PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33688971-0	2021	Effect of irradiation on the expression of E-cadherin and beta-catenin in early and late radiation sequelae of the urinary bladder and its modulation by NF-kappaB inhibitor thalidomide.	Thalidomide	173-184	cadherin 1	Mus musculus	43-53
6548496-0	1984	Thalidomide in lepra reaction (ENL) in lepromatous leprosy patients.	Thalidomide	0-11	MLLT1 super elongation complex subunit	Homo sapiens	31-34
6548496-6	1984	Control of ENL reaction by thalidomide in these patients is probably due to its immunosuppressive effect, more likely by its stablising action on lysosomes.	Thalidomide	27-38	MLLT1 super elongation complex subunit	Homo sapiens	11-14
5300279-0	1966	[Thalidomide: effect on serum ceruloplasmin].	Thalidomide	1-12	ceruloplasmin	Homo sapiens	30-43
33878647-0	2021	Design and linkage optimization of ursane-thalidomide-based PROTACs and identification of their targeted-degradation properties to MDM2 protein.	Thalidomide	42-53	transformed mouse 3T3 cell double minute 2	Mus musculus	131-135
3970671-7	1985	Glucagon administration (GLUPAN) transiently increased CI and QP but failed to improve O2CP and did not change QAVS.	Thalidomide	25-31	glucagon	Canis lupus familiaris	0-8
700507-3	1978	Contrary to N-ethyl-maleimide, thalidomide does not block the SH groups irreversible, and they can be reactivated with BAL.	Thalidomide	31-42	solute carrier family 27 member 5	Rattus norvegicus	119-122
5593734-1	1967	On the necessary 2nd noxa in experimental thalidomide embryopathies].	Thalidomide	42-53	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	21-25
33780898-0	2021	Discovery of thalidomide-based PROTAC small molecules as the highly efficient SHP2 degraders.	Thalidomide	13-24	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	78-82
33780898-4	2021	Herein we described the design, synthesis and evaluation of a series of thalidomide-based heterobifunctional molecules and identified 11(ZB-S-29) as the highly efficient SHP2 degrader with a DC50 of 6.02 nM.	Thalidomide	72-83	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	170-174
33688971-0	2021	Effect of irradiation on the expression of E-cadherin and beta-catenin in early and late radiation sequelae of the urinary bladder and its modulation by NF-kappaB inhibitor thalidomide.	Thalidomide	173-184	catenin (cadherin associated protein), beta 1	Mus musculus	58-70
33688971-0	2021	Effect of irradiation on the expression of E-cadherin and beta-catenin in early and late radiation sequelae of the urinary bladder and its modulation by NF-kappaB inhibitor thalidomide.	Thalidomide	173-184	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	153-162
33688971-1	2021	PURPOSE: In a previous study we have shown in a mouse model that administration of nuclear factor-kappa B (NF-kappaB) inhibitor thalidomide has promising therapeutic effects on early radiation cystitis (ERC) and late radiation sequelae (LRS) of the urinary bladder.	Thalidomide	128-139	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-105
33688971-1	2021	PURPOSE: In a previous study we have shown in a mouse model that administration of nuclear factor-kappa B (NF-kappaB) inhibitor thalidomide has promising therapeutic effects on early radiation cystitis (ERC) and late radiation sequelae (LRS) of the urinary bladder.	Thalidomide	128-139	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	107-116
33688971-7	2021	Early administration of thalidomide (day 1-15) resulted in a steeper rise in the first days, an extended and increased expression at the end of the early phase and a higher expression of beta-catenin alone at the beginning of the late phase.	Thalidomide	24-35	catenin (cadherin associated protein), beta 1	Mus musculus	187-199
33688971-9	2021	Early administration of thalidomide improves these compensatory mechanisms by inhibiting NF-kappaB signaling and its interfering effects.	Thalidomide	24-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	89-98
33751979-3	2021	We firstly screened CRBN ligands as the E3 ligase moiety, then obtained a series of potent ALK degraders based on different CRBN ligands, exemplified by SIAIS091 and SIAIS001 with lenalidomide/thalidomide-based linkers.	Thalidomide	193-204	ALK receptor tyrosine kinase	Homo sapiens	91-94
34048672-6	2021	Fusing thalidomide-the ligand of the cereblon ubiquitin ligase-to O4I2 led to a new PROTAC-O4I2, which selectively degraded SF3B1 and induced cellular apoptosis in a CRBN-dependent manner.	Thalidomide	7-18	splicing factor 3b subunit 1	Homo sapiens	124-129
34048672-6	2021	Fusing thalidomide-the ligand of the cereblon ubiquitin ligase-to O4I2 led to a new PROTAC-O4I2, which selectively degraded SF3B1 and induced cellular apoptosis in a CRBN-dependent manner.	Thalidomide	7-18	cereblon	Homo sapiens	166-170
33975771-0	2021	Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-kappaB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	74-83
33975771-0	2021	Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-kappaB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.	Thalidomide	0-11	NLR family, pyrin domain containing 3	Mus musculus	85-90
33975771-0	2021	Thalidomide reduces glycerol-induced acute kidney injury by inhibition of NF-kappaB, NLRP3 inflammasome, COX-2 and inflammatory cytokines.	Thalidomide	0-11	cytochrome c oxidase II, mitochondrial	Mus musculus	105-110
33687083-12	2021	Thalidomide (30-100 microM) inhibited noradrenaline-, phenylephrine-, and methoxamine-induced contractions, as well as nonadrenergic contractions induced by endothelin-1 and U46619, and neurogenic contractions induced by EFS.	Thalidomide	0-11	endothelin 1	Homo sapiens	157-169
34033753-1	2021	Cereblon (CRBN), originally identified as a gene associated with intellectual disability, was identified as primary target of thalidomide.	Thalidomide	126-137	cereblon	Homo sapiens	0-8
34033753-1	2021	Cereblon (CRBN), originally identified as a gene associated with intellectual disability, was identified as primary target of thalidomide.	Thalidomide	126-137	cereblon	Homo sapiens	10-14
34033753-2	2021	Accumulating evidence has shown that CRBN is a substrate receptor of Cullin Ring E3 ubiquitin ligase 4 (CRL4) containing DDB1, CUL4, and RBX1, which recognizes specific neosubstrates in the presence of thalidomide or its analogs and induces their ubiquitination and proteasomal degradation.	Thalidomide	202-213	cereblon	Homo sapiens	37-41
34033753-2	2021	Accumulating evidence has shown that CRBN is a substrate receptor of Cullin Ring E3 ubiquitin ligase 4 (CRL4) containing DDB1, CUL4, and RBX1, which recognizes specific neosubstrates in the presence of thalidomide or its analogs and induces their ubiquitination and proteasomal degradation.	Thalidomide	202-213	CDK2 associated cullin domain 1	Homo sapiens	69-75
34033753-2	2021	Accumulating evidence has shown that CRBN is a substrate receptor of Cullin Ring E3 ubiquitin ligase 4 (CRL4) containing DDB1, CUL4, and RBX1, which recognizes specific neosubstrates in the presence of thalidomide or its analogs and induces their ubiquitination and proteasomal degradation.	Thalidomide	202-213	interleukin 17 receptor B	Homo sapiens	104-108
34033753-2	2021	Accumulating evidence has shown that CRBN is a substrate receptor of Cullin Ring E3 ubiquitin ligase 4 (CRL4) containing DDB1, CUL4, and RBX1, which recognizes specific neosubstrates in the presence of thalidomide or its analogs and induces their ubiquitination and proteasomal degradation.	Thalidomide	202-213	damage specific DNA binding protein 1	Homo sapiens	121-125
34033753-2	2021	Accumulating evidence has shown that CRBN is a substrate receptor of Cullin Ring E3 ubiquitin ligase 4 (CRL4) containing DDB1, CUL4, and RBX1, which recognizes specific neosubstrates in the presence of thalidomide or its analogs and induces their ubiquitination and proteasomal degradation.	Thalidomide	202-213	ring-box 1	Homo sapiens	137-141
33938033-1	2021	Thalidomide and its derivatives lenalidomide and pomalidomide, known as immunomodulatory drugs, (IMiDs) bind directly to cereblon (CRBN), a substrate receptor of an E3 ubiquitin ligase, resulting in the rapid ubiquitination and degradation of the substrate protein.	Thalidomide	0-11	cereblon	Homo sapiens	131-135
33938033-3	2021	To date, almost all CRBN ligands are derived from thalidomide and there are few structural differences between them.	Thalidomide	50-61	cereblon	Homo sapiens	20-24
33206273-0	2021	Thalidomide Inhibits Angiogenesis via Downregulation of VEGF and Angiopoietin-2 in Crohn"s Disease.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	56-60
33926033-0	2021	Chemical Degradation of Androgen Receptor (AR) Using Bicalutamide Analog-Thalidomide PROTACs.	Thalidomide	73-84	androgen receptor	Homo sapiens	24-41
33926033-0	2021	Chemical Degradation of Androgen Receptor (AR) Using Bicalutamide Analog-Thalidomide PROTACs.	Thalidomide	73-84	androgen receptor	Homo sapiens	43-45
33926033-1	2021	A series of PROTACs (PROteolysis-TArgeting Chimeras) consisting of bicalutamide analogs and thalidomides were designed, synthesized, and biologically evaluated as novel androgen receptor (AR) degraders.	Thalidomide	92-104	androgen receptor	Homo sapiens	169-186
33926033-1	2021	A series of PROTACs (PROteolysis-TArgeting Chimeras) consisting of bicalutamide analogs and thalidomides were designed, synthesized, and biologically evaluated as novel androgen receptor (AR) degraders.	Thalidomide	92-104	androgen receptor	Homo sapiens	188-190
33206273-8	2021	Thalidomide produced a significant reduction in protein expression of Ang-2 and VEGF, along with a decrease in mRNA expression of Ang-2.	Thalidomide	0-11	angiopoietin 2	Homo sapiens	70-75
33206273-8	2021	Thalidomide produced a significant reduction in protein expression of Ang-2 and VEGF, along with a decrease in mRNA expression of Ang-2.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	80-84
33206273-0	2021	Thalidomide Inhibits Angiogenesis via Downregulation of VEGF and Angiopoietin-2 in Crohn"s Disease.	Thalidomide	0-11	angiopoietin 2	Homo sapiens	65-79
33206273-8	2021	Thalidomide produced a significant reduction in protein expression of Ang-2 and VEGF, along with a decrease in mRNA expression of Ang-2.	Thalidomide	0-11	angiopoietin 2	Homo sapiens	130-135
33206273-13	2021	It also indicated that thalidomide can be able to deactivate endothelium by the downregulation effect on angiogenic factors by targeting VEGF and Ang-2.	Thalidomide	23-34	vascular endothelial growth factor A	Homo sapiens	137-141
33206273-13	2021	It also indicated that thalidomide can be able to deactivate endothelium by the downregulation effect on angiogenic factors by targeting VEGF and Ang-2.	Thalidomide	23-34	angiopoietin 2	Homo sapiens	146-151
33465355-1	2021	In the present investigation, we tested the hypothesis that suppression of the phospho-extracellular signal regulated kinase (pERK1/2)-nuclear factor kappa (NFkappa)-B signaling, subsequent to tumor necrosis factor-alpha (TNF-alpha) inhibition, underlies thalidomide (TLM) mediated neuroprotection.	Thalidomide	255-266	tumor necrosis factor	Rattus norvegicus	193-220
33249990-2	2021	The pharmacological effects of thalidomide are attributed to its anti-angiogenic, anti-inflammatory and modulatory effect on cytokines principally tumor necrosis factor-alpha, while the teratogenic effects are linked to two molecular targets, namely cereblon and tubulin.	Thalidomide	31-42	tumor necrosis factor	Homo sapiens	147-174
33517358-8	2021	Metformin, thalidomide and cytokines (IFN, tumor necrosis factor (TNF), interleukin-2 (IL-2) and others) have pleiomorphic activities, some of which can enhance tumorigenesis.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	43-64
33517358-8	2021	Metformin, thalidomide and cytokines (IFN, tumor necrosis factor (TNF), interleukin-2 (IL-2) and others) have pleiomorphic activities, some of which can enhance tumorigenesis.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	66-69
33517358-8	2021	Metformin, thalidomide and cytokines (IFN, tumor necrosis factor (TNF), interleukin-2 (IL-2) and others) have pleiomorphic activities, some of which can enhance tumorigenesis.	Thalidomide	11-22	interleukin 2	Homo sapiens	72-85
33517358-8	2021	Metformin, thalidomide and cytokines (IFN, tumor necrosis factor (TNF), interleukin-2 (IL-2) and others) have pleiomorphic activities, some of which can enhance tumorigenesis.	Thalidomide	11-22	interleukin 2	Homo sapiens	87-91
33465355-1	2021	In the present investigation, we tested the hypothesis that suppression of the phospho-extracellular signal regulated kinase (pERK1/2)-nuclear factor kappa (NFkappa)-B signaling, subsequent to tumor necrosis factor-alpha (TNF-alpha) inhibition, underlies thalidomide (TLM) mediated neuroprotection.	Thalidomide	255-266	tumor necrosis factor	Rattus norvegicus	222-231
33465355-1	2021	In the present investigation, we tested the hypothesis that suppression of the phospho-extracellular signal regulated kinase (pERK1/2)-nuclear factor kappa (NFkappa)-B signaling, subsequent to tumor necrosis factor-alpha (TNF-alpha) inhibition, underlies thalidomide (TLM) mediated neuroprotection.	Thalidomide	268-271	tumor necrosis factor	Rattus norvegicus	193-220
33465355-1	2021	In the present investigation, we tested the hypothesis that suppression of the phospho-extracellular signal regulated kinase (pERK1/2)-nuclear factor kappa (NFkappa)-B signaling, subsequent to tumor necrosis factor-alpha (TNF-alpha) inhibition, underlies thalidomide (TLM) mediated neuroprotection.	Thalidomide	268-271	tumor necrosis factor	Rattus norvegicus	222-231
33465355-5	2021	Unilateral intra-hippocampal TLM ameliorated these behavioral deficits along with the following ex vivo hippocampal effects: (i) abrogation of the IR-evoked elevations in hippocampal TNF-alpha, pERK1/2, NFkappaB, BDNF, iNOS contents and (ii) partial restoration of the reduced anti-inflammatory cytokine IL-10 and p-nNOS S852.	Thalidomide	29-32	tumor necrosis factor	Rattus norvegicus	183-192
33465355-5	2021	Unilateral intra-hippocampal TLM ameliorated these behavioral deficits along with the following ex vivo hippocampal effects: (i) abrogation of the IR-evoked elevations in hippocampal TNF-alpha, pERK1/2, NFkappaB, BDNF, iNOS contents and (ii) partial restoration of the reduced anti-inflammatory cytokine IL-10 and p-nNOS S852.	Thalidomide	29-32	brain-derived neurotrophic factor	Rattus norvegicus	213-217
33465355-5	2021	Unilateral intra-hippocampal TLM ameliorated these behavioral deficits along with the following ex vivo hippocampal effects: (i) abrogation of the IR-evoked elevations in hippocampal TNF-alpha, pERK1/2, NFkappaB, BDNF, iNOS contents and (ii) partial restoration of the reduced anti-inflammatory cytokine IL-10 and p-nNOS S852.	Thalidomide	29-32	nitric oxide synthase 2	Rattus norvegicus	219-223
33465355-5	2021	Unilateral intra-hippocampal TLM ameliorated these behavioral deficits along with the following ex vivo hippocampal effects: (i) abrogation of the IR-evoked elevations in hippocampal TNF-alpha, pERK1/2, NFkappaB, BDNF, iNOS contents and (ii) partial restoration of the reduced anti-inflammatory cytokine IL-10 and p-nNOS S852.	Thalidomide	29-32	interleukin 10	Rattus norvegicus	304-309
33465355-5	2021	Unilateral intra-hippocampal TLM ameliorated these behavioral deficits along with the following ex vivo hippocampal effects: (i) abrogation of the IR-evoked elevations in hippocampal TNF-alpha, pERK1/2, NFkappaB, BDNF, iNOS contents and (ii) partial restoration of the reduced anti-inflammatory cytokine IL-10 and p-nNOS S852.	Thalidomide	29-32	nitric oxide synthase 1	Rattus norvegicus	316-320
33015978-8	2021	Altered expression of miR-141 and HDAC6 was introduced to identify their functions in thalidomide-mediated events.	Thalidomide	86-97	histone deacetylase 6	Rattus norvegicus	34-39
33470442-0	2021	Thalidomide and its metabolite 5-hydroxythalidomide induce teratogenicity via the cereblon neosubstrate PLZF.	Thalidomide	0-11	zinc finger and BTB domain containing 16	Homo sapiens	104-108
33470442-1	2021	Thalidomide causes teratogenic effects by inducing protein degradation via cereblon (CRBN)-containing ubiquitin ligase and modification of its substrate specificity.	Thalidomide	0-11	cereblon	Gallus gallus	85-89
33470442-3	2021	Here, we report that promyelocytic leukaemia zinc finger (PLZF)/ZBTB16 is a CRBN target protein whose degradation is involved in thalidomide- and 5-hydroxythalidomide-induced teratogenicity.	Thalidomide	129-140	zinc finger and BTB domain containing 16	Homo sapiens	58-62
33470442-3	2021	Here, we report that promyelocytic leukaemia zinc finger (PLZF)/ZBTB16 is a CRBN target protein whose degradation is involved in thalidomide- and 5-hydroxythalidomide-induced teratogenicity.	Thalidomide	129-140	zinc finger and BTB domain containing 32	Gallus gallus	64-70
33470442-3	2021	Here, we report that promyelocytic leukaemia zinc finger (PLZF)/ZBTB16 is a CRBN target protein whose degradation is involved in thalidomide- and 5-hydroxythalidomide-induced teratogenicity.	Thalidomide	129-140	cereblon	Homo sapiens	76-80
33547076-3	2021	For example, thalidomide-like drugs (IMiDs) degrade the critical multiple myeloma transcription factors IKZF1 and IKZF3 by recruiting them to the cereblon E3 ubiquitin ligase.	Thalidomide	13-24	IKAROS family zinc finger 1	Homo sapiens	104-109
33547076-3	2021	For example, thalidomide-like drugs (IMiDs) degrade the critical multiple myeloma transcription factors IKZF1 and IKZF3 by recruiting them to the cereblon E3 ubiquitin ligase.	Thalidomide	13-24	IKAROS family zinc finger 3	Homo sapiens	114-119
33015978-8	2021	Altered expression of miR-141 and HDAC6 was introduced to identify their functions in thalidomide-mediated events.	Thalidomide	86-97	microRNA 141	Rattus norvegicus	22-29
33015978-12	2021	miR-141 was responsible for thalidomide-mediated protective events by targeting HDAC6.	Thalidomide	28-39	microRNA 141	Rattus norvegicus	0-7
33015978-12	2021	miR-141 was responsible for thalidomide-mediated protective events by targeting HDAC6.	Thalidomide	28-39	histone deacetylase 6	Rattus norvegicus	80-85
33470442-4	2021	Using a human transcription factor protein array produced in a wheat cell-free protein synthesis system, PLZF was identified as a thalidomide-dependent CRBN substrate.	Thalidomide	130-141	zinc finger and BTB domain containing 16	Homo sapiens	105-109
33470442-4	2021	Using a human transcription factor protein array produced in a wheat cell-free protein synthesis system, PLZF was identified as a thalidomide-dependent CRBN substrate.	Thalidomide	130-141	cereblon	Homo sapiens	152-156
33470442-5	2021	PLZF is degraded by the ubiquitin ligase CRL4CRBN in complex with thalidomide, its derivatives or 5-hydroxythalidomide in a manner dependent on the conserved first and third zinc finger domains of PLZF.	Thalidomide	66-77	zinc finger and BTB domain containing 16	Homo sapiens	0-4
33470442-5	2021	PLZF is degraded by the ubiquitin ligase CRL4CRBN in complex with thalidomide, its derivatives or 5-hydroxythalidomide in a manner dependent on the conserved first and third zinc finger domains of PLZF.	Thalidomide	66-77	cereblon	Homo sapiens	45-49
33470442-5	2021	PLZF is degraded by the ubiquitin ligase CRL4CRBN in complex with thalidomide, its derivatives or 5-hydroxythalidomide in a manner dependent on the conserved first and third zinc finger domains of PLZF.	Thalidomide	66-77	zinc finger and BTB domain containing 16	Homo sapiens	197-201
33470442-6	2021	Surprisingly, thalidomide and 5-hydroxythalidomide confer distinctly different substrate specificities to mouse and chicken CRBN, and both compounds cause teratogenic phenotypes in chicken embryos.	Thalidomide	14-25	cereblon	Gallus gallus	124-128
33470442-8	2021	Most importantly, degradation of PLZF protein, but not of the known thalidomide-dependent CRBN substrate SALL4, was induced by thalidomide or 5-hydroxythalidomide treatment in chicken embryos.	Thalidomide	127-138	zinc finger and BTB domain containing 16	Homo sapiens	33-37
33470442-9	2021	Furthermore, PLZF overexpression partially rescued the thalidomide-induced phenotypes.	Thalidomide	55-66	zinc finger and BTB domain containing 16	Homo sapiens	13-17
33470442-10	2021	Our findings implicate PLZF as an important thalidomide-induced CRBN neosubstrate involved in thalidomide teratogenicity.	Thalidomide	44-55	zinc finger and BTB domain containing 16	Homo sapiens	23-27
33470442-10	2021	Our findings implicate PLZF as an important thalidomide-induced CRBN neosubstrate involved in thalidomide teratogenicity.	Thalidomide	44-55	cereblon	Gallus gallus	64-68
33470442-10	2021	Our findings implicate PLZF as an important thalidomide-induced CRBN neosubstrate involved in thalidomide teratogenicity.	Thalidomide	94-105	zinc finger and BTB domain containing 16	Homo sapiens	23-27
33470442-10	2021	Our findings implicate PLZF as an important thalidomide-induced CRBN neosubstrate involved in thalidomide teratogenicity.	Thalidomide	94-105	cereblon	Gallus gallus	64-68
33015978-13	2021	Overexpression of HDAC6 blocked the protection of thalidomide against PQ-induced injury via activating the IkBalpha-NF-kappaB signalling pathway.	Thalidomide	50-61	histone deacetylase 6	Rattus norvegicus	18-23
33015978-14	2021	Collectively, this study evidenced that thalidomide protects lung tissues from PQ-induced injury through a miR-141/HDAC6/IkBalpha-NF-kappaB axis.	Thalidomide	40-51	microRNA 141	Rattus norvegicus	107-114
33015978-14	2021	Collectively, this study evidenced that thalidomide protects lung tissues from PQ-induced injury through a miR-141/HDAC6/IkBalpha-NF-kappaB axis.	Thalidomide	40-51	histone deacetylase 6	Rattus norvegicus	115-120
33333254-7	2021	The mean reduction rates at 7-10 days after treatment for serum interleukin-6 and interferon-gamma concentrations were greater in the thalidomide group compared to the controls.	Thalidomide	134-145	interleukin 6	Homo sapiens	64-77
33333254-7	2021	The mean reduction rates at 7-10 days after treatment for serum interleukin-6 and interferon-gamma concentrations were greater in the thalidomide group compared to the controls.	Thalidomide	134-145	interferon gamma	Homo sapiens	82-98
33416146-2	2021	The expression level of DEPTOR is closely related to the prognosis of patients with MM treated with the antiangiogenic agent thalidomide; however, its role in the regulation of angiogenesis has not yet been elucidated.	Thalidomide	125-136	DEP domain containing MTOR interacting protein	Homo sapiens	24-30
32008086-0	2020	Thalidomide targets EGFL6 to inhibit EGFL6/PAX6 axis-driven angiogenesis in small bowel vascular malformation.	Thalidomide	0-11	EGF like domain multiple 6	Homo sapiens	20-25
33127336-8	2021	An examination of the contribution of Tnfa in allograft response revealed that it was prospectively antagonized by etanercept or thalidomide, which resolved cytokine, chemokine, and receptor cascades.	Thalidomide	129-140	tumor necrosis factor	Rattus norvegicus	38-42
33310190-1	2021	Cereblon (CRBN), the substrate receptor of an E3 ubiquitin ligase complex, is a target of thalidomide and thalidomide-derived immunomodulatory drugs (IMiDs).	Thalidomide	90-101	cereblon	Homo sapiens	0-8
33310190-1	2021	Cereblon (CRBN), the substrate receptor of an E3 ubiquitin ligase complex, is a target of thalidomide and thalidomide-derived immunomodulatory drugs (IMiDs).	Thalidomide	90-101	cereblon	Homo sapiens	10-14
33310190-1	2021	Cereblon (CRBN), the substrate receptor of an E3 ubiquitin ligase complex, is a target of thalidomide and thalidomide-derived immunomodulatory drugs (IMiDs).	Thalidomide	106-117	cereblon	Homo sapiens	0-8
33310190-1	2021	Cereblon (CRBN), the substrate receptor of an E3 ubiquitin ligase complex, is a target of thalidomide and thalidomide-derived immunomodulatory drugs (IMiDs).	Thalidomide	106-117	cereblon	Homo sapiens	10-14
33745380-7	2021	Pharmacological inhibition of PI3K or JNK, using thalidomide, quercetin, or SP600125, attenuated the development of morphine tolerance in mice with SNL as measured by thermal paw withdrawal.	Thalidomide	49-60	mitogen-activated protein kinase 8	Mus musculus	38-41
33317522-0	2020	Oxidative stress mediates thalidomide-induced pain by targeting peripheral TRPA1 and central TRPV4.	Thalidomide	26-37	transient receptor potential cation channel subfamily A member 1	Homo sapiens	75-80
33317522-0	2020	Oxidative stress mediates thalidomide-induced pain by targeting peripheral TRPA1 and central TRPV4.	Thalidomide	26-37	transient receptor potential cation channel subfamily V member 4	Homo sapiens	93-98
33317522-11	2020	CONCLUSIONS: Targeting of peripheral TRPA1 and central TRPV4 may be required to attenuate pain associated with CIPN elicited by thalidomide and related drugs.	Thalidomide	128-139	transient receptor potential cation channel subfamily A member 1	Homo sapiens	37-42
33317522-11	2020	CONCLUSIONS: Targeting of peripheral TRPA1 and central TRPV4 may be required to attenuate pain associated with CIPN elicited by thalidomide and related drugs.	Thalidomide	128-139	transient receptor potential cation channel subfamily V member 4	Homo sapiens	55-60
33527793-8	2021	Corresponding to increased CTLA-4 expression in T cells, the expression of ligand molecules for CTLA-4 significantly increased in splenic dendritic cells in TM/DX-treated groups.	Thalidomide	157-159	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	27-33
33527793-8	2021	Corresponding to increased CTLA-4 expression in T cells, the expression of ligand molecules for CTLA-4 significantly increased in splenic dendritic cells in TM/DX-treated groups.	Thalidomide	157-159	cytotoxic T-lymphocyte-associated protein 4	Mus musculus	96-102
32979866-3	2021	However, this may not be the sole mechanism involved since the blockade of TNF-alpha synthesis by thalidomide prevents hyperalgesia without interrupting the synthesis of IL-1beta, IL-6 and CINC-1.	Thalidomide	98-109	tumor necrosis factor	Rattus norvegicus	75-84
33275735-2	2020	Currently, there are 3 CD38 antibody-based regimens approved for the treatment of both transplant-eligible (daratumumab plus bortezomib-thalidomide-dexamethasone [D-VTd]) and transplant-ineligible (daratumumab plus lenalidomide-dexamethasone [D-Rd] or daratumumab plus bortezomib-melphalan-prednisone [D-VMP]) patients with newly diagnosed MM (NDMM).	Thalidomide	136-147	CD38 molecule	Homo sapiens	23-27
32008086-0	2020	Thalidomide targets EGFL6 to inhibit EGFL6/PAX6 axis-driven angiogenesis in small bowel vascular malformation.	Thalidomide	0-11	EGF like domain multiple 6	Homo sapiens	37-42
32008086-0	2020	Thalidomide targets EGFL6 to inhibit EGFL6/PAX6 axis-driven angiogenesis in small bowel vascular malformation.	Thalidomide	0-11	paired box 6	Homo sapiens	43-47
32008086-8	2020	Furthermore, through in vitro and in vivo assays, we elucidated that thalidomide can function as anti-angiogenesis medicine through the regulation of EGFL6 in a proteasome-dependent manner.	Thalidomide	69-80	EGF like domain multiple 6	Homo sapiens	150-155
32008086-9	2020	Finally, we found that CRBN can mediate the effect of thalidomide on EGFL6 expression and that the CRBN protein interacts with EGFL6 via a Lon N-terminal peptide.	Thalidomide	54-65	cereblon	Homo sapiens	23-27
32008086-9	2020	Finally, we found that CRBN can mediate the effect of thalidomide on EGFL6 expression and that the CRBN protein interacts with EGFL6 via a Lon N-terminal peptide.	Thalidomide	54-65	EGF like domain multiple 6	Homo sapiens	69-74
32008086-9	2020	Finally, we found that CRBN can mediate the effect of thalidomide on EGFL6 expression and that the CRBN protein interacts with EGFL6 via a Lon N-terminal peptide.	Thalidomide	54-65	EGF like domain multiple 6	Homo sapiens	127-132
32008086-10	2020	CONCLUSION: Our findings revealed a key role for EGFL6 in SBVM pathogenesis and provided a mechanism explaining why thalidomide can cure small bowel bleeding resulting from SBVM.	Thalidomide	116-127	EGF like domain multiple 6	Homo sapiens	49-54
32865967-1	2020	Cereblon (CRBN) is an E3 ligase adapter protein that can be reprogrammed by imide-class compounds such as thalidomide, lenalidomide, and pomalidomide to induce the degradation of neo-substrate proteins.	Thalidomide	106-117	cereblon	Homo sapiens	0-8
32778513-12	2020	Splicing mutations were common in both cohorts, though thalidomide-treated patients were more likely to have a high-risk SRSF2 or U2AF1 Q157 mutation (P = .01).	Thalidomide	55-66	serine and arginine rich splicing factor 2	Homo sapiens	121-126
32778513-12	2020	Splicing mutations were common in both cohorts, though thalidomide-treated patients were more likely to have a high-risk SRSF2 or U2AF1 Q157 mutation (P = .01).	Thalidomide	55-66	U2 small nuclear RNA auxiliary factor 1	Homo sapiens	130-135
33070611-7	2020	Our cereblon TR-FRET binding assay was very stable and detected changes in phthalimide activity due to thalidomide isomerization.	Thalidomide	103-114	cereblon	Homo sapiens	4-12
32865967-1	2020	Cereblon (CRBN) is an E3 ligase adapter protein that can be reprogrammed by imide-class compounds such as thalidomide, lenalidomide, and pomalidomide to induce the degradation of neo-substrate proteins.	Thalidomide	106-117	cereblon	Homo sapiens	10-14
32729462-1	2020	None: Recent developments in the genetics of restless legs syndrome (RLS) revealed associations of disease risk with genetic loci containing the genes coding cereblon, the protein bound by thalidomide, and its endogenous substrate MEIS2 whose degradation is inhibited by the thalidomide-cereblon interaction.	Thalidomide	275-286	Meis homeobox 2	Homo sapiens	231-236
32848052-1	2020	Thalidomide exerts its teratogenic and immunomodulatory effects by binding to cereblon (CRBN) and thereby inhibiting/modifying the CRBN-mediated ubiquitination pathway consisting of the Cullin4-DDB1-ROC1 E3 ligase complex.	Thalidomide	0-11	cereblon	Mus musculus	88-92
33008427-5	2020	METHODS: MUK eight is a randomised, controlled, open, parallel group, multi-centre phase II trial that will recruit patients with RRMM who have relapsed after treatment with thalidomide, lenalidomide, and a proteasome inhibitor.	Thalidomide	174-185	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	9-12
32800337-5	2020	Immunofluorescence analysis showed decrease of VEGFA expression in both ARPE-19 cells and HUVECs after treatment only with thalidomide but not with senicapoc or sodium butyrate.	Thalidomide	123-134	vascular endothelial growth factor A	Homo sapiens	47-52
32800337-9	2020	Thalidomide also reduced cobalt chloride induced increase of VEGFA mRNA in ARPE-19 (-33%) and protein in culture medium (-20%).	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	61-66
32848052-1	2020	Thalidomide exerts its teratogenic and immunomodulatory effects by binding to cereblon (CRBN) and thereby inhibiting/modifying the CRBN-mediated ubiquitination pathway consisting of the Cullin4-DDB1-ROC1 E3 ligase complex.	Thalidomide	0-11	cereblon	Mus musculus	131-135
32929090-2	2020	Here, we report the structural bases for the SALL4-specific proteasomal degradation induced by 5-hydroxythalidomide, a primary thalidomide metabolite generated by the enzymatic activity of cytochrome P450 isozymes, through the interaction with cereblon (CRBN).	Thalidomide	104-115	spalt like transcription factor 4	Homo sapiens	45-50
32848052-1	2020	Thalidomide exerts its teratogenic and immunomodulatory effects by binding to cereblon (CRBN) and thereby inhibiting/modifying the CRBN-mediated ubiquitination pathway consisting of the Cullin4-DDB1-ROC1 E3 ligase complex.	Thalidomide	0-11	damage specific DNA binding protein 1	Mus musculus	194-198
32848052-1	2020	Thalidomide exerts its teratogenic and immunomodulatory effects by binding to cereblon (CRBN) and thereby inhibiting/modifying the CRBN-mediated ubiquitination pathway consisting of the Cullin4-DDB1-ROC1 E3 ligase complex.	Thalidomide	0-11	ring-box 1	Mus musculus	199-203
32848052-3	2020	Here we examined whether CRBN is involved in the hypnotic effect of thalidomide by generating mice harboring a thalidomide-resistant mutant allele of Crbn (Crbn YW/AA knock-in mice).	Thalidomide	68-79	cereblon	Mus musculus	25-29
32848052-4	2020	Thalidomide increased non-REM sleep time in Crbn YW/AA knock-in homozygotes and heterozygotes to a similar degree as seen in wild-type littermates.	Thalidomide	0-11	cereblon	Mus musculus	44-48
32848052-5	2020	Thalidomide similarly depressed excitatory synaptic transmission in the cortical slices obtained from wild-type and Crbn YW/AA homozygous knock-in mice without affecting GABAergic inhibition.	Thalidomide	0-11	cereblon	Mus musculus	116-120
32848052-6	2020	Thalidomide induced Fos expression in vasopressin-containing neurons of the supraoptic nucleus and reduced Fos expression in the tuberomammillary nuclei.	Thalidomide	0-11	FBJ osteosarcoma oncogene	Mus musculus	20-23
32848052-6	2020	Thalidomide induced Fos expression in vasopressin-containing neurons of the supraoptic nucleus and reduced Fos expression in the tuberomammillary nuclei.	Thalidomide	0-11	FBJ osteosarcoma oncogene	Mus musculus	107-110
32929090-1	2020	Thalidomide and its derivatives exert not only therapeutic effects as immunomodulatory drugs (IMiDs) but also adverse effects such as teratogenicity, which are due in part to different C2H2 zinc-finger (ZF) transcription factors, IKZF1 (or IKZF3) and SALL4, respectively.	Thalidomide	0-11	IKAROS family zinc finger 1	Homo sapiens	230-235
32929090-1	2020	Thalidomide and its derivatives exert not only therapeutic effects as immunomodulatory drugs (IMiDs) but also adverse effects such as teratogenicity, which are due in part to different C2H2 zinc-finger (ZF) transcription factors, IKZF1 (or IKZF3) and SALL4, respectively.	Thalidomide	0-11	IKAROS family zinc finger 3	Homo sapiens	240-245
32929090-1	2020	Thalidomide and its derivatives exert not only therapeutic effects as immunomodulatory drugs (IMiDs) but also adverse effects such as teratogenicity, which are due in part to different C2H2 zinc-finger (ZF) transcription factors, IKZF1 (or IKZF3) and SALL4, respectively.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	251-256
32929090-2	2020	Here, we report the structural bases for the SALL4-specific proteasomal degradation induced by 5-hydroxythalidomide, a primary thalidomide metabolite generated by the enzymatic activity of cytochrome P450 isozymes, through the interaction with cereblon (CRBN).	Thalidomide	104-115	cereblon	Homo sapiens	254-258
32367505-7	2020	In contrast to this, Snap25 expression, studied in males, was increased in the hippocampus and cerebellum in both, VPA- and THAL-treated rats.	Thalidomide	124-128	synaptosome associated protein 25	Rattus norvegicus	21-27
32387854-0	2020	The association of HBG2, BCL11A, and HBS1L-MYB polymorphisms to thalidomide response in Chinese beta-thalassemia patients.	Thalidomide	64-75	hemoglobin subunit gamma 2	Homo sapiens	19-23
32387854-0	2020	The association of HBG2, BCL11A, and HBS1L-MYB polymorphisms to thalidomide response in Chinese beta-thalassemia patients.	Thalidomide	64-75	HBS1 like translational GTPase	Homo sapiens	37-42
32387854-0	2020	The association of HBG2, BCL11A, and HBS1L-MYB polymorphisms to thalidomide response in Chinese beta-thalassemia patients.	Thalidomide	64-75	MYB proto-oncogene, transcription factor	Homo sapiens	43-46
32387854-10	2020	It was demonstrated that SNPs in HBG2 and HBS1L-MYB contributed significantly to thalidomide response in Chinese patients with beta-thalassemia and that the cumulative number of minor SNP alleles may serve as good predictors of treatment response in this population.	Thalidomide	81-92	hemoglobin subunit gamma 2	Homo sapiens	33-37
32387854-10	2020	It was demonstrated that SNPs in HBG2 and HBS1L-MYB contributed significantly to thalidomide response in Chinese patients with beta-thalassemia and that the cumulative number of minor SNP alleles may serve as good predictors of treatment response in this population.	Thalidomide	81-92	HBS1 like translational GTPase	Homo sapiens	42-47
32387854-10	2020	It was demonstrated that SNPs in HBG2 and HBS1L-MYB contributed significantly to thalidomide response in Chinese patients with beta-thalassemia and that the cumulative number of minor SNP alleles may serve as good predictors of treatment response in this population.	Thalidomide	81-92	MYB proto-oncogene, transcription factor	Homo sapiens	48-51
32634680-2	2020	These proteolysis targeted chimeras (PROTACs) are based on an ATP competitive inhibitor of p38alpha and p38beta, which is linked to thalidomide analogues to recruit the Cereblon E3 ubiquitin ligase complex.	Thalidomide	132-143	mitogen-activated protein kinase 14	Homo sapiens	91-99
32634680-2	2020	These proteolysis targeted chimeras (PROTACs) are based on an ATP competitive inhibitor of p38alpha and p38beta, which is linked to thalidomide analogues to recruit the Cereblon E3 ubiquitin ligase complex.	Thalidomide	132-143	mitogen-activated protein kinase 11	Homo sapiens	104-111
32935774-1	2020	INTRODUCTION: Thalidomide is an anti- tumor necrosis factor alpha (TNF-a) drug used mainly in the management of moderate to severe form of Erythema Nodosum Leprosum (ENL).	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	38-65
32935774-1	2020	INTRODUCTION: Thalidomide is an anti- tumor necrosis factor alpha (TNF-a) drug used mainly in the management of moderate to severe form of Erythema Nodosum Leprosum (ENL).	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	67-72
32819116-0	2020	Thalidomide inhibits the gene promoter of connective tissue growth factor in human embryonic lung fibroblasts.	Thalidomide	0-11	cellular communication network factor 2	Homo sapiens	42-73
32819116-2	2020	It"s necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-beta1 (TGF-beta1) in human embryonic lung fibroblast (HELF).	Thalidomide	44-55	cellular communication network factor 2	Homo sapiens	91-122
32819116-2	2020	It"s necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-beta1 (TGF-beta1) in human embryonic lung fibroblast (HELF).	Thalidomide	44-55	cellular communication network factor 2	Homo sapiens	124-128
32819116-2	2020	It"s necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-beta1 (TGF-beta1) in human embryonic lung fibroblast (HELF).	Thalidomide	44-55	transforming growth factor beta 1	Homo sapiens	141-173
32819116-2	2020	It"s necessary to investigate the effect of thalidomide on the gene promoter activation of connective tissue growth factor (CTGF) induced by transforming growth factor-beta1 (TGF-beta1) in human embryonic lung fibroblast (HELF).	Thalidomide	44-55	transforming growth factor beta 1	Homo sapiens	175-184
32819116-5	2020	The activity of luciferase was measured to observe the effect of TGF-beta1 and THALIDOMIDE on the activity of CTGF gene promoter.	Thalidomide	79-90	cellular communication network factor 2	Homo sapiens	110-114
32819116-7	2020	The thalidomide inhibited the TGF-beta1-induced activation of CTGF gene promoter in HELF, and the effect peaked in the 25 microg/L group (all P<0.001).	Thalidomide	4-15	transforming growth factor beta 1	Homo sapiens	30-39
32819116-7	2020	The thalidomide inhibited the TGF-beta1-induced activation of CTGF gene promoter in HELF, and the effect peaked in the 25 microg/L group (all P<0.001).	Thalidomide	4-15	cellular communication network factor 2	Homo sapiens	62-66
32819116-8	2020	CONCLUSIONS: Thalidomide produces a significant inhibitory effect on the gene promoter activation of CTGF induced by TGF-beta1 in HELF, it may be a potentially effective drug for the treatment of pulmonary fibrosis.	Thalidomide	13-24	cellular communication network factor 2	Homo sapiens	101-105
32819116-8	2020	CONCLUSIONS: Thalidomide produces a significant inhibitory effect on the gene promoter activation of CTGF induced by TGF-beta1 in HELF, it may be a potentially effective drug for the treatment of pulmonary fibrosis.	Thalidomide	13-24	transforming growth factor beta 1	Homo sapiens	117-126
32268442-1	2020	The use of dexamethasone plus thalidomide in combination with a continuous infusion of cisplatin, doxorubicin, cyclophosphamide, and etoposide (DTPACE) was first described in relapsed myeloma (MM) and showed effectiveness as induction therapy before autologous stem cell transplant (ASCT)1 .	Thalidomide	30-41	solute carrier family 1 member 4	Homo sapiens	283-289
32908940-11	2020	Tha 200 mug/ml suppressed iNOS and TNF-alpha, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05).	Thalidomide	0-3	nitric oxide synthase 2, inducible	Mus musculus	26-30
32908940-11	2020	Tha 200 mug/ml suppressed iNOS and TNF-alpha, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05).	Thalidomide	0-3	tumor necrosis factor	Mus musculus	35-44
32908940-11	2020	Tha 200 mug/ml suppressed iNOS and TNF-alpha, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05).	Thalidomide	0-3	mannose receptor, C type 1	Mus musculus	59-64
32908940-11	2020	Tha 200 mug/ml suppressed iNOS and TNF-alpha, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05).	Thalidomide	0-3	arginase, liver	Mus musculus	69-74
32908940-13	2020	The (Tha 200 mug/ml) MS group exhibited a decrease in TNF-alpha and IL-1beta level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05).	Thalidomide	5-8	tumor necrosis factor	Mus musculus	54-63
32908940-13	2020	The (Tha 200 mug/ml) MS group exhibited a decrease in TNF-alpha and IL-1beta level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05).	Thalidomide	5-8	interleukin 1 alpha	Rattus norvegicus	68-76
32908940-13	2020	The (Tha 200 mug/ml) MS group exhibited a decrease in TNF-alpha and IL-1beta level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05).	Thalidomide	5-8	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	107-114
32908940-13	2020	The (Tha 200 mug/ml) MS group exhibited a decrease in TNF-alpha and IL-1beta level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05).	Thalidomide	5-8	NPHS2 stomatin family member, podocin	Rattus norvegicus	119-126
32908940-14	2020	Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-alpha and IL-1beta levels via its modulation on M1/M2 differentiation.	Thalidomide	145-148	tumor necrosis factor	Mus musculus	184-193
32908940-14	2020	Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-alpha and IL-1beta levels via its modulation on M1/M2 differentiation.	Thalidomide	145-148	interleukin 1 alpha	Rattus norvegicus	198-206
32573072-5	2020	To exert the anti-metastatic effects of thalidomide, both IFN-g production and direct cytotoxicity of NK cells were essential, without notable contribution from T cells.	Thalidomide	40-51	interferon gamma	Mus musculus	58-63
32573072-6	2020	In thalidomide-treated mice, there was a significant increase in the terminally differentiated mature CD27lo NK cells in the peripheral tissues and NK cells in thalidomide-treated mice exhibited significantly higher cytotoxicity and IFN-g production.	Thalidomide	3-14	CD27 antigen	Mus musculus	102-106
32573072-6	2020	In thalidomide-treated mice, there was a significant increase in the terminally differentiated mature CD27lo NK cells in the peripheral tissues and NK cells in thalidomide-treated mice exhibited significantly higher cytotoxicity and IFN-g production.	Thalidomide	3-14	interferon gamma	Mus musculus	233-238
32573072-6	2020	In thalidomide-treated mice, there was a significant increase in the terminally differentiated mature CD27lo NK cells in the peripheral tissues and NK cells in thalidomide-treated mice exhibited significantly higher cytotoxicity and IFN-g production.	Thalidomide	160-171	interferon gamma	Mus musculus	233-238
32573072-7	2020	The NK cell expression of T-bet was up-regulated by thalidomide treatment and the down-regulation of glycogen synthase kinase 3b expression was observed in thalidomide-treated NK cells.	Thalidomide	52-63	T-box 21	Mus musculus	26-31
32573072-7	2020	The NK cell expression of T-bet was up-regulated by thalidomide treatment and the down-regulation of glycogen synthase kinase 3b expression was observed in thalidomide-treated NK cells.	Thalidomide	156-167	T-box 21	Mus musculus	26-31
32573072-7	2020	The NK cell expression of T-bet was up-regulated by thalidomide treatment and the down-regulation of glycogen synthase kinase 3b expression was observed in thalidomide-treated NK cells.	Thalidomide	156-167	glycogen synthase kinase 3 beta	Mus musculus	101-128
32573072-8	2020	Collectively, our study suggests that thalidomide induces the functional maturation of peripheral NK cells through alteration of T-bet expression to inhibit lung metastasis of cancer cells.	Thalidomide	38-49	T-box 21	Mus musculus	129-134
32447240-16	2020	NO synthase (NOS) inhibitors significantly augmented the anticonvulsant effects of combined low doses of thalidomide and morphine, whereas the inducible NOS inhibitor aminoguanidine (100 mg/kg, i.p.)	Thalidomide	105-116	nitric oxide synthase 1, neuronal	Mus musculus	0-11
32766176-6	2020	Analytical testing (immunohistochemistry, western blot, and qRT-PCR) shows that IL-6, IL-17, IL-23, and RORgammat protein and mRNA expression levels were significantly reduced by thalidomide (p < 0.05 for all) and that these levels were significantly lower in the high-dose thalidomide group than in the low-dose thalidomide group (p < 0.05 for all).	Thalidomide	179-190	interleukin 6	Rattus norvegicus	80-84
32407871-6	2020	In addition, thalidomide treatment also regulated cytokine production by inhibiting the production of angiogenesis-related cytokines, such as G-CSF, VEGF-B, VEGFR1, VEGFR3 and IL-10.	Thalidomide	13-24	colony stimulating factor 3 (granulocyte)	Mus musculus	142-147
32407871-6	2020	In addition, thalidomide treatment also regulated cytokine production by inhibiting the production of angiogenesis-related cytokines, such as G-CSF, VEGF-B, VEGFR1, VEGFR3 and IL-10.	Thalidomide	13-24	vascular endothelial growth factor B	Mus musculus	149-155
32407871-6	2020	In addition, thalidomide treatment also regulated cytokine production by inhibiting the production of angiogenesis-related cytokines, such as G-CSF, VEGF-B, VEGFR1, VEGFR3 and IL-10.	Thalidomide	13-24	FMS-like tyrosine kinase 1	Mus musculus	157-163
32407871-6	2020	In addition, thalidomide treatment also regulated cytokine production by inhibiting the production of angiogenesis-related cytokines, such as G-CSF, VEGF-B, VEGFR1, VEGFR3 and IL-10.	Thalidomide	13-24	FMS-like tyrosine kinase 4	Mus musculus	165-171
32407871-6	2020	In addition, thalidomide treatment also regulated cytokine production by inhibiting the production of angiogenesis-related cytokines, such as G-CSF, VEGF-B, VEGFR1, VEGFR3 and IL-10.	Thalidomide	13-24	interleukin 10	Mus musculus	176-181
32622642-0	2020	Facile skin targeting of a thalidomide analog containing benzyl chloride moiety alleviates experimental psoriasis via the suppression of MAPK/NF-kappaB/AP-1 phosphorylation in keratinocytes.	Thalidomide	27-38	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	142-151
32622642-0	2020	Facile skin targeting of a thalidomide analog containing benzyl chloride moiety alleviates experimental psoriasis via the suppression of MAPK/NF-kappaB/AP-1 phosphorylation in keratinocytes.	Thalidomide	27-38	jun proto-oncogene	Mus musculus	152-156
32622642-1	2020	BACKGROUND: Thalidomide can be a TNF-alpha inhibitor for treating skin inflammation.	Thalidomide	12-23	tumor necrosis factor	Mus musculus	33-42
32801749-9	2020	It follows that PD-1 antibody, chidamide, etoposide, and thalidomide (PCET) regimen may be a promising choice for patients with R/R ENKTL and warrants further investigation.	Thalidomide	57-68	programmed cell death 1	Homo sapiens	16-20
32766176-6	2020	Analytical testing (immunohistochemistry, western blot, and qRT-PCR) shows that IL-6, IL-17, IL-23, and RORgammat protein and mRNA expression levels were significantly reduced by thalidomide (p < 0.05 for all) and that these levels were significantly lower in the high-dose thalidomide group than in the low-dose thalidomide group (p < 0.05 for all).	Thalidomide	179-190	interleukin 17A	Rattus norvegicus	86-91
32035188-9	2020	Both early thalidomide treatments reduced NF-kappaB activation and shifted the ED50 value for ERC and late radiation sequelae (LRS) to higher doses.	Thalidomide	11-22	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	42-51
32304852-4	2020	Thalidomide analogues were recently found to hijack CRL4CRBN ubiquitin ligase to target a number of cellular proteins for ubiquitination and proteasomal degradation.	Thalidomide	0-11	interleukin 17 receptor B	Homo sapiens	52-56
32304852-5	2020	Thalidomide-mediated degradation of SALL4 and p63, transcription factors essential for embryonic development, very likely plays a critical role in thalidomide embryopathy.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	36-41
32304852-5	2020	Thalidomide-mediated degradation of SALL4 and p63, transcription factors essential for embryonic development, very likely plays a critical role in thalidomide embryopathy.	Thalidomide	0-11	tumor protein p63	Homo sapiens	46-49
32304852-5	2020	Thalidomide-mediated degradation of SALL4 and p63, transcription factors essential for embryonic development, very likely plays a critical role in thalidomide embryopathy.	Thalidomide	147-158	spalt like transcription factor 4	Homo sapiens	36-41
32304852-5	2020	Thalidomide-mediated degradation of SALL4 and p63, transcription factors essential for embryonic development, very likely plays a critical role in thalidomide embryopathy.	Thalidomide	147-158	tumor protein p63	Homo sapiens	46-49
32172013-6	2020	Response to thalidomide was better in patients with POEMS-CD than those with POEMS alone (90% vs 43% clinical response, [p = .012]; 80% vs 45% normalization of serum VEGF levels, [p = .079]).	Thalidomide	12-23	vascular endothelial growth factor A	Homo sapiens	166-170
31721534-13	2020	Conclusion: Combined treatment with ATO and THAL can inhibit proliferation and invasion of AML cells by down-regulating ULK1 and BECLIN1 and up-regulating PTEN and IL6, and this effect was more marked than the effects of ATO and THAL alone.	Thalidomide	44-48	unc-51 like autophagy activating kinase 1	Homo sapiens	120-124
31721534-13	2020	Conclusion: Combined treatment with ATO and THAL can inhibit proliferation and invasion of AML cells by down-regulating ULK1 and BECLIN1 and up-regulating PTEN and IL6, and this effect was more marked than the effects of ATO and THAL alone.	Thalidomide	44-48	beclin 1	Homo sapiens	129-136
31721534-13	2020	Conclusion: Combined treatment with ATO and THAL can inhibit proliferation and invasion of AML cells by down-regulating ULK1 and BECLIN1 and up-regulating PTEN and IL6, and this effect was more marked than the effects of ATO and THAL alone.	Thalidomide	44-48	phosphatase and tensin homolog	Homo sapiens	155-159
31721534-13	2020	Conclusion: Combined treatment with ATO and THAL can inhibit proliferation and invasion of AML cells by down-regulating ULK1 and BECLIN1 and up-regulating PTEN and IL6, and this effect was more marked than the effects of ATO and THAL alone.	Thalidomide	44-48	interleukin 6	Homo sapiens	164-167
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	chemokine (C-C motif) ligand 3	Mus musculus	147-151
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	interferon gamma	Mus musculus	153-162
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	vascular endothelial growth factor A	Mus musculus	167-171
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	interleukin 6	Mus musculus	205-209
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	interleukin 1 beta	Mus musculus	211-219
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	interleukin 17A	Mus musculus	221-226
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	26-30	transforming growth factor, beta 1	Mus musculus	232-241
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	chemokine (C-C motif) ligand 3	Mus musculus	147-151
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	interferon gamma	Mus musculus	153-162
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	vascular endothelial growth factor A	Mus musculus	167-171
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	interleukin 6	Mus musculus	205-209
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	interleukin 1 beta	Mus musculus	211-219
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	interleukin 17A	Mus musculus	221-226
31578565-8	2020	The mice treated with ITC/Thal and CMX/Thal showed intense weight loss, increased deposition of reticulin fibers, high pulmonary concentrations of CCL3, IFN-gamma and VEGF, and decreased concentrations of IL-6, IL-1beta, IL-17, and TGF-beta1.	Thalidomide	39-43	transforming growth factor, beta 1	Mus musculus	232-241
32621419-8	2020	On the other hand, several CRL activators have been reported, such as plant auxin and immunomodulatory imide drugs, thalidomide.	Thalidomide	116-127	interleukin 31 receptor A	Homo sapiens	27-30
32223235-5	2020	In this study, we developed thalidomide-based heterobifunctional compounds that induced selective degradation of BRAF-V600E, but not the wild-type BRAF.	Thalidomide	28-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	113-117
32443710-0	2020	Thalidomide Reduces Vascular Endothelial Growth Factor Immunostaining in Canine Splenic Hemangiosarcoma.	Thalidomide	0-11	vascular endothelial growth factor A	Canis lupus familiaris	20-54
32443710-2	2020	Recently it was demonstrated that thalidomide extends the survival time of dogs with HSA, potentially due to thalidomide-induced inhibition of vascular endothelial growth factor (VEGF) production by the neoplastic cells.	Thalidomide	34-45	vascular endothelial growth factor A	Canis lupus familiaris	143-177
32443710-2	2020	Recently it was demonstrated that thalidomide extends the survival time of dogs with HSA, potentially due to thalidomide-induced inhibition of vascular endothelial growth factor (VEGF) production by the neoplastic cells.	Thalidomide	34-45	vascular endothelial growth factor A	Canis lupus familiaris	179-183
32443710-2	2020	Recently it was demonstrated that thalidomide extends the survival time of dogs with HSA, potentially due to thalidomide-induced inhibition of vascular endothelial growth factor (VEGF) production by the neoplastic cells.	Thalidomide	109-120	vascular endothelial growth factor A	Canis lupus familiaris	143-177
32443710-2	2020	Recently it was demonstrated that thalidomide extends the survival time of dogs with HSA, potentially due to thalidomide-induced inhibition of vascular endothelial growth factor (VEGF) production by the neoplastic cells.	Thalidomide	109-120	vascular endothelial growth factor A	Canis lupus familiaris	179-183
32443710-3	2020	To investigate this, immunostaining was used to evaluate VEGF within HSA metastases that developed after thalidomide treatment.	Thalidomide	105-116	vascular endothelial growth factor A	Canis lupus familiaris	57-61
32443710-7	2020	This supports the hypothesis that thalidomide prolongs survival time in dogs with HSA due to inhibition of VEGF production by the neoplastic cells.	Thalidomide	34-45	vascular endothelial growth factor A	Canis lupus familiaris	107-111
32443710-8	2020	As VEGF remained visible within HSAs exposed to thalidomide, additional treatments to inhibit VEGF production may further prolong survival times of dogs with these common canine neoplasms.	Thalidomide	48-59	vascular endothelial growth factor A	Canis lupus familiaris	3-7
32443710-8	2020	As VEGF remained visible within HSAs exposed to thalidomide, additional treatments to inhibit VEGF production may further prolong survival times of dogs with these common canine neoplasms.	Thalidomide	48-59	vascular endothelial growth factor A	Canis lupus familiaris	94-98
32009091-1	2020	Objective A randomized controlled trial has shown the efficacy of thalidomide against Polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes (POEMS) syndrome; however, there are still refractory patients.	Thalidomide	66-77	myomesin 2	Homo sapiens	132-141
32414180-3	2020	The discovery of cereblon (CRBN), the direct target of thalidomide, a decade ago greatly improved our understanding of its mechanism of action.	Thalidomide	55-66	cereblon	Homo sapiens	27-31
32414180-4	2020	Accumulating evidence has shown that CRBN functions as a substrate of Cullin RING E3 ligase (CRL4CRBN), whose specificity is controlled by ligands such as thalidomide.	Thalidomide	155-166	cereblon	Homo sapiens	37-41
32414180-4	2020	Accumulating evidence has shown that CRBN functions as a substrate of Cullin RING E3 ligase (CRL4CRBN), whose specificity is controlled by ligands such as thalidomide.	Thalidomide	155-166	CDK2 associated cullin domain 1	Homo sapiens	70-76
32414180-5	2020	For example, lenalidomide and pomalidomide, well-known thalidomide derivatives, degrade the neosubstrates Ikaros and Aiolos, resulting in anti-proliferative effects in multiple myeloma.	Thalidomide	55-66	IKAROS family zinc finger 1	Homo sapiens	106-112
32414180-5	2020	For example, lenalidomide and pomalidomide, well-known thalidomide derivatives, degrade the neosubstrates Ikaros and Aiolos, resulting in anti-proliferative effects in multiple myeloma.	Thalidomide	55-66	IKAROS family zinc finger 3	Homo sapiens	117-123
32414180-9	2020	Recently, several CRBN neosubstrates (e.g., SALL4 (Spalt Like Transcription Factor 4) and p63 (Tumor Protein P63)) have been identified as candidate mediators of thalidomide teratogenicity.	Thalidomide	162-173	cereblon	Homo sapiens	18-22
32414180-9	2020	Recently, several CRBN neosubstrates (e.g., SALL4 (Spalt Like Transcription Factor 4) and p63 (Tumor Protein P63)) have been identified as candidate mediators of thalidomide teratogenicity.	Thalidomide	162-173	spalt like transcription factor 4	Homo sapiens	44-49
32414180-9	2020	Recently, several CRBN neosubstrates (e.g., SALL4 (Spalt Like Transcription Factor 4) and p63 (Tumor Protein P63)) have been identified as candidate mediators of thalidomide teratogenicity.	Thalidomide	162-173	spalt like transcription factor 4	Homo sapiens	51-84
32414180-9	2020	Recently, several CRBN neosubstrates (e.g., SALL4 (Spalt Like Transcription Factor 4) and p63 (Tumor Protein P63)) have been identified as candidate mediators of thalidomide teratogenicity.	Thalidomide	162-173	tumor protein p63	Homo sapiens	90-93
32414180-9	2020	Recently, several CRBN neosubstrates (e.g., SALL4 (Spalt Like Transcription Factor 4) and p63 (Tumor Protein P63)) have been identified as candidate mediators of thalidomide teratogenicity.	Thalidomide	162-173	tumor protein p63	Homo sapiens	95-113
32223235-5	2020	In this study, we developed thalidomide-based heterobifunctional compounds that induced selective degradation of BRAF-V600E, but not the wild-type BRAF.	Thalidomide	28-39	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	147-151
32018067-9	2020	Protein content, N-acetyl-b-glucosaminidase (NAG) and myeloperoxidase (MPO) activities were elevated in ocular tissues after disease induction, further decreasing post-treatment with intravitreal thalidomide.	Thalidomide	196-207	N-acetyl-alpha-glucosaminidase	Homo sapiens	17-43
32317922-7	2020	We then identified the autophosphorylation site T2524 as a so far not described 14-3-3 binding site at the very C-terminus of LRRK2.	Thalidomide	48-53	leucine rich repeat kinase 2	Homo sapiens	126-131
32018067-9	2020	Protein content, N-acetyl-b-glucosaminidase (NAG) and myeloperoxidase (MPO) activities were elevated in ocular tissues after disease induction, further decreasing post-treatment with intravitreal thalidomide.	Thalidomide	196-207	myeloperoxidase	Homo sapiens	71-74
32018067-9	2020	Protein content, N-acetyl-b-glucosaminidase (NAG) and myeloperoxidase (MPO) activities were elevated in ocular tissues after disease induction, further decreasing post-treatment with intravitreal thalidomide.	Thalidomide	196-207	N-acetyl-alpha-glucosaminidase	Homo sapiens	45-48
32018067-9	2020	Protein content, N-acetyl-b-glucosaminidase (NAG) and myeloperoxidase (MPO) activities were elevated in ocular tissues after disease induction, further decreasing post-treatment with intravitreal thalidomide.	Thalidomide	196-207	myeloperoxidase	Homo sapiens	54-69
33133483-6	2020	Proteolysis targeting chimeras (PROTACs) structurally based on the cereblon (CRBN) ligand thalidomide have recently been described to degrade the targets CDK4/6.	Thalidomide	90-101	cereblon	Homo sapiens	77-81
32251415-1	2020	Thalidomide-dependent degradation of the embryonic transcription factor SALL4 by the CRL4CRBN E3 ubiquitin ligase is a plausible major driver of thalidomide teratogenicity.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	72-77
32251415-1	2020	Thalidomide-dependent degradation of the embryonic transcription factor SALL4 by the CRL4CRBN E3 ubiquitin ligase is a plausible major driver of thalidomide teratogenicity.	Thalidomide	145-156	spalt like transcription factor 4	Homo sapiens	72-77
33133483-6	2020	Proteolysis targeting chimeras (PROTACs) structurally based on the cereblon (CRBN) ligand thalidomide have recently been described to degrade the targets CDK4/6.	Thalidomide	90-101	cyclin dependent kinase 4	Homo sapiens	154-160
31840939-7	2020	CONCLUSION: Thal can effectively prevent skin and pulmonary tissue fibrosis in a mouse model of SSc through the TGF-beta1/Smad3 signaling pathway and can rectify the distortion of the Th17/Treg balance in SSc by potentially regulating Th17 and Treg cell production, as well as their related factors expression.	Thalidomide	12-16	transforming growth factor, beta 1	Mus musculus	112-121
32132601-7	2020	By contrast, the cytoplasmic translation factor GSPT1 was degraded following treatment with the thalidomide derivative CC-885 only when CRBN was present in the cytoplasm, indicating that subcellular distribution of CRBN is critical for the efficacy of thalidomide-based medications.	Thalidomide	96-107	G1 to S phase transition 1	Homo sapiens	48-53
32132601-7	2020	By contrast, the cytoplasmic translation factor GSPT1 was degraded following treatment with the thalidomide derivative CC-885 only when CRBN was present in the cytoplasm, indicating that subcellular distribution of CRBN is critical for the efficacy of thalidomide-based medications.	Thalidomide	96-107	cereblon	Homo sapiens	136-140
32132601-7	2020	By contrast, the cytoplasmic translation factor GSPT1 was degraded following treatment with the thalidomide derivative CC-885 only when CRBN was present in the cytoplasm, indicating that subcellular distribution of CRBN is critical for the efficacy of thalidomide-based medications.	Thalidomide	96-107	cereblon	Homo sapiens	215-219
32132601-7	2020	By contrast, the cytoplasmic translation factor GSPT1 was degraded following treatment with the thalidomide derivative CC-885 only when CRBN was present in the cytoplasm, indicating that subcellular distribution of CRBN is critical for the efficacy of thalidomide-based medications.	Thalidomide	252-263	G1 to S phase transition 1	Homo sapiens	48-53
32132601-7	2020	By contrast, the cytoplasmic translation factor GSPT1 was degraded following treatment with the thalidomide derivative CC-885 only when CRBN was present in the cytoplasm, indicating that subcellular distribution of CRBN is critical for the efficacy of thalidomide-based medications.	Thalidomide	252-263	cereblon	Homo sapiens	215-219
31840939-6	2020	RESULTS: Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P &lt; .001) in BLM-induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)-17A expression (both P &lt; .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P &lt; .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P &lt; .01); (d) Thal inhibited TGF-beta1 expression and Smad3 phosphorylation (both P &lt; .05); (e) TGF-beta1 was positively correlated with the IL-17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively).	Thalidomide	9-13	forkhead box P3	Mus musculus	340-345
31840939-7	2020	CONCLUSION: Thal can effectively prevent skin and pulmonary tissue fibrosis in a mouse model of SSc through the TGF-beta1/Smad3 signaling pathway and can rectify the distortion of the Th17/Treg balance in SSc by potentially regulating Th17 and Treg cell production, as well as their related factors expression.	Thalidomide	12-16	SMAD family member 3	Mus musculus	122-127
31840939-6	2020	RESULTS: Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P &lt; .001) in BLM-induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)-17A expression (both P &lt; .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P &lt; .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P &lt; .01); (d) Thal inhibited TGF-beta1 expression and Smad3 phosphorylation (both P &lt; .05); (e) TGF-beta1 was positively correlated with the IL-17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively).	Thalidomide	9-13	transforming growth factor, beta 1	Mus musculus	678-687
31422568-10	2020	Hesperidin found stronger binding strength and IC50 was relative to thalidomide on TNF alpha, IL 6, and caspase 3.	Thalidomide	68-79	interleukin 6	Rattus norvegicus	94-98
31840939-6	2020	RESULTS: Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P &lt; .001) in BLM-induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)-17A expression (both P &lt; .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P &lt; .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P &lt; .01); (d) Thal inhibited TGF-beta1 expression and Smad3 phosphorylation (both P &lt; .05); (e) TGF-beta1 was positively correlated with the IL-17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively).	Thalidomide	9-13	SMAD family member 3	Mus musculus	703-708
31840939-6	2020	RESULTS: Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P &lt; .001) in BLM-induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)-17A expression (both P &lt; .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P &lt; .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P &lt; .01); (d) Thal inhibited TGF-beta1 expression and Smad3 phosphorylation (both P &lt; .05); (e) TGF-beta1 was positively correlated with the IL-17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively).	Thalidomide	9-13	transforming growth factor, beta 1	Mus musculus	748-757
31840939-6	2020	RESULTS: Thal treatment: (a) reduced skin, and pulmonary tissue fibrosis, inflammation score, and hydroxyproline content (P &lt; .001) in BLM-induced SSc mice; (b) reduced the percentages of Th17 cells and associated interleukin (IL)-17A expression (both P &lt; .05) but increased the percentages of Treg cells and its transcription factor Foxp3 expression (both P &lt; .05); (c) correlation analysis found positive correlations between Th17/Treg ratio, the inflammatory score of the skin and pulmonary tissues, hydroxyproline content, and type I collagen messenger RNA expression (r = .8546, .8656, .6902, .6807, .8118, and .8424, respectively, P &lt; .01); (d) Thal inhibited TGF-beta1 expression and Smad3 phosphorylation (both P &lt; .05); (e) TGF-beta1 was positively correlated with the IL-17A and Th17/Treg ratio (r = .5856, P = .005; r = .6684, P = .0107, respectively).	Thalidomide	9-13	interleukin 17A	Mus musculus	793-799
32071327-0	2020	Thalidomide Inhibits Human iPSC Mesendoderm Differentiation by Modulating CRBN-dependent Degradation of SALL4.	Thalidomide	0-11	cereblon	Homo sapiens	74-78
32071327-0	2020	Thalidomide Inhibits Human iPSC Mesendoderm Differentiation by Modulating CRBN-dependent Degradation of SALL4.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	104-109
32071327-2	2020	Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex.	Thalidomide	0-11	cereblon	Rattus norvegicus	76-80
32071327-2	2020	Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex.	Thalidomide	0-11	cullin 4A	Homo sapiens	113-118
32071327-2	2020	Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex.	Thalidomide	0-11	damage specific DNA binding protein 1	Homo sapiens	119-123
32071327-2	2020	Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex.	Thalidomide	0-11	cereblon	Rattus norvegicus	124-128
32071327-2	2020	Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex.	Thalidomide	0-11	ring-box 1	Homo sapiens	129-133
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	0-11	cereblon	Homo sapiens	23-27
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	0-11	cereblon	Homo sapiens	93-97
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	122-127
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	185-196	cereblon	Homo sapiens	23-27
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	185-196	cereblon	Homo sapiens	93-97
32071327-3	2020	Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans.	Thalidomide	185-196	spalt like transcription factor 4	Homo sapiens	122-127
32071327-4	2020	Herein, thalidomide-induced degradation of SALL4 was examined in human induced pluripotent stem cells (hiPSCs) that were differentiated either to lateral plate mesoderm (LPM)-like cells, the developmental ontology of the limb bud, or definitive endoderm.	Thalidomide	8-19	spalt like transcription factor 4	Homo sapiens	43-48
32071327-6	2020	Thalidomide- and IMiD-induced SALL4 degradation can be abrogated by CRBN V388I mutation or SALL4 G416A mutation in hiPSCs.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	30-35
32071327-6	2020	Thalidomide- and IMiD-induced SALL4 degradation can be abrogated by CRBN V388I mutation or SALL4 G416A mutation in hiPSCs.	Thalidomide	0-11	cereblon	Homo sapiens	68-72
32071327-6	2020	Thalidomide- and IMiD-induced SALL4 degradation can be abrogated by CRBN V388I mutation or SALL4 G416A mutation in hiPSCs.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	91-96
32071327-9	2020	The data here show that thalidomide, lenalidomide, and pomalidomide affect stem cell mesendoderm differentiation through CRBN-mediated degradation of SALL4 and highlight the utility of the LPM differentiation model for studying the teratogenicity of new CRBN modulating agents.	Thalidomide	24-35	cereblon	Homo sapiens	121-125
32071327-9	2020	The data here show that thalidomide, lenalidomide, and pomalidomide affect stem cell mesendoderm differentiation through CRBN-mediated degradation of SALL4 and highlight the utility of the LPM differentiation model for studying the teratogenicity of new CRBN modulating agents.	Thalidomide	24-35	spalt like transcription factor 4	Homo sapiens	150-155
32071327-9	2020	The data here show that thalidomide, lenalidomide, and pomalidomide affect stem cell mesendoderm differentiation through CRBN-mediated degradation of SALL4 and highlight the utility of the LPM differentiation model for studying the teratogenicity of new CRBN modulating agents.	Thalidomide	24-35	cereblon	Homo sapiens	254-258
31392724-5	2020	In the LOT1 setting, from 2008 to 2015, there was a decrease in the use of thalidomide-based therapy, from 66 7% to 42 6%, and chemotherapy from, 20 2% to 5 9%, whereas use of bortezomib-based therapy or bortezomib + thalidomide increased from 10 7% to 45 5%.	Thalidomide	75-86	PLAG1 like zinc finger 1	Homo sapiens	7-11
31392724-5	2020	In the LOT1 setting, from 2008 to 2015, there was a decrease in the use of thalidomide-based therapy, from 66 7% to 42 6%, and chemotherapy from, 20 2% to 5 9%, whereas use of bortezomib-based therapy or bortezomib + thalidomide increased from 10 7% to 45 5%.	Thalidomide	217-228	PLAG1 like zinc finger 1	Homo sapiens	7-11
31620907-7	2020	In addition, the PDCD1LG1 rs4143815 CC and CG types (high-expression types) were associated significantly with higher frequency of patients who were treated with thalidomide and/or bortezomib.	Thalidomide	162-173	CD274 molecule	Homo sapiens	17-25
31916702-1	2020	OBJECTIVE: To explore the relationship between hepatic cytochrome P450 2C19 (CYP2C19) gene polymorphisms and the effectiveness and safety of thalidomide in the treatment of patients with immune-related bowel disease (IRBD).	Thalidomide	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-75
31916702-1	2020	OBJECTIVE: To explore the relationship between hepatic cytochrome P450 2C19 (CYP2C19) gene polymorphisms and the effectiveness and safety of thalidomide in the treatment of patients with immune-related bowel disease (IRBD).	Thalidomide	141-152	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
31916702-2	2020	METHODS: CYP2C19 variants in 79 patients treated with thalidomide were analyzed using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).	Thalidomide	54-65	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	9-16
31422568-10	2020	Hesperidin found stronger binding strength and IC50 was relative to thalidomide on TNF alpha, IL 6, and caspase 3.	Thalidomide	68-79	tumor necrosis factor	Rattus norvegicus	83-92
31422568-10	2020	Hesperidin found stronger binding strength and IC50 was relative to thalidomide on TNF alpha, IL 6, and caspase 3.	Thalidomide	68-79	caspase 3	Rattus norvegicus	104-113
31767403-3	2020	We describe herein the design, synthesis, and evaluation of PROTAC BET degraders, based on the BET inhibitor with selectivity for the first Bromodomain benzo[cd]indole-2-one, alkylamide linker and cereblon ligand thalidomide.	Thalidomide	213-224	delta/notch like EGF repeat containing	Homo sapiens	67-70
31964914-0	2020	CRL4-Cereblon complex in Thalidomide Embryopathy: a translational investigation.	Thalidomide	25-36	interleukin 17 receptor B	Homo sapiens	0-4
31964914-0	2020	CRL4-Cereblon complex in Thalidomide Embryopathy: a translational investigation.	Thalidomide	25-36	cereblon	Homo sapiens	5-13
31964914-1	2020	The Cereblon-CRL4 complex has been studied predominantly with regards to thalidomide treatment of multiple myeloma.	Thalidomide	73-84	cereblon	Homo sapiens	4-12
31964914-1	2020	The Cereblon-CRL4 complex has been studied predominantly with regards to thalidomide treatment of multiple myeloma.	Thalidomide	73-84	interleukin 17 receptor B	Homo sapiens	13-17
31964914-2	2020	Nevertheless, the role of Cereblon-CRL4 in Thalidomide Embryopathy (TE) is still not understood.	Thalidomide	43-54	cereblon	Homo sapiens	26-34
31964914-2	2020	Nevertheless, the role of Cereblon-CRL4 in Thalidomide Embryopathy (TE) is still not understood.	Thalidomide	43-54	interleukin 17 receptor B	Homo sapiens	35-39
31964914-9	2020	In conclusion, we suggest that CRL4-Cereblon variants act through several regulatory mechanisms, which may influence CRL4-Cereblon complex assembly and its ability to bind thalidomide.	Thalidomide	172-183	interleukin 17 receptor B	Homo sapiens	31-35
31964914-9	2020	In conclusion, we suggest that CRL4-Cereblon variants act through several regulatory mechanisms, which may influence CRL4-Cereblon complex assembly and its ability to bind thalidomide.	Thalidomide	172-183	cereblon	Homo sapiens	36-44
31964914-9	2020	In conclusion, we suggest that CRL4-Cereblon variants act through several regulatory mechanisms, which may influence CRL4-Cereblon complex assembly and its ability to bind thalidomide.	Thalidomide	172-183	interleukin 17 receptor B	Homo sapiens	117-121
31964914-9	2020	In conclusion, we suggest that CRL4-Cereblon variants act through several regulatory mechanisms, which may influence CRL4-Cereblon complex assembly and its ability to bind thalidomide.	Thalidomide	172-183	cereblon	Homo sapiens	122-130
31963193-13	2020	IMiDs decreased TLR4-induced mediator release; this effect was stronger for pomalidomide than for lenalidomide and especially thalidomide.	Thalidomide	126-137	toll like receptor 4	Homo sapiens	16-20
32021103-0	2020	Curcumin Combined with Thalidomide Reduces Expression of STAT3 and Bcl-xL, Leading to Apoptosis in Acute Myeloid Leukemia Cell Lines.	Thalidomide	23-34	signal transducer and activator of transcription 3	Homo sapiens	57-62
32021103-0	2020	Curcumin Combined with Thalidomide Reduces Expression of STAT3 and Bcl-xL, Leading to Apoptosis in Acute Myeloid Leukemia Cell Lines.	Thalidomide	23-34	BCL2 like 1	Homo sapiens	67-73
32021103-9	2020	The expression level of STAT3 and BCL-XL was significantly down-regulated in KG-1 cells after treatment by CUR and THAL and their combination.	Thalidomide	115-119	signal transducer and activator of transcription 3	Homo sapiens	24-29
32021103-9	2020	The expression level of STAT3 and BCL-XL was significantly down-regulated in KG-1 cells after treatment by CUR and THAL and their combination.	Thalidomide	115-119	BCL2 like 1	Homo sapiens	34-40
32021103-10	2020	Conclusion: Overall, our findings suggested that down-regulation of STAT3 and BCL-XL mRNA expression in response to CUR and THAL treatment lead to inhibition of cell growth and induction of apoptosis.	Thalidomide	124-128	signal transducer and activator of transcription 3	Homo sapiens	68-73
32021103-10	2020	Conclusion: Overall, our findings suggested that down-regulation of STAT3 and BCL-XL mRNA expression in response to CUR and THAL treatment lead to inhibition of cell growth and induction of apoptosis.	Thalidomide	124-128	BCL2 like 1	Homo sapiens	78-84
32010638-7	2019	Thalidomide, an inhibitor of monocyte-derived TNF-alpha, was evaluated in the rabbit model of TBM and shown to improve survival and reduce inflammation of the brain and the meninges.	Thalidomide	0-11	tumor necrosis factor	Oryctolagus cuniculus	46-55
31767403-3	2020	We describe herein the design, synthesis, and evaluation of PROTAC BET degraders, based on the BET inhibitor with selectivity for the first Bromodomain benzo[cd]indole-2-one, alkylamide linker and cereblon ligand thalidomide.	Thalidomide	213-224	delta/notch like EGF repeat containing	Homo sapiens	95-98
31044460-0	2019	Blockade of angiogenin by thalidomide inhibits the tumorigenesis of murine hemangioendothelioma.	Thalidomide	26-37	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	12-22
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	interferon gamma	Mus musculus	184-193
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	insulin-like growth factor 1	Mus musculus	195-200
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	interleukin 6	Mus musculus	202-206
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	interleukin 17A	Mus musculus	208-213
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	tumor necrosis factor	Mus musculus	215-224
31920668-4	2019	Herein, our study demonstrated that thalidomide protected colon mucosa against trinitro-benzene-sulfonic acid (TNBS)-induced injury, diminished inflammatory infiltration and levels of IFN-gamma, IGF-1, IL-6, IL-17, TNF-alpha, while increased the levels of IL-10 and TGF-gamma.	Thalidomide	36-47	interleukin 10	Mus musculus	256-261
30914422-1	2020	AIM: To determine whether changes in the serum levels of vascular endothelial growth factor (VEGF) after thalidomide therapy will affect the peripapillary retinal thickness (pRT) associated with optic disc oedema (ODE) in patients with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome.	Thalidomide	105-116	vascular endothelial growth factor A	Homo sapiens	57-91
30914422-4	2020	We determined whether a change in the pRT from baseline was significantly correlated with the serum level of VEGF from that at 6 months after the thalidomide treatment.	Thalidomide	146-157	vascular endothelial growth factor A	Homo sapiens	109-113
32522938-2	2020	Although the molecular mechanisms of thalidomide and its derivatives remained poorly understood until recently, we identified cereblon (CRBN), a primary direct target of thalidomide, using ferrite glycidyl methacrylate (FG) beads.	Thalidomide	37-48	cereblon	Homo sapiens	136-140
32522938-2	2020	Although the molecular mechanisms of thalidomide and its derivatives remained poorly understood until recently, we identified cereblon (CRBN), a primary direct target of thalidomide, using ferrite glycidyl methacrylate (FG) beads.	Thalidomide	170-181	cereblon	Homo sapiens	136-140
32522938-4	2020	When a ligand such as thalidomide binds to CRBN, it recognizes various "neosubstrates" depending on the shape of the ligand.	Thalidomide	22-33	cereblon	Homo sapiens	43-47
31867326-4	2019	Thalidomide and its derivatives, termed immunomodulatory imide drugs (IMiDs), are a class of drugs that target the 3"-untranslated region (3"-UTR) of TNF-alpha mRNA, inhibiting TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	150-159
31867326-4	2019	Thalidomide and its derivatives, termed immunomodulatory imide drugs (IMiDs), are a class of drugs that target the 3"-untranslated region (3"-UTR) of TNF-alpha mRNA, inhibiting TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	177-186
31044460-5	2019	By qRT-PCR screening, we observed that the expression of angiogenin was downregulated by thalidomide treatment.	Thalidomide	89-100	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	57-67
31044460-7	2019	Moreover, we confirmed that the antitumoral role of thalidomide is dependent on angiogenin expression both in vivo and in vitro.	Thalidomide	52-63	angiogenin	Homo sapiens	80-90
32186620-2	2019	Since 2013, the treatment of these patients in the public system is based on CTD (cyclophosphamide, thalidomide, and dexamethasone).	Thalidomide	100-111	CTD	Homo sapiens	77-80
30890040-3	2019	This study is to assess if serum PF4 could be a prognostic factor in predicting treatment response and survival of MM treated with thalidomide and VAD regimens.	Thalidomide	131-142	platelet factor 4	Homo sapiens	33-36
30890040-12	2019	CONCLUSIONS: We speculate serum PF4 is a promising response and prognostic factor in newly diagnosed MM treated with thalidomide and VAD regimens.	Thalidomide	117-128	platelet factor 4	Homo sapiens	32-35
31335998-1	2019	BACKGROUND: Thalidomide and closely related analogues are used clinically for their immunomodulatory and antiangiogenic properties mediated by the inhibition of the proinflammatory cytokine tumor necrosis factor alpha.	Thalidomide	12-23	tumor necrosis factor	Rattus norvegicus	190-217
31591562-0	2019	p63 is a cereblon substrate involved in thalidomide teratogenicity.	Thalidomide	40-51	tumor protein p63	Danio rerio	0-3
31819606-11	2019	Furthermore, the GFAP and Iba1 expressions and TNF-alpha levels of the ipsilateral spinal dorsal horn in SNL+Tha group were significantly weaker from day 3 to day 14 after SNL than those in SNL+Veh group (P &lt; 0.05).	Thalidomide	109-112	glial fibrillary acidic protein	Homo sapiens	17-21
31819606-11	2019	Furthermore, the GFAP and Iba1 expressions and TNF-alpha levels of the ipsilateral spinal dorsal horn in SNL+Tha group were significantly weaker from day 3 to day 14 after SNL than those in SNL+Veh group (P &lt; 0.05).	Thalidomide	109-112	allograft inflammatory factor 1	Homo sapiens	26-30
31819606-11	2019	Furthermore, the GFAP and Iba1 expressions and TNF-alpha levels of the ipsilateral spinal dorsal horn in SNL+Tha group were significantly weaker from day 3 to day 14 after SNL than those in SNL+Veh group (P &lt; 0.05).	Thalidomide	109-112	tumor necrosis factor	Homo sapiens	47-56
32128089-0	2019	Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-alpha, IL-6 inhibition, and SOCS1 activation.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	124-133
32128089-0	2019	Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-alpha, IL-6 inhibition, and SOCS1 activation.	Thalidomide	0-11	interleukin 6	Rattus norvegicus	135-139
32128089-0	2019	Thalidomide attenuates the hyporesponsiveness of isolated atria to chronotropic stimulation in BDL rats: The involvement of TNF-alpha, IL-6 inhibition, and SOCS1 activation.	Thalidomide	0-11	suppressor of cytokine signaling 1	Rattus norvegicus	156-161
32128089-14	2019	On the other hand, hepatic SOCS1 expression was up-regulated by thalidomide treatment in this group.	Thalidomide	64-75	suppressor of cytokine signaling 1	Rattus norvegicus	27-32
30962579-4	2019	WL40 was synthesized by linking the Rpn13 covalent inhibitor RA190 with the cereblon (CRBN) binding ligand thalidomide.	Thalidomide	107-118	cereblon	Homo sapiens	86-90
31591562-1	2019	Cereblon (CRBN) is a primary target of thalidomide and mediates its multiple pharmacological activities, including teratogenic and antimyeloma activities.	Thalidomide	39-50	cereblon	Danio rerio	10-14
31591562-2	2019	CRBN functions as a substrate receptor of the E3 ubiquitin ligase CRL4, whose substrate specificity is modulated by thalidomide and its analogs.	Thalidomide	116-127	cereblon	Danio rerio	0-4
31591562-4	2019	Here we show that p63 isoforms are thalidomide-dependent CRL4CRBN neosubstrates that are responsible, at least in part, for its teratogenic effects.	Thalidomide	35-46	tumor protein p63	Danio rerio	18-21
30934098-0	2019	A Cautious Note on Thalidomide Usage in Cancer Treatment: Genetic Profiling of the TBX2 Sub-Family Gene Expression is Required.	Thalidomide	19-30	T-box transcription factor 2	Homo sapiens	83-87
31670229-11	2019	Compared with vehicle (phosphate-buffered saline), thalidomide significantly inhibited the secretion of IFN-gamma and IL-17 in ITP mouse and reduced the expression of CD68 in spleen.	Thalidomide	51-62	interferon gamma	Mus musculus	104-113
31670229-11	2019	Compared with vehicle (phosphate-buffered saline), thalidomide significantly inhibited the secretion of IFN-gamma and IL-17 in ITP mouse and reduced the expression of CD68 in spleen.	Thalidomide	51-62	interleukin 17A	Mus musculus	118-123
31670229-11	2019	Compared with vehicle (phosphate-buffered saline), thalidomide significantly inhibited the secretion of IFN-gamma and IL-17 in ITP mouse and reduced the expression of CD68 in spleen.	Thalidomide	51-62	CD68 antigen	Mus musculus	167-171
31487824-8	2019	Based on the structure of dicarboximides and thalidomide, novel proteolysis-targeting chimeras (PROTACs) were synthesized and used as tools to downregulate ABC50 in leukemia cells.	Thalidomide	45-56	ATP binding cassette subfamily F member 1	Homo sapiens	156-161
31487824-0	2019	New Thalidomide-Resembling Dicarboximides Target ABC50 Protein and Show Antileukemic and Immunomodulatory Activities.	Thalidomide	4-15	ATP binding cassette subfamily F member 1	Homo sapiens	49-54
31115923-0	2019	Polymorphisms in the promotor region of the CRBN gene as a predictive factor for peripheral neuropathy in the course of thalidomide-based chemotherapy in multiple myeloma patients.	Thalidomide	120-131	cereblon	Homo sapiens	44-48
31115923-2	2019	This study aimed to analyse the influence of clinical and molecular factors - single nucleotide polymorphisms (SNPs) of the CRBN gene: rs6768972 and rs1672753, on the risk of adverse effects (AEs) of thalidomide-based chemotherapy in patients with MM.	Thalidomide	200-211	cereblon	Homo sapiens	124-128
31115923-8	2019	Selected CRBN SNPs may be useful in assessing the probability of AEs in the form of peripheral polyneuropathy and gastrointestinal motility disorders associated with the use of thalidomide in patients with MM.	Thalidomide	177-188	cereblon	Homo sapiens	9-13
30934098-5	2019	The identification of CRBN and TBX5 as potential direct ligands for this drug have opened the way to better understand its efficiency and its failure.We hereby review these mechanisms and provide evidence that could explain why thalidomide failed to make it as a drug of choice in lung cancer treatment.	Thalidomide	228-239	cereblon	Homo sapiens	22-26
30934098-5	2019	The identification of CRBN and TBX5 as potential direct ligands for this drug have opened the way to better understand its efficiency and its failure.We hereby review these mechanisms and provide evidence that could explain why thalidomide failed to make it as a drug of choice in lung cancer treatment.	Thalidomide	228-239	T-box transcription factor 5	Homo sapiens	31-35
30934098-6	2019	Linking the genetic signature of TBX2 subfamily in these tumors to their inability to respond properly to thalidomide raises concerns of worsening lung cancer patients" health if this drug is utilized.	Thalidomide	106-117	T-box transcription factor 2	Homo sapiens	33-37
31175889-3	2019	In this study, we used two mouse models of depression and investigated the possible role of nitric oxide (NO), NO synthase (NOS) and inducible NOS (iNOS) in the ant-depressant-like effects of thalidomide.	Thalidomide	192-203	nitric oxide synthase 2, inducible	Mus musculus	133-146
30806135-0	2019	Thalidomide alleviates bone cancer pain by down-regulating expressions of NF-kappaB and GFAP in spinal astrocytes in a mouse model.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	74-83
30806135-0	2019	Thalidomide alleviates bone cancer pain by down-regulating expressions of NF-kappaB and GFAP in spinal astrocytes in a mouse model.	Thalidomide	0-11	glial fibrillary acidic protein	Mus musculus	88-92
30806135-2	2019	Previous study has shown that thalidomide decreases the expression of tumor necrosis factor alpha in the mouse spinal cord.	Thalidomide	30-41	tumor necrosis factor	Mus musculus	70-97
30806135-4	2019	Here, we investigated the effect of thalidomide on the expression level of NF-kappaB as well as glial fibrillary acidic protein (GFAP) in the spinal cord astrocyte in a mice model.	Thalidomide	36-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
30806135-11	2019	Treating the tumor-bearing mice with thalidomide results in a dramatic reduction in pain behaviors and a significant decrease of NF-kappaB and GFAP expressions.	Thalidomide	37-48	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	129-138
30806135-11	2019	Treating the tumor-bearing mice with thalidomide results in a dramatic reduction in pain behaviors and a significant decrease of NF-kappaB and GFAP expressions.	Thalidomide	37-48	glial fibrillary acidic protein	Mus musculus	143-147
30806135-12	2019	Conclusions: Thalidomide alleviates the pain behaviors probably by down-regulating the expression of NF-kappaB and GFAP.	Thalidomide	13-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	101-110
30806135-12	2019	Conclusions: Thalidomide alleviates the pain behaviors probably by down-regulating the expression of NF-kappaB and GFAP.	Thalidomide	13-24	glial fibrillary acidic protein	Mus musculus	115-119
31168767-0	2019	Post-treatment improvement of NK cell numbers predicts better survival in myeloma patients treated with thalidomide-based regimens.	Thalidomide	104-115	solute carrier family 35 member G1	Homo sapiens	0-4
31388035-0	2019	The role of ESCO2, SALL4 and TBX5 genes in the susceptibility to thalidomide teratogenesis.	Thalidomide	65-76	establishment of sister chromatid cohesion N-acetyltransferase 2	Homo sapiens	12-17
31132355-0	2019	Synergistic effects of gefitinib and thalidomide treatment on EGFR-TKI-sensitive and -resistant NSCLC.	Thalidomide	37-48	epidermal growth factor receptor	Homo sapiens	62-66
31132355-8	2019	The inhibition of EGFR phosphorylation and downstream signaling was more pronounced in the thalidomide and gefitinib co-treatment group as compared with the single agent treatment groups.	Thalidomide	91-102	epidermal growth factor receptor	Homo sapiens	18-22
31132355-9	2019	Further study revealed that the inhibitors of AKT, MEK/ERK, and p38 increased the antiproliferative and proapoptotic effects of the combined treatment of thalidomide and gefitinib.	Thalidomide	154-165	AKT serine/threonine kinase 1	Homo sapiens	46-49
31132355-9	2019	Further study revealed that the inhibitors of AKT, MEK/ERK, and p38 increased the antiproliferative and proapoptotic effects of the combined treatment of thalidomide and gefitinib.	Thalidomide	154-165	mitogen-activated protein kinase kinase 7	Homo sapiens	51-54
31132355-9	2019	Further study revealed that the inhibitors of AKT, MEK/ERK, and p38 increased the antiproliferative and proapoptotic effects of the combined treatment of thalidomide and gefitinib.	Thalidomide	154-165	EPH receptor B2	Homo sapiens	55-58
31132355-9	2019	Further study revealed that the inhibitors of AKT, MEK/ERK, and p38 increased the antiproliferative and proapoptotic effects of the combined treatment of thalidomide and gefitinib.	Thalidomide	154-165	mitogen-activated protein kinase 14	Homo sapiens	64-67
31132355-11	2019	In conclusion, thalidomide and gefitinib exhibit synergistic effects on both TKI-sensitive and -resistant NSCLC cells by targeting the EGFR signaling pathways, suggesting that the combination strategy is promising for the treatment of NSCLC.	Thalidomide	15-26	epidermal growth factor receptor	Homo sapiens	135-139
31388035-0	2019	The role of ESCO2, SALL4 and TBX5 genes in the susceptibility to thalidomide teratogenesis.	Thalidomide	65-76	spalt like transcription factor 4	Homo sapiens	19-24
31388035-0	2019	The role of ESCO2, SALL4 and TBX5 genes in the susceptibility to thalidomide teratogenesis.	Thalidomide	65-76	T-box transcription factor 5	Homo sapiens	29-33
31388035-4	2019	Recently, SALL4 and TBX5 were demonstrated to be thalidomide targets.	Thalidomide	49-60	spalt like transcription factor 4	Homo sapiens	10-15
31388035-4	2019	Recently, SALL4 and TBX5 were demonstrated to be thalidomide targets.	Thalidomide	49-60	T-box transcription factor 5	Homo sapiens	20-24
31132668-13	2019	Particularly, we showed thalidomide reduced CD4+ T helper cell infiltration and downregulated Th1- and Th17-polarizing genes.	Thalidomide	24-35	CD4 antigen	Mus musculus	44-47
31388035-10	2019	DGE analysis showed a significant reduction of ESCO2 in hPSCs after thalidomide exposure.	Thalidomide	68-79	establishment of sister chromatid cohesion N-acetyltransferase 2	Homo sapiens	47-52
31132668-13	2019	Particularly, we showed thalidomide reduced CD4+ T helper cell infiltration and downregulated Th1- and Th17-polarizing genes.	Thalidomide	24-35	negative elongation factor complex member C/D, Th1l	Mus musculus	94-97
31043423-4	2019	Thalidomide analogs bind the CRL4CRBN ubiquitin ligase and induce degradation of particular proteins, but each of the molecules studied has distinct patterns of substrate specificity that likely underlie the clinical activity and toxicities of each drug.	Thalidomide	0-11	interleukin 17 receptor B	Homo sapiens	29-33
31132668-14	2019	In addition, thalidomide treatment lowered the microvessel density and vascular endothelial growth factor (VEGF) expression.	Thalidomide	13-24	vascular endothelial growth factor A	Mus musculus	71-105
31132668-14	2019	In addition, thalidomide treatment lowered the microvessel density and vascular endothelial growth factor (VEGF) expression.	Thalidomide	13-24	vascular endothelial growth factor A	Mus musculus	107-111
31132668-15	2019	We further demonstrated that thalidomide suppressed NF-kappaB activation in LL37-treated skin and in TNF-alpha-stimulated HaCaT keratinocytes in vitro.	Thalidomide	29-40	tumor necrosis factor	Mus musculus	101-110
31251063-0	2019	De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.	Thalidomide	85-96	cereblon	Homo sapiens	18-26
31251063-0	2019	De-Novo Design of Cereblon (CRBN) Effectors Guided by Natural Hydrolysis Products of Thalidomide Derivatives.	Thalidomide	85-96	cereblon	Homo sapiens	28-32
31030100-0	2019	Thalidomide induce response in patients with corticosteroid-resistant or relapsed ITP by upregulating Neuropilin-1 expression.	Thalidomide	0-11	neuropilin 1	Homo sapiens	102-114
31030100-10	2019	In vitro, THD treatment upregulated expression of NRP-1and Tregs only in ITP patients.	Thalidomide	10-13	neuropilin 1	Homo sapiens	50-55
31030100-12	2019	Additionally, rhTPO plus THD or THD therapy significantly increased the levels of NRP-1, Tregs and Bregs in responders.	Thalidomide	25-28	neuropilin 1	Homo sapiens	82-87
31030100-12	2019	Additionally, rhTPO plus THD or THD therapy significantly increased the levels of NRP-1, Tregs and Bregs in responders.	Thalidomide	32-35	neuropilin 1	Homo sapiens	82-87
31030100-13	2019	CONCLUSIONS: Our study shows for the first time that NRP-1 is involved in the pathogenesis of ITP, THD could induce response in ITP patients by upregulating NRP-1 expression and restoring the proportion of Tregs and Bregs.	Thalidomide	99-102	neuropilin 1	Homo sapiens	53-58
31030100-13	2019	CONCLUSIONS: Our study shows for the first time that NRP-1 is involved in the pathogenesis of ITP, THD could induce response in ITP patients by upregulating NRP-1 expression and restoring the proportion of Tregs and Bregs.	Thalidomide	99-102	neuropilin 1	Homo sapiens	157-162
31055217-1	2019	Thalidomide is a teratogen that causes multiple malformations in the developing baby through its interaction with cereblon (CRBN), a substrate receptor subunit of the CRL4 E3 ubiquitin ligase complex.	Thalidomide	0-11	cereblon	Danio rerio	124-128
31289557-7	2019	The present data indicate that thalidomide contributes to an improvement of prognosis for patients with locally advanced EC with elevated serum VEGF levels during radiotherapy.	Thalidomide	31-42	vascular endothelial growth factor A	Homo sapiens	144-148
31464258-1	2019	Thalidomide, which is an angiogenesis inhibitor and immunomodulator that reduces tumor necrosis factor-alpha, has regained value in the treatment of multiple myeloma.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	81-108
31055217-5	2019	Knockdown of CRBN in zebrafish embryos impaired brain development and led to small brains, as did treatment with thalidomide.	Thalidomide	113-124	cereblon	Danio rerio	13-17
30612232-7	2019	Long-term follow-up found that all 12 patients received autologous stem cell transplant, melphalan-based therapy or lenalidomide/thalidomide-based therapy obtained clinical improvement, of which eight experienced decreased levels of VEGF by 50% or back to normal.	Thalidomide	129-140	vascular endothelial growth factor A	Homo sapiens	233-237
30834740-0	2019	Thalidomide and Its Analogs Differentially Target Fibroblast Growth Factor Receptors: Thalidomide Suppresses FGFR Gene Expression while Pomalidomide Dampens FGFR2 Activity.	Thalidomide	0-11	fibroblast growth factor receptor 2	Gallus gallus	157-162
30834740-8	2019	Corroboration with previous studies suggests that thalidomide might affect FGFR expression through the transcription factor, E2F1.	Thalidomide	50-61	E2F transcription factor 1	Gallus gallus	125-129
30834740-11	2019	Kinome analysis revealed that kinase activities of FGFR2 and FGFR3 (G697C) reduced by 31% and 65%, respectively, in the presence of 10 muM thalidomide.	Thalidomide	139-150	fibroblast growth factor receptor 2	Gallus gallus	51-56
30834740-11	2019	Kinome analysis revealed that kinase activities of FGFR2 and FGFR3 (G697C) reduced by 31% and 65%, respectively, in the presence of 10 muM thalidomide.	Thalidomide	139-150	fibroblast growth factor receptor 3	Gallus gallus	61-66
31157769-1	2019	The immunomodulatory drugs (IMiDs) thalidomide and its analogs, lenalidomide and pomalidomide, all FDA approved drugs for the treatment of multiple myeloma, induce ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase for proteasomal degradation.	Thalidomide	35-46	IKAROS family zinc finger 1	Homo sapiens	241-246
31157769-1	2019	The immunomodulatory drugs (IMiDs) thalidomide and its analogs, lenalidomide and pomalidomide, all FDA approved drugs for the treatment of multiple myeloma, induce ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase for proteasomal degradation.	Thalidomide	35-46	IKAROS family zinc finger 3	Homo sapiens	252-258
31157769-1	2019	The immunomodulatory drugs (IMiDs) thalidomide and its analogs, lenalidomide and pomalidomide, all FDA approved drugs for the treatment of multiple myeloma, induce ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase for proteasomal degradation.	Thalidomide	35-46	IKAROS family zinc finger 3	Homo sapiens	260-265
31157769-1	2019	The immunomodulatory drugs (IMiDs) thalidomide and its analogs, lenalidomide and pomalidomide, all FDA approved drugs for the treatment of multiple myeloma, induce ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase for proteasomal degradation.	Thalidomide	35-46	cereblon	Homo sapiens	285-289
31157769-1	2019	The immunomodulatory drugs (IMiDs) thalidomide and its analogs, lenalidomide and pomalidomide, all FDA approved drugs for the treatment of multiple myeloma, induce ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase for proteasomal degradation.	Thalidomide	35-46	mitochondrial E3 ubiquitin protein ligase 1	Homo sapiens	291-310
30687387-8	2018	The observed limb phenotype is similar to the severe proximal truncations observed in human babies exposed to thalidomide, which has been proposed to block the Fgf10-AER-Fgf8 feedback loop.	Thalidomide	110-121	fibroblast growth factor 10	Homo sapiens	160-165
30683719-3	2019	The thalidomide-like molecules (collectively called the IMiDs) bind to the ubiquitously expressed cereblon ubiquitin ligase complex and alter its substrate specificity such that it targets the IKZF1 and IKZF3 lymphocyte transcription factors for destruction.	Thalidomide	4-15	IKAROS family zinc finger 1	Homo sapiens	193-198
30683719-3	2019	The thalidomide-like molecules (collectively called the IMiDs) bind to the ubiquitously expressed cereblon ubiquitin ligase complex and alter its substrate specificity such that it targets the IKZF1 and IKZF3 lymphocyte transcription factors for destruction.	Thalidomide	4-15	IKAROS family zinc finger 3	Homo sapiens	203-208
30736806-7	2019	Importantly, intraperitoneal injection of the TNF-alpha inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyperacetylation in the Scn8a promoter, thus subsequently attenuating Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT.	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	46-55
30736806-7	2019	Importantly, intraperitoneal injection of the TNF-alpha inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyperacetylation in the Scn8a promoter, thus subsequently attenuating Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT.	Thalidomide	66-77	signal transducer and activator of transcription 3	Homo sapiens	109-114
30736806-7	2019	Importantly, intraperitoneal injection of the TNF-alpha inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyperacetylation in the Scn8a promoter, thus subsequently attenuating Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT.	Thalidomide	66-77	signal transducer and activator of transcription 3	Homo sapiens	148-153
30736806-7	2019	Importantly, intraperitoneal injection of the TNF-alpha inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyperacetylation in the Scn8a promoter, thus subsequently attenuating Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT.	Thalidomide	66-77	sodium voltage-gated channel alpha subunit 8	Homo sapiens	193-198
30736806-7	2019	Importantly, intraperitoneal injection of the TNF-alpha inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyperacetylation in the Scn8a promoter, thus subsequently attenuating Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT.	Thalidomide	66-77	neuron navigator 1	Homo sapiens	239-243
30717761-10	2019	Thalidomide AEs occurred at more similar rates in males (25 AEs in 41 men, 60.9%) and females (12 in 26 (46.2%), but were more common in ENG patients (17 in 17) than in ACVRL1 (14 in 34, p &lt; 0.0001).	Thalidomide	0-11	activin A receptor like type 1	Homo sapiens	169-175
30682785-4	2019	We have previously shown that 3,6"-dithiothalidomide (3,6"-DT), a thalidomide analog that is more potent than thalidomide with similar brain penetration, selectively inhibits the synthesis of TNF-alpha in cultured cells and reverses behavioral impairments induced by mild TBI in mice.	Thalidomide	41-52	tumor necrosis factor	Mus musculus	192-201
30682785-4	2019	We have previously shown that 3,6"-dithiothalidomide (3,6"-DT), a thalidomide analog that is more potent than thalidomide with similar brain penetration, selectively inhibits the synthesis of TNF-alpha in cultured cells and reverses behavioral impairments induced by mild TBI in mice.	Thalidomide	66-77	tumor necrosis factor	Mus musculus	192-201
30687387-8	2018	The observed limb phenotype is similar to the severe proximal truncations observed in human babies exposed to thalidomide, which has been proposed to block the Fgf10-AER-Fgf8 feedback loop.	Thalidomide	110-121	fibroblast growth factor 8	Homo sapiens	170-174
30362282-8	2019	We emphasize targeting a more specific Th1 mechanism via the tumour necrosis factor (TNF)-alpha cytokine antagonist thalidomide, as it is the only TNF-alpha antagonist currently approved for use in infectious disease settings and has been shown to decrease Th1 overreaction, restoring immune balance in HIV-CM IRIS.	Thalidomide	116-127	negative elongation factor complex member C/D	Homo sapiens	39-42
30602127-3	2019	Notably, targeting CRL4 has recently emerged as a noval anti-cancer strategy, including thalidomide and its derivatives that bind to the substrate recognition receptor cereblon (CRBN), and anticancer sulfonamides that target DCAF15 to suppress the neoplastic proliferation of multiple myeloma and colorectal cancers, respectively.	Thalidomide	88-99	cereblon	Homo sapiens	178-182
30651882-12	2019	Taken together, these results suggest that Thd may have therapeutic potential in diabetic renal injury via the AMPK signaling pathway.	Thalidomide	43-46	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	111-115
30651882-0	2019	Thalidomide decreases high glucose-induced extracellular matrix protein synthesis in mesangial cells via the AMPK pathway.	Thalidomide	0-11	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	109-113
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	138-186
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	188-192
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	nuclear factor kappa B subunit 1	Homo sapiens	239-248
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	C-C motif chemokine ligand 2	Rattus norvegicus	250-284
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	C-C motif chemokine ligand 2	Rattus norvegicus	286-291
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	61-72	transforming growth factor, beta 1	Rattus norvegicus	297-335
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	138-186
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	188-192
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	nuclear factor kappa B subunit 1	Homo sapiens	239-248
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	C-C motif chemokine ligand 2	Rattus norvegicus	250-284
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	C-C motif chemokine ligand 2	Rattus norvegicus	286-291
30651882-1	2019	A previous study demonstrated the renal-protective effect of thalidomide (Thd) in diabetic nephropathy rats through the activation of the adenosine monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling pathways.	Thalidomide	74-77	transforming growth factor, beta 1	Rattus norvegicus	297-335
30362282-8	2019	We emphasize targeting a more specific Th1 mechanism via the tumour necrosis factor (TNF)-alpha cytokine antagonist thalidomide, as it is the only TNF-alpha antagonist currently approved for use in infectious disease settings and has been shown to decrease Th1 overreaction, restoring immune balance in HIV-CM IRIS.	Thalidomide	116-127	tumor necrosis factor	Homo sapiens	61-95
30362282-8	2019	We emphasize targeting a more specific Th1 mechanism via the tumour necrosis factor (TNF)-alpha cytokine antagonist thalidomide, as it is the only TNF-alpha antagonist currently approved for use in infectious disease settings and has been shown to decrease Th1 overreaction, restoring immune balance in HIV-CM IRIS.	Thalidomide	116-127	tumor necrosis factor	Homo sapiens	147-156
30362282-8	2019	We emphasize targeting a more specific Th1 mechanism via the tumour necrosis factor (TNF)-alpha cytokine antagonist thalidomide, as it is the only TNF-alpha antagonist currently approved for use in infectious disease settings and has been shown to decrease Th1 overreaction, restoring immune balance in HIV-CM IRIS.	Thalidomide	116-127	negative elongation factor complex member C/D	Homo sapiens	257-260
30155589-1	2018	Cancer-related fatigue (CRF) is one of the adverse events in multiple myeloma (MM) patients treated with cytotoxic agents, proteasome inhibitors (PIs), and immunomodulatory drugs (IMiDs) such as bortezomib, lenalidomide, and thalidomide.	Thalidomide	225-236	complement C1q like 1	Homo sapiens	0-22
31031470-2	2019	Erythema nodosum leprosum(ENL) in special cases need to be managed with capsule thalidomide in varying doses.	Thalidomide	80-91	MLLT1 super elongation complex subunit	Homo sapiens	26-29
31031470-3	2019	We report such a case of bradycardia in thalidomide dose dependent manner in a young ENL male.	Thalidomide	40-51	MLLT1 super elongation complex subunit	Homo sapiens	85-88
30597765-0	2018	Thalidomide Teratogenic Effects Linked to Degradation of SALL4: After 60 years, researchers have now shed light on the mechanism underlying thalidomide"s devastating teratogenic effects.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	57-62
30597765-0	2018	Thalidomide Teratogenic Effects Linked to Degradation of SALL4: After 60 years, researchers have now shed light on the mechanism underlying thalidomide"s devastating teratogenic effects.	Thalidomide	140-151	spalt like transcription factor 4	Homo sapiens	57-62
30339882-0	2018	Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-beta/Smad3 signaling pathway in an Nrf2-dependent manner.	Thalidomide	0-11	SMAD family member 3	Mus musculus	100-105
30339882-0	2018	Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-beta/Smad3 signaling pathway in an Nrf2-dependent manner.	Thalidomide	0-11	nuclear factor, erythroid derived 2, like 2	Mus musculus	130-134
31068561-5	2019	A randomized controlled trial on thalidomide plus dexamethasone for POEMS syndrome showed reduced serum VEGF levels after therapy; however, the incidence of peripheral neuropathy, a well-known side effect of both thalidomide and bortezomib, increased.	Thalidomide	33-44	vascular endothelial growth factor A	Homo sapiens	104-108
30344721-0	2018	Association of CD117 and HLA-DR expression with shorter overall survival and/or progression-free survival in patients with multiple myeloma treated with bortezomib and thalidomide combination treatment without transplantation.	Thalidomide	168-179	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	15-20
30534560-2	2018	Based on reports that vascular endothelial growth factor- (VEGF-) mediated angiogenesis is critical for MM pathogenesis, the antiangiogenic compound thalidomide has been added to VAD (T-VAD).	Thalidomide	149-160	vascular endothelial growth factor A	Homo sapiens	22-64
30373817-7	2018	We have also tested a thalidomide derivative, FPFT-2216, which showed an inhibitory effect toward IKZF1 protein level.	Thalidomide	22-33	IKAROS family zinc finger 1	Mus musculus	98-103
30385546-0	2018	Defining the human C2H2 zinc finger degrome targeted by thalidomide analogs through CRBN.	Thalidomide	56-67	cereblon	Homo sapiens	84-88
30385546-1	2018	The small molecules thalidomide, lenalidomide, and pomalidomide induce the ubiquitination and proteasomal degradation of the transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) by recruiting a Cys2-His2 (C2H2) zinc finger domain to Cereblon (CRBN), the substrate receptor of the CRL4CRBN E3 ubiquitin ligase.	Thalidomide	20-31	IKAROS family zinc finger 1	Homo sapiens	155-160
30385546-1	2018	The small molecules thalidomide, lenalidomide, and pomalidomide induce the ubiquitination and proteasomal degradation of the transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) by recruiting a Cys2-His2 (C2H2) zinc finger domain to Cereblon (CRBN), the substrate receptor of the CRL4CRBN E3 ubiquitin ligase.	Thalidomide	20-31	IKAROS family zinc finger 3	Homo sapiens	174-179
30385546-1	2018	The small molecules thalidomide, lenalidomide, and pomalidomide induce the ubiquitination and proteasomal degradation of the transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) by recruiting a Cys2-His2 (C2H2) zinc finger domain to Cereblon (CRBN), the substrate receptor of the CRL4CRBN E3 ubiquitin ligase.	Thalidomide	20-31	cereblon	Homo sapiens	236-244
30385546-1	2018	The small molecules thalidomide, lenalidomide, and pomalidomide induce the ubiquitination and proteasomal degradation of the transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) by recruiting a Cys2-His2 (C2H2) zinc finger domain to Cereblon (CRBN), the substrate receptor of the CRL4CRBN E3 ubiquitin ligase.	Thalidomide	20-31	cereblon	Homo sapiens	246-250
30252647-1	2018	A transcription factor called SALL4 could be the missing link between thalidomide and the limb defects caused by the drug.	Thalidomide	70-81	spalt like transcription factor 4	Homo sapiens	30-35
30190590-0	2018	SALL4 mediates teratogenicity as a thalidomide-dependent cereblon substrate.	Thalidomide	35-46	spalt like transcription factor 4	Homo sapiens	0-5
30190590-4	2018	Instead, we identify SALL4 as a thalidomide-dependent cereblon neosubstrate.	Thalidomide	32-43	spalt like transcription factor 4	Homo sapiens	21-26
30190590-5	2018	Human mutations in SALL4 cause Duane-radial ray, IVIC, and acro-renal-ocular syndromes with overlapping clinical presentations to thalidomide embryopathy, including phocomelia.	Thalidomide	130-141	spalt like transcription factor 4	Homo sapiens	19-24
30301277-5	2018	Among them, 2-[1-(3-chlorobenzyl)-2,6-dioxopiperidin-3-yl]isoindoline-1,3-dione (5c) was found to inhibit TNF-alpha and IL-6 expression in HaCaT cells with a higher potency than thalidomide and no significant cell cytotoxicity was detected at 10 muM.	Thalidomide	178-189	tumor necrosis factor	Homo sapiens	106-115
30064974-0	2018	Crbn I391V is sufficient to confer in vivo sensitivity to thalidomide and its derivatives in mice.	Thalidomide	58-69	cereblon	Mus musculus	0-4
30064974-3	2018	Here, we report the development of a mouse model that is sensitive to thalidomide derivatives because of a single amino acid change in the direct target of thalidomide derivatives, cereblon (Crbn).	Thalidomide	70-81	cereblon	Mus musculus	191-195
30064974-3	2018	Here, we report the development of a mouse model that is sensitive to thalidomide derivatives because of a single amino acid change in the direct target of thalidomide derivatives, cereblon (Crbn).	Thalidomide	156-167	cereblon	Mus musculus	191-195
30064974-4	2018	In human cells, thalidomide and its analogs bind CRBN and recruit protein targets to the CRL4CRBN E3 ubiquitin ligase, resulting in their ubiquitination and subsequent degradation by the proteasome.	Thalidomide	16-27	cereblon	Homo sapiens	49-53
30064974-5	2018	We show that mice with a single I391V amino acid change in Crbn exhibit thalidomide-induced degradation of drug targets previously identified in human cells, including Ikaros (Ikzf1), Aiolos (Ikzf3), Zfp91, and casein kinase 1a1 (Ck1alpha), both in vitro and in vivo.	Thalidomide	72-83	cereblon	Mus musculus	59-63
30064974-5	2018	We show that mice with a single I391V amino acid change in Crbn exhibit thalidomide-induced degradation of drug targets previously identified in human cells, including Ikaros (Ikzf1), Aiolos (Ikzf3), Zfp91, and casein kinase 1a1 (Ck1alpha), both in vitro and in vivo.	Thalidomide	72-83	IKAROS family zinc finger 1	Homo sapiens	168-174
30064974-5	2018	We show that mice with a single I391V amino acid change in Crbn exhibit thalidomide-induced degradation of drug targets previously identified in human cells, including Ikaros (Ikzf1), Aiolos (Ikzf3), Zfp91, and casein kinase 1a1 (Ck1alpha), both in vitro and in vivo.	Thalidomide	72-83	IKAROS family zinc finger 1	Homo sapiens	176-181
30064974-5	2018	We show that mice with a single I391V amino acid change in Crbn exhibit thalidomide-induced degradation of drug targets previously identified in human cells, including Ikaros (Ikzf1), Aiolos (Ikzf3), Zfp91, and casein kinase 1a1 (Ck1alpha), both in vitro and in vivo.	Thalidomide	72-83	IKAROS family zinc finger 3	Homo sapiens	192-197
30064974-5	2018	We show that mice with a single I391V amino acid change in Crbn exhibit thalidomide-induced degradation of drug targets previously identified in human cells, including Ikaros (Ikzf1), Aiolos (Ikzf3), Zfp91, and casein kinase 1a1 (Ck1alpha), both in vitro and in vivo.	Thalidomide	72-83	ZFP91 zinc finger protein, atypical E3 ubiquitin ligase	Homo sapiens	200-205
30064974-8	2018	We further demonstrate that Crbn I391V is sufficient to confer thalidomide-induced fetal loss in mice, capturing a major toxicity of this class of drugs.	Thalidomide	63-74	cereblon	Mus musculus	28-32
30118587-7	2018	Homobifunctional CRBN degraders will be useful tools for future biomedical investigations of CRBN-related signaling and may help to further elucidate the molecular mechanism of thalidomide analogues.	Thalidomide	177-188	cereblon	Homo sapiens	17-21
30118587-1	2018	The immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide, all approved for the treatment of multiple myeloma, induce targeted ubiquitination and degradation of Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase.	Thalidomide	35-46	IKAROS family zinc finger 1	Homo sapiens	182-188
30118587-1	2018	The immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide, all approved for the treatment of multiple myeloma, induce targeted ubiquitination and degradation of Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase.	Thalidomide	35-46	IKAROS family zinc finger 1	Homo sapiens	190-195
30118587-7	2018	Homobifunctional CRBN degraders will be useful tools for future biomedical investigations of CRBN-related signaling and may help to further elucidate the molecular mechanism of thalidomide analogues.	Thalidomide	177-188	cereblon	Homo sapiens	93-97
30118587-1	2018	The immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide, all approved for the treatment of multiple myeloma, induce targeted ubiquitination and degradation of Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase.	Thalidomide	35-46	IKAROS family zinc finger 3	Homo sapiens	201-207
30118587-1	2018	The immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide, all approved for the treatment of multiple myeloma, induce targeted ubiquitination and degradation of Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase.	Thalidomide	35-46	IKAROS family zinc finger 3	Homo sapiens	209-214
29938270-9	2018	Thalidomide, as an inhibitor of ubiquitin ligase, was able to prevent the decrease in claudin-1 protein expression and the TEER reduction in Caco-2 cells.	Thalidomide	0-11	claudin 1	Homo sapiens	86-95
30118587-1	2018	The immunomodulatory drugs (IMiDs) thalidomide, lenalidomide, and pomalidomide, all approved for the treatment of multiple myeloma, induce targeted ubiquitination and degradation of Ikaros (IKZF1) and Aiolos (IKZF3) via the cereblon (CRBN) E3 ubiquitin ligase.	Thalidomide	35-46	cereblon	Homo sapiens	234-238
30288348-5	2018	Results: We found that high IKZF3, but not IKZF1, expression in T-cells correlates with superior overall survival in MMIII patients treated with immunomodulatory drugs (thalidomide, lenalidomide and pomalidomide).	Thalidomide	169-180	IKAROS family zinc finger 3	Homo sapiens	28-33
30029933-15	2018	CONCLUSIONS: Thalidomide, which is a specific VEGF inhibitor, significantly inhibited neointimal hyperplasia and vascular restenosis after balloon injury to the carotid artery in rats, thus potentially providing a novel method for the prevention and treatment of restenosis, especially in-stent restenosis.	Thalidomide	13-24	vascular endothelial growth factor A	Rattus norvegicus	46-50
30067223-0	2018	Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray syndrome.	Thalidomide	0-11	spalt like transcription factor 4	Homo sapiens	36-41
30067223-4	2018	Strikingly, heterozygous loss of function mutations in SALL4 result in a human developmental condition that phenocopies thalidomide-induced birth defects such as absence of thumbs, phocomelia, defects in ear and eye development, and congenital heart disease.	Thalidomide	120-131	spalt like transcription factor 4	Homo sapiens	55-60
30067223-5	2018	We find that thalidomide induces degradation of SALL4 exclusively in humans, primates, and rabbits, but not in rodents or fish, providing a mechanistic link for the species-specific pathogenesis of thalidomide syndrome.	Thalidomide	13-24	spalt like transcription factor 4	Homo sapiens	48-53
30067223-5	2018	We find that thalidomide induces degradation of SALL4 exclusively in humans, primates, and rabbits, but not in rodents or fish, providing a mechanistic link for the species-specific pathogenesis of thalidomide syndrome.	Thalidomide	198-209	spalt like transcription factor 4	Homo sapiens	48-53
30069488-0	2018	PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-kappaB Inactivation.	Thalidomide	11-22	melanotransferrin	Homo sapiens	144-147
30069488-0	2018	PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-kappaB Inactivation.	Thalidomide	11-22	SEC61 translocon subunit alpha 1	Homo sapiens	152-157
30069488-0	2018	PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-kappaB Inactivation.	Thalidomide	11-22	nuclear factor kappa B subunit 1	Homo sapiens	162-171
30069488-5	2018	We demonstrated that the inhibition of endosomal recruitment of p97 and Sec61, together with attenuated NF-kappaB activation and Myddosome formation, contributes to PYR-41- and thalidomide-impaired cross-presentation and thereby reverses cross-activation of T cells.	Thalidomide	177-188	melanotransferrin	Homo sapiens	64-67
30069488-5	2018	We demonstrated that the inhibition of endosomal recruitment of p97 and Sec61, together with attenuated NF-kappaB activation and Myddosome formation, contributes to PYR-41- and thalidomide-impaired cross-presentation and thereby reverses cross-activation of T cells.	Thalidomide	177-188	SEC61 translocon subunit alpha 1	Homo sapiens	72-77
30069488-5	2018	We demonstrated that the inhibition of endosomal recruitment of p97 and Sec61, together with attenuated NF-kappaB activation and Myddosome formation, contributes to PYR-41- and thalidomide-impaired cross-presentation and thereby reverses cross-activation of T cells.	Thalidomide	177-188	nuclear factor kappa B subunit 1	Homo sapiens	104-113
30069488-6	2018	These observations suggest that NF-kappaB signaling and p97 and Sec61 molecules are candidates for dealing with the side effects of PYR-41 and thalidomide.	Thalidomide	143-154	nuclear factor kappa B subunit 1	Homo sapiens	32-41
30069488-6	2018	These observations suggest that NF-kappaB signaling and p97 and Sec61 molecules are candidates for dealing with the side effects of PYR-41 and thalidomide.	Thalidomide	143-154	melanotransferrin	Homo sapiens	56-59
30069488-6	2018	These observations suggest that NF-kappaB signaling and p97 and Sec61 molecules are candidates for dealing with the side effects of PYR-41 and thalidomide.	Thalidomide	143-154	SEC61 translocon subunit alpha 1	Homo sapiens	64-69
29763936-0	2018	Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling.	Thalidomide	26-37	AKT serine/threonine kinase 1	Homo sapiens	107-110
30029250-7	2018	Results: Thalidomide and three novel analogs all showed inhibitory effects on endothelial cell proliferation and VEGF expression in vitro.	Thalidomide	9-20	vascular endothelial growth factor A	Rattus norvegicus	113-117
29750304-2	2018	Thalidomide is a drug that has been reported to inhibit angiogenesis and reduce VEGF production by downregulating VEGF expression.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	80-84
29750304-2	2018	Thalidomide is a drug that has been reported to inhibit angiogenesis and reduce VEGF production by downregulating VEGF expression.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	114-118
29750304-13	2018	Thus, the results of the present study demonstrated that intraperitoneal administration of thalidomide may alleviate the development of early OA by suppressing VEGF expression in mice and may have potential as a novel therapy for the treatment of OA.	Thalidomide	91-102	vascular endothelial growth factor A	Mus musculus	160-164
29763936-0	2018	Synergistic Inhibition of Thalidomide and Icotinib on Human Non-Small Cell Lung Carcinomas Through ERK and AKT Signaling.	Thalidomide	26-37	EPH receptor B2	Homo sapiens	99-102
29750304-0	2018	Intraperitoneal injection of thalidomide alleviates early osteoarthritis development by suppressing vascular endothelial growth factor expression in mice.	Thalidomide	29-40	vascular endothelial growth factor A	Mus musculus	100-134
29854627-4	2018	Thalidomide and carboplatin induced up-regulation of the expression of p53, tumor necrosis factor-alpha and interleukin-6 in brain and kidney.	Thalidomide	0-11	tumor protein p53	Homo sapiens	71-74
29593101-13	2018	Thalidomide reduced the burden of CD68+ cells and the expression of inflammatory cytokines in the bAVM lesions.	Thalidomide	0-11	CD68 antigen	Mus musculus	34-38
29593101-15	2018	Thalidomide increased Pdgfb expression in bAVM lesion.	Thalidomide	0-11	platelet derived growth factor, B polypeptide	Mus musculus	22-27
29593101-16	2018	Overexpression of PDGFB mimicked the effect of thalidomide.	Thalidomide	47-58	platelet derived growth factor, B polypeptide	Mus musculus	18-23
29593101-17	2018	CONCLUSIONS: Thalidomide and lenalidomide improve mural cell coverage of bAVM vessels and reduce bAVM hemorrhage, which is likely through upregulation of Pdgfb expression.	Thalidomide	13-24	platelet derived growth factor, B polypeptide	Mus musculus	154-159
29854627-8	2018	GSPE co-treatment with thalidomide and carboplatin reduced their brain and renal damage, oxidative stress, diminished cytokines, p53, neurotransmitters and biochemical parameters, and inhibited brain and renal cell apoptosis.	Thalidomide	23-34	tumor protein p53	Homo sapiens	129-132
29746508-0	2018	CUL5 is required for thalidomide-dependent inhibition of cellular proliferation.	Thalidomide	21-32	cullin 5	Homo sapiens	0-4
29746508-3	2018	We discovered that CUL5 (previously identified as VACM-1), a scaffold protein in E3 ligase complexes, is involved in thalidomide-dependent inhibition of endothelial cell growth.	Thalidomide	117-128	cullin 5	Homo sapiens	19-23
29746508-3	2018	We discovered that CUL5 (previously identified as VACM-1), a scaffold protein in E3 ligase complexes, is involved in thalidomide-dependent inhibition of endothelial cell growth.	Thalidomide	117-128	cullin 5	Homo sapiens	50-56
29746508-4	2018	Our results show that in human endothelial cells (HUVEC), thalidomide-dependent decrease in cell growth was associated with decreased nuclear localization of CUL5.	Thalidomide	58-69	cullin 5	Homo sapiens	158-162
29746508-7	2018	In this study, the antiproliferative response to thalidomide was compromised in RAMEC expressing mutated CUL5.	Thalidomide	49-60	cullin 5	Homo sapiens	105-109
29746508-8	2018	These results suggest that CUL5 protein is involved in the thalidomide-dependent regulation of cellular proliferation in vitro.	Thalidomide	59-70	cullin 5	Homo sapiens	27-31
29746508-9	2018	Consequently, CUL5 may be an important part of the mechanism for thalidomide-dependent inhibition of cellular proliferation, as well as a novel biomarker for predicting a response to thalidomide for the treatment of disorders such as multiple myeloma and HIV infection.	Thalidomide	65-76	cullin 5	Homo sapiens	14-18
29746508-9	2018	Consequently, CUL5 may be an important part of the mechanism for thalidomide-dependent inhibition of cellular proliferation, as well as a novel biomarker for predicting a response to thalidomide for the treatment of disorders such as multiple myeloma and HIV infection.	Thalidomide	183-194	cullin 5	Homo sapiens	14-18
29844872-2	2018	The aim of this study was to evaluate the influence of selected clinical and molecular factors including single nucleotide polymorphisms (SNPs) in CRBN gene on the efficacy of first line CTD (cyclophosphamide, thalidomide, dexamethasone) chemotherapy in patients with multiple myeloma.	Thalidomide	210-221	cereblon	Homo sapiens	147-151
29844872-2	2018	The aim of this study was to evaluate the influence of selected clinical and molecular factors including single nucleotide polymorphisms (SNPs) in CRBN gene on the efficacy of first line CTD (cyclophosphamide, thalidomide, dexamethasone) chemotherapy in patients with multiple myeloma.	Thalidomide	210-221	CTD	Homo sapiens	187-190
29844872-11	2018	In conclusion, SNPs of the CRBN gene may be useful in qualifying patients for treatment with regimens containing thalidomide.	Thalidomide	113-124	cereblon	Homo sapiens	27-31
29653983-5	2018	Adoptive transfer of wild-type Gr-1+CD11b+ MDSCs from tumor-bearing mice reversed this antitumor response, whereas caspase-1 inhibiting thalidomide-treated MDSCs phenocopied the antitumor response found in caspase-1 null mice.	Thalidomide	136-147	caspase 1	Mus musculus	115-124
29653983-5	2018	Adoptive transfer of wild-type Gr-1+CD11b+ MDSCs from tumor-bearing mice reversed this antitumor response, whereas caspase-1 inhibiting thalidomide-treated MDSCs phenocopied the antitumor response found in caspase-1 null mice.	Thalidomide	136-147	caspase 1	Mus musculus	206-215
29854627-4	2018	Thalidomide and carboplatin induced up-regulation of the expression of p53, tumor necrosis factor-alpha and interleukin-6 in brain and kidney.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	76-103
29854627-4	2018	Thalidomide and carboplatin induced up-regulation of the expression of p53, tumor necrosis factor-alpha and interleukin-6 in brain and kidney.	Thalidomide	0-11	interleukin 6	Homo sapiens	108-121
29449372-1	2018	Upon binding to thalidomide and other immunomodulatory drugs, the E3 ligase substrate receptor cereblon (CRBN) promotes proteosomal destruction by engaging the DDB1-CUL4A-Roc1-RBX1 E3 ubiquitin ligase in human cells but not in mouse cells, suggesting that sequence variations in CRBN may cause its inactivation.	Thalidomide	16-27	cereblon	Mus musculus	105-109
29719394-1	2018	Introduction: Thalidomide (THA) is an angiogenesis inhibitor and an efficient inhibitor of the tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	95-122
29719394-1	2018	Introduction: Thalidomide (THA) is an angiogenesis inhibitor and an efficient inhibitor of the tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	124-133
29719394-1	2018	Introduction: Thalidomide (THA) is an angiogenesis inhibitor and an efficient inhibitor of the tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	27-30	tumor necrosis factor	Homo sapiens	95-122
29719394-1	2018	Introduction: Thalidomide (THA) is an angiogenesis inhibitor and an efficient inhibitor of the tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	27-30	tumor necrosis factor	Homo sapiens	124-133
29695106-3	2018	Additionally, BSG is implicated in response to treatment with immunomodulatory drugs (thalidomide and its derivatives).	Thalidomide	86-97	basigin (Ok blood group)	Homo sapiens	14-17
29449372-1	2018	Upon binding to thalidomide and other immunomodulatory drugs, the E3 ligase substrate receptor cereblon (CRBN) promotes proteosomal destruction by engaging the DDB1-CUL4A-Roc1-RBX1 E3 ubiquitin ligase in human cells but not in mouse cells, suggesting that sequence variations in CRBN may cause its inactivation.	Thalidomide	16-27	damage specific DNA binding protein 1	Mus musculus	160-164
29449372-1	2018	Upon binding to thalidomide and other immunomodulatory drugs, the E3 ligase substrate receptor cereblon (CRBN) promotes proteosomal destruction by engaging the DDB1-CUL4A-Roc1-RBX1 E3 ubiquitin ligase in human cells but not in mouse cells, suggesting that sequence variations in CRBN may cause its inactivation.	Thalidomide	16-27	cullin 4A	Mus musculus	165-182
29449372-1	2018	Upon binding to thalidomide and other immunomodulatory drugs, the E3 ligase substrate receptor cereblon (CRBN) promotes proteosomal destruction by engaging the DDB1-CUL4A-Roc1-RBX1 E3 ubiquitin ligase in human cells but not in mouse cells, suggesting that sequence variations in CRBN may cause its inactivation.	Thalidomide	16-27	cereblon	Mus musculus	279-283
29449372-4	2018	With a series of recombinant thalidomide-binding domain (TBD) proteins, we show that CRBN sequence variants retain their drug-binding properties to both classical immunomodulatory drugs and dBET1, a chemical compound and targeting ligand designed to degrade bromodomain-containing 4 (BRD4) via a CRBN-dependent mechanism.	Thalidomide	29-40	cereblon	Mus musculus	85-89
29449372-4	2018	With a series of recombinant thalidomide-binding domain (TBD) proteins, we show that CRBN sequence variants retain their drug-binding properties to both classical immunomodulatory drugs and dBET1, a chemical compound and targeting ligand designed to degrade bromodomain-containing 4 (BRD4) via a CRBN-dependent mechanism.	Thalidomide	29-40	Blocked early in transport 1	Drosophila melanogaster	190-195
29552137-7	2018	Furthermore, vincristine administration induced the upregulation of tumor necrosis factor (TNF)-alpha production in DRGs, and inhibition of TNF-alpha synthesis with thalidomide in vivo reversed TRPV1 protein expression, as well as pain hypersensitivity induced by vincristine in rats.	Thalidomide	165-176	tumor necrosis factor	Rattus norvegicus	140-149
29530986-8	2018	These results strongly suggest that increased BK channel activity is the pathological mechanism of intellectual disability in CRBN mutations.SIGNIFICANCE STATEMENTCereblon (CRBN), a well known target of the immunomodulatory drug thalidomide, was originally identified as a gene that causes human intellectual disability when mutated.	Thalidomide	229-240	cereblon	Homo sapiens	126-130
29530986-8	2018	These results strongly suggest that increased BK channel activity is the pathological mechanism of intellectual disability in CRBN mutations.SIGNIFICANCE STATEMENTCereblon (CRBN), a well known target of the immunomodulatory drug thalidomide, was originally identified as a gene that causes human intellectual disability when mutated.	Thalidomide	229-240	cereblon	Homo sapiens	173-177
29552137-7	2018	Furthermore, vincristine administration induced the upregulation of tumor necrosis factor (TNF)-alpha production in DRGs, and inhibition of TNF-alpha synthesis with thalidomide in vivo reversed TRPV1 protein expression, as well as pain hypersensitivity induced by vincristine in rats.	Thalidomide	165-176	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	194-199
29632537-3	2018	Recent studies also show that thalidomide analogs, cyclophosphamide, and other small molecules are able to act on TNFR2, resulting in the elimination of TNFR2-expressing Tregs.	Thalidomide	30-41	TNF receptor superfamily member 1B	Homo sapiens	114-119
29632537-3	2018	Recent studies also show that thalidomide analogs, cyclophosphamide, and other small molecules are able to act on TNFR2, resulting in the elimination of TNFR2-expressing Tregs.	Thalidomide	30-41	TNF receptor superfamily member 1B	Homo sapiens	153-158
29496670-5	2018	Using a thalidomide analog bead pull-down assay, we showed that IMiD compounds directly bind CRBN in CD34+ cells.	Thalidomide	8-19	cereblon	Mus musculus	93-97
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	fibroblast growth factor 8	Homo sapiens	68-72
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	fibroblast growth factor 10	Homo sapiens	74-79
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	bone morphogenetic protein 4	Homo sapiens	81-85
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	sonic hedgehog signaling molecule	Homo sapiens	87-90
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	tumor protein p53	Homo sapiens	92-96
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	tumor protein p63	Homo sapiens	98-102
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	tumor protein p73	Homo sapiens	108-112
29496670-5	2018	Using a thalidomide analog bead pull-down assay, we showed that IMiD compounds directly bind CRBN in CD34+ cells.	Thalidomide	8-19	CD34 antigen	Mus musculus	101-105
29681766-12	2018	In addition, the TNF-alpha synthesis inhibitor thalidomide significantly attenuated the number of paclitaxel-induced TUNEL-positive neurons in the hippocampus and restored the impaired spatial learning and memory function in paclitaxel-treated rats.	Thalidomide	47-58	tumor necrosis factor	Rattus norvegicus	17-26
29223784-0	2018	Thalidomide attenuates development of morphine dependence in mice by inhibiting PI3K/Akt and nitric oxide signaling pathways.	Thalidomide	0-11	thymoma viral proto-oncogene 1	Mus musculus	85-88
29223784-6	2018	In the present study, we aimed to explore the effect of thalidomide on the development of morphine dependence targeting PI3K/Akt (PKB) and nitric oxide (NO) pathways.	Thalidomide	56-67	thymoma viral proto-oncogene 1	Mus musculus	125-128
29223784-6	2018	In the present study, we aimed to explore the effect of thalidomide on the development of morphine dependence targeting PI3K/Akt (PKB) and nitric oxide (NO) pathways.	Thalidomide	56-67	AKT serine/threonine kinase 1	Homo sapiens	130-133
29223784-8	2018	In both models the consequent effect of thalidomide on PI3K/Akt and/or NO signaling in morphine dependence was determined.	Thalidomide	40-51	thymoma viral proto-oncogene 1	Mus musculus	60-63
29223784-9	2018	Thalidomide alone or in combination with PI3K inhibitor, Akt inhibitor or nitric oxide synthase (NOS) inhibitors significantly reduced naloxone induced withdrawal signs in morphine dependent mice.	Thalidomide	0-11	nitric oxide synthase 1, neuronal	Mus musculus	74-95
29223784-11	2018	In T98G human glioblastoma cells, thalidomide alone or in combination with PI3K and Akt inhibitors significantly reduced iNOS expression in comparison to the morphine treated cells.	Thalidomide	34-45	nitric oxide synthase 2	Homo sapiens	121-125
29223784-12	2018	Also, morphine-induced p-Akt was suppressed when T98G cells were pretreated with thalidomide.	Thalidomide	81-92	thymoma viral proto-oncogene 1	Mus musculus	25-28
29223784-14	2018	Moreover, these data indicate that thalidomide attenuates the development of morphine dependence in vivo and in vitro by inhibition of PI3K/Akt and nitric oxide signaling pathways.	Thalidomide	35-46	thymoma viral proto-oncogene 1	Mus musculus	140-143
29383859-6	2018	The pro-angiogenic effect of GDF15 was through the activation of Src and its downstream AKT, MAPK, and NF-kappaB signaling, which was blocked by thalidomide.	Thalidomide	145-156	growth differentiation factor 15	Mus musculus	29-34
29383859-6	2018	The pro-angiogenic effect of GDF15 was through the activation of Src and its downstream AKT, MAPK, and NF-kappaB signaling, which was blocked by thalidomide.	Thalidomide	145-156	Rous sarcoma oncogene	Mus musculus	65-68
29383859-6	2018	The pro-angiogenic effect of GDF15 was through the activation of Src and its downstream AKT, MAPK, and NF-kappaB signaling, which was blocked by thalidomide.	Thalidomide	145-156	thymoma viral proto-oncogene 1	Mus musculus	88-91
29410497-0	2018	The Neuroprotective Effect of Thalidomide against Ischemia through the Cereblon-mediated Repression of AMPK Activity.	Thalidomide	30-41	cereblon	Homo sapiens	71-79
29410497-4	2018	Here we examined the molecular mechanism of thalidomide"s neuroprotective effects, focusing on its target protein, cereblon (CRBN), and its binding protein, AMP-activated protein kinase (AMPK), which plays an important role in maintaining intracellular energy homeostasis in the brain.	Thalidomide	44-55	cereblon	Homo sapiens	115-123
29410497-4	2018	Here we examined the molecular mechanism of thalidomide"s neuroprotective effects, focusing on its target protein, cereblon (CRBN), and its binding protein, AMP-activated protein kinase (AMPK), which plays an important role in maintaining intracellular energy homeostasis in the brain.	Thalidomide	44-55	cereblon	Homo sapiens	125-129
29410497-8	2018	Furthermore, we considered that the AMPK-CRBN interaction was altered when neuroprotective action by thalidomide occurred in cells under ischemic conditions.	Thalidomide	101-112	cereblon	Homo sapiens	41-45
29410497-10	2018	However, when thalidomide was administered at the same time as H2O2, the binding of AMPK and CRBN was partly restored.	Thalidomide	14-25	cereblon	Homo sapiens	93-97
29410497-11	2018	These results suggest that thalidomide inhibits the activity of AMPK via CRBN under oxidative stress and suppresses nerve cell death.	Thalidomide	27-38	cereblon	Homo sapiens	73-77
29108926-3	2018	Thalidomide analogs have the ability to induce HbF production while inhibiting the release of tumor necrosis factor-alpha.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	94-121
28786198-12	2018	Moreover, IL23R polymorphisms may contribute to poor prognosis in patients with MM treated with thalidomide and/or bortezomib.	Thalidomide	96-107	interleukin 23 receptor	Homo sapiens	10-15
29130642-1	2018	Thalidomide and its derivatives, lenalidomide and pomalidomide (also known as IMiDs), have significantly changed the treatment landscape of multiple myeloma, and the recent discovery of cereblon (CRBN) as their direct biological target has led to a deeper understanding of their complex mechanism of action.	Thalidomide	0-11	cereblon	Homo sapiens	196-200
28758232-8	2018	Finally, we found that repeated thalidomide treatment robustly enhanced CB2 receptor expression, but slightly reduced CB1 receptor expression, in the RVM.	Thalidomide	32-43	cannabinoid receptor 2	Rattus norvegicus	72-75
28758232-8	2018	Finally, we found that repeated thalidomide treatment robustly enhanced CB2 receptor expression, but slightly reduced CB1 receptor expression, in the RVM.	Thalidomide	32-43	cannabinoid receptor 1	Rattus norvegicus	118-121
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	166-177	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	49-58
29251720-2	2018	We characterized NVP-2, a selective ATP-competitive CDK9 inhibitor, and THAL-SNS-032, a selective CDK9 degrader consisting of a CDK-binding SNS-032 ligand linked to a thalidomide derivative that binds the E3 ubiquitin ligase Cereblon (CRBN).	Thalidomide	167-178	cyclin dependent kinase 9	Homo sapiens	98-102
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	27-38	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	49-58
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	166-177	tumor necrosis factor	Mus musculus	120-123
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	27-38	tumor necrosis factor	Mus musculus	120-123
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	27-38	interferon gamma	Mus musculus	128-132
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	166-177	interferon gamma	Mus musculus	128-132
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	27-38	ECSIT signalling integrator	Mus musculus	237-242
29291352-7	2018	The immunosuppressive drug thalidomide prevented NF-kappaB from binding to the promoters of its target genes (including TNF and IFNG), and combination treatment with thalidomide and dexamethasone extended survival of mice engrafted with ECSIT-T419C-transfected ENKTL cells.	Thalidomide	166-177	ECSIT signalling integrator	Mus musculus	237-242
29291352-8	2018	We added thalidomide to the conventional dexamethasone-containing therapy regimen for two patients with HPS who expressed ECSIT-V140A, and we observed reversal of their HPS and disease-free survival for longer than 3 years.	Thalidomide	9-20	ECSIT signaling integrator	Homo sapiens	122-127
28365861-4	2018	Application of the TNF-synthesis inhibitor thalidomide and the TNF-alpha antagonist etanercept dose-dependently suppressed acute itch.	Thalidomide	43-54	itchy, E3 ubiquitin protein ligase	Mus musculus	129-133
28365861-7	2018	Furthermore, chronic itch induced by dry skin was reduced by administration of thalidomide and etanercept and in TNFR1/R2 DKO mice.	Thalidomide	79-90	itchy, E3 ubiquitin protein ligase	Mus musculus	21-25
29397841-6	2018	The ratio of Th17 cells in peripheral blood and serum levels of IL-17 in patients with multiple myeloma after treatment with thalidomide were significantly lower than those before treatment, and the ratio of Treg cells and levels of IL-35 were significantly higher than those before treatment, and the ratio of Th17 / Treg cells was higher than that before treatment (P&lt;0.05).	Thalidomide	125-136	interleukin 17A	Homo sapiens	64-69
29108922-2	2018	In our previously clinical practice, we observed that thalidomide, a potent VEGF inhibitor, can significantly decrease the tumor size of one EGFR-TKI resistance patient with lung cancer cachexia.	Thalidomide	54-65	vascular endothelial growth factor A	Homo sapiens	76-80
29108922-2	2018	In our previously clinical practice, we observed that thalidomide, a potent VEGF inhibitor, can significantly decrease the tumor size of one EGFR-TKI resistance patient with lung cancer cachexia.	Thalidomide	54-65	epidermal growth factor receptor	Homo sapiens	141-145
29397841-9	2018	The anti-MM mechanism of thalidomide may relate with the regulation of Th17 / Treg cell ratio and expression levels of IL-17 and IL-35.	Thalidomide	25-36	interleukin 17A	Homo sapiens	119-124
29513882-1	2018	In the present study, we successfully developed a docetaxel (DTX) and thalidomide (TDD) co-delivery system based on low density lipoprotein (LDL) modified silica nanoparticles (LDL/SLN/DTX/TDD).	Thalidomide	70-81	aldo-keto reductase family 1 member C2	Homo sapiens	83-86
28379698-1	2018	Here we report the development of a proteolysis targeting chimera (PROTAC) based on the combination of the unique features of the sirtuin rearranging ligands (SirReals) as highly potent and isotype-selective Sirt2 inhibitors with thalidomide, a bona fide cereblon ligand.	Thalidomide	230-241	sirtuin 2	Homo sapiens	208-213
29732020-6	2018	The rele-vance of TNF-alpha to the pathogenesis of RAS has stemmed from the observations that anti- TNF-alpha drugs such as thalidomide and pentoxifylline have been found to be effective in the treatment of RAS.	Thalidomide	124-135	tumor necrosis factor	Homo sapiens	18-27
29386886-9	2018	Compared with diabetic control rats, those treated with thalidomide showed significantly improved histological alterations and biomarkers of renal function, as well as reduced expression of renal inflammatory cytokines, including NF-kappaB and MCP-1.	Thalidomide	56-67	mast cell protease 1-like 1	Rattus norvegicus	244-249
29358579-0	2018	Structural basis of thalidomide enantiomer binding to cereblon.	Thalidomide	20-31	cereblon	Danio rerio	54-62
29358579-3	2018	Here, we present structural and biochemical studies of (S)- and (R)-enantiomers bound to the primary target of thalidomide, cereblon (CRBN).	Thalidomide	111-122	cereblon	Danio rerio	124-132
29358579-3	2018	Here, we present structural and biochemical studies of (S)- and (R)-enantiomers bound to the primary target of thalidomide, cereblon (CRBN).	Thalidomide	111-122	cereblon	Danio rerio	134-138
29358579-5	2018	The crystal structures of the thalidomide-binding domain of CRBN bound to each enantiomer show that both enantiomers bind the tri-Trp pocket, although the bound form of the (S)-enantiomer exhibited a more relaxed glutarimide ring conformation.	Thalidomide	30-41	cereblon	Danio rerio	60-64
28982338-0	2018	Thalidomide Improves Psoriasis-like Lesions and Inhibits Cutaneous VEGF Expression without Alteration of Microvessel Density in Imiquimod- induced Psoriatic Mouse Model.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	67-71
28982338-3	2018	Thalidomide has been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	67-93
28982338-3	2018	Thalidomide has been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	98-132
28982338-3	2018	Thalidomide has been reported being able to inhibit the effects of fibroblast growth factor 2 and vascular endothelial growth factor (VEGF), and inhibit tumour necrosis factor-alpha synthesis, and suppress tumour necrosis factor-induced nuclear factor-kappa B activation in Jurkat cells, resulting in suppression of proliferation inflammation, angiogenesis, and the immune system, which are related to the pathogenesis of psoriasis.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	134-138
28982338-10	2018	The cutaneous VEGF protein levels down-expressed significantly in the moderate- and high-dose thalidomide groups (p&lt;0.05 for both), while those in the low-dose thalidomide and acitretin did not (p&gt;0.05 for both).	Thalidomide	94-105	vascular endothelial growth factor A	Mus musculus	14-18
28982338-12	2018	CONCLUSION: Thalidomide can improve the psoriasis-like lesions and inhibit the expression of cutaneous VEGF in imiquimod-induced psoriatic model with dose-dependence, however, it does not alter circulating VEGF-A levels and microvessel density in dermis.	Thalidomide	12-23	vascular endothelial growth factor A	Mus musculus	103-107
29732020-6	2018	The rele-vance of TNF-alpha to the pathogenesis of RAS has stemmed from the observations that anti- TNF-alpha drugs such as thalidomide and pentoxifylline have been found to be effective in the treatment of RAS.	Thalidomide	124-135	tumor necrosis factor	Homo sapiens	100-109
29272525-6	2017	Thalidomide treatment reduced PTX3 in the serum 7 days after starting treatment.	Thalidomide	0-11	pentraxin 3	Homo sapiens	30-34
30175757-5	2018	To recruit the von Hippel-Lindau (VHL) E3 ligase complex and the cereblon (CRBN) E3 ligase complex, a VHL inhibitor and a thalidomide derivative have been integrated into PROTAC and Degronimid constructs, respectively.	Thalidomide	122-133	cereblon	Homo sapiens	75-79
29272525-7	2017	In situ analyses have also demonstrated enhancement of PTX3 in ENL lesions and showed that treatment with thalidomide reduced its expression and the prominent neutrophilic infiltrate, a hallmark of the disease.	Thalidomide	106-117	pentraxin 3	Homo sapiens	55-59
29172279-0	2017	Anti-Vascular Endothelial Growth Factor Targeting by Curcumin and Thalidomide in Acute Myeloid Leukemia Cells Acute myeloid leukemias (AMLs) are blood disorders that exhibit uncontrolled growth and reduction of apoptosisrates.	Thalidomide	66-77	vascular endothelial growth factor A	Homo sapiens	5-39
27405747-0	2017	Polymorphism of IL-10 receptor beta affects the prognosis of multiple myeloma patients treated with thalidomide and/or bortezomib.	Thalidomide	100-111	interleukin 10	Homo sapiens	16-21
27405747-12	2017	In particular, IL-10RB K47E polymorphism may contribute to the poor prognosis of MM patients treated with thalidomide and/or bortezomib.	Thalidomide	106-117	interleukin 10 receptor subunit beta	Homo sapiens	15-22
29344159-7	2017	P38 cDNA was transfected into esophageal cancer cells to assess tumor cell viability, sensitivity to thalidomide treatment and IDO gene expression.	Thalidomide	101-112	mitogen-activated protein kinase 14	Homo sapiens	0-3
29344159-10	2017	In vitro experiments revealed that the expression of p-p38 induced esophageal cancer Eca-109 and TE-1 cell viability, and resistance to thalidomide treatment, as well as in the expression of IDO without the application of lipopolysaccharides.	Thalidomide	136-147	mitogen-activated protein kinase 14	Homo sapiens	55-58
29238068-7	2017	Thalidomide, a TNF-alpha and NF-kappaB inhibitor, significantly weakened the metastasis and homing capacity of miR-105-overexpressed CRC cells in nude mice.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	15-24
29238068-7	2017	Thalidomide, a TNF-alpha and NF-kappaB inhibitor, significantly weakened the metastasis and homing capacity of miR-105-overexpressed CRC cells in nude mice.	Thalidomide	0-11	microRNA 105	Mus musculus	111-118
29172279-11	2017	Thalidomide as a VEGF inhibitor in combination with curcumin appears to have a synergistic impacton inhibition of cell proliferation and promotion of apoptosis.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	17-21
28869897-9	2017	Single administration of thalidomide significantly reduced production of cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta) in serum but not in the brain, and attenuated upregulation of NMDA receptor (NR) 2A/B subunits in the hippocampus at POD 14.	Thalidomide	25-36	tumor necrosis factor	Rattus norvegicus	84-117
29116196-0	2017	Thalidomide Inhibits TGF-beta1-induced Epithelial to Mesenchymal Transition in Alveolar Epithelial Cells via Smad-Dependent and Smad-Independent Signaling Pathways.	Thalidomide	0-11	transforming growth factor beta 1	Homo sapiens	21-30
29116196-4	2017	CCL-149 cells were treated with TGF-beta1 in the presence of THL at the indicated concentrations.	Thalidomide	61-64	transforming growth factor beta 1	Homo sapiens	32-41
29116196-7	2017	THL inhibited the TGF-beta1 induction of alpha-SMA, vimentin, MMP-2/-9 and collagen type IV expression and restored the morphological changes in primary alveolar epithelial cells caused by TGF-beta1.	Thalidomide	0-3	transforming growth factor beta 1	Homo sapiens	18-27
29116196-7	2017	THL inhibited the TGF-beta1 induction of alpha-SMA, vimentin, MMP-2/-9 and collagen type IV expression and restored the morphological changes in primary alveolar epithelial cells caused by TGF-beta1.	Thalidomide	0-3	vimentin	Homo sapiens	52-60
29116196-7	2017	THL inhibited the TGF-beta1 induction of alpha-SMA, vimentin, MMP-2/-9 and collagen type IV expression and restored the morphological changes in primary alveolar epithelial cells caused by TGF-beta1.	Thalidomide	0-3	matrix metallopeptidase 2	Homo sapiens	62-70
29116196-7	2017	THL inhibited the TGF-beta1 induction of alpha-SMA, vimentin, MMP-2/-9 and collagen type IV expression and restored the morphological changes in primary alveolar epithelial cells caused by TGF-beta1.	Thalidomide	0-3	transforming growth factor beta 1	Homo sapiens	189-198
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	transforming growth factor beta 1	Homo sapiens	24-33
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	mitogen-activated protein kinase 14	Homo sapiens	61-64
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	mitogen-activated protein kinase 8	Homo sapiens	66-69
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	mitogen-activated protein kinase 1	Homo sapiens	71-74
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	AKT serine/threonine kinase 1	Homo sapiens	76-79
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	glycogen synthase kinase 3 beta	Homo sapiens	81-89
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	SMAD family member 2	Homo sapiens	91-97
29116196-9	2017	Moreover, THL inhibited TGF-beta1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3beta, Smad 2 and Smad3 without altering the total expression levels of those proteins.	Thalidomide	10-13	SMAD family member 3	Homo sapiens	102-107
29116196-10	2017	These findings indicate that TGF-beta1-induced EMT in alveolar epithelial cells is inhibited by THL via both Smad-dependent and non-Smad-dependent signaling pathways and suggests therapeutic approaches for targeting this process in pulmonary fibrosis.	Thalidomide	96-99	transforming growth factor beta 1	Homo sapiens	29-38
28869897-9	2017	Single administration of thalidomide significantly reduced production of cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta) in serum but not in the brain, and attenuated upregulation of NMDA receptor (NR) 2A/B subunits in the hippocampus at POD 14.	Thalidomide	25-36	interleukin 1 beta	Rattus norvegicus	122-144
28993730-8	2017	However, targeting the altered biological pathways (mTOR, PDGFRB, FGF2, HDAC) guided identification of possibly beneficial treatment with a combination of sirolimus, thalidomide, sunitinib, and vorinostat.	Thalidomide	166-177	mechanistic target of rapamycin kinase	Homo sapiens	52-56
28672061-8	2017	Measurement of intragraft cytokine levels after thalidomide treatment revealed downregulation of matrix metalloproteinase 8 and monocyte chemotactic protein 1, cytokines involved in tissue remodelling and inflammation, respectively.	Thalidomide	48-59	matrix metallopeptidase 8	Rattus norvegicus	97-123
28672061-8	2017	Measurement of intragraft cytokine levels after thalidomide treatment revealed downregulation of matrix metalloproteinase 8 and monocyte chemotactic protein 1, cytokines involved in tissue remodelling and inflammation, respectively.	Thalidomide	48-59	C-C motif chemokine ligand 2	Rattus norvegicus	128-158
28538510-3	2017	Thalidomide, a drug known for its immunomodulating and antiangiogenic properties, has recently been demonstrated to induce gamma-globin gene expression and to increase the proliferation of erythroid cells.	Thalidomide	0-11	hemoglobin subunit gamma 1	Homo sapiens	123-135
29151411-13	2017	CONCLUSIONS: Thalidomide has a protective effect on ALI induced by PQ poisoning in rats in a dose-dependent manner, the mechanism may be achieved by reducing the level of oxygen free radicals, reducing the inflammatory factor and inhibiting the IkappaB-alpha/NF-kappaB signal pathway activation.	Thalidomide	13-24	NFKB inhibitor alpha	Rattus norvegicus	245-258
28902348-4	2017	Silencing CUL4A expression or CUL4A inhibition by thalidomide suppressed the EMT process induced by TGF-beta1.	Thalidomide	50-61	cullin 4A	Homo sapiens	30-35
28902348-4	2017	Silencing CUL4A expression or CUL4A inhibition by thalidomide suppressed the EMT process induced by TGF-beta1.	Thalidomide	50-61	transforming growth factor beta 1	Homo sapiens	100-109
28993730-8	2017	However, targeting the altered biological pathways (mTOR, PDGFRB, FGF2, HDAC) guided identification of possibly beneficial treatment with a combination of sirolimus, thalidomide, sunitinib, and vorinostat.	Thalidomide	166-177	histone deacetylase 9	Homo sapiens	72-76
28636891-2	2017	Thalidomide or bortezomib may be combined with cyclophosphamide and dexamethasone, in what are known as the CTD and VCD protocols, respectively.	Thalidomide	0-11	CTD	Homo sapiens	108-111
28822719-11	2017	During thalidomide treatment, a decrease in CD4/CD8 ratio (p=0.04), a decrease in CD4 count (p=0.04), an increase in cell activation calculated by the percentage of CD38 +/HLA-DR+ CD8 cells (p&lt;0.05) and an increase in US-CRP (p&lt;0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption.	Thalidomide	7-18	CD4 molecule	Homo sapiens	44-47
28822719-11	2017	During thalidomide treatment, a decrease in CD4/CD8 ratio (p=0.04), a decrease in CD4 count (p=0.04), an increase in cell activation calculated by the percentage of CD38 +/HLA-DR+ CD8 cells (p&lt;0.05) and an increase in US-CRP (p&lt;0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption.	Thalidomide	7-18	CD8a molecule	Homo sapiens	48-51
28822719-11	2017	During thalidomide treatment, a decrease in CD4/CD8 ratio (p=0.04), a decrease in CD4 count (p=0.04), an increase in cell activation calculated by the percentage of CD38 +/HLA-DR+ CD8 cells (p&lt;0.05) and an increase in US-CRP (p&lt;0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption.	Thalidomide	7-18	CD4 molecule	Homo sapiens	82-85
28822719-11	2017	During thalidomide treatment, a decrease in CD4/CD8 ratio (p=0.04), a decrease in CD4 count (p=0.04), an increase in cell activation calculated by the percentage of CD38 +/HLA-DR+ CD8 cells (p&lt;0.05) and an increase in US-CRP (p&lt;0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption.	Thalidomide	7-18	CD38 molecule	Homo sapiens	165-169
28822719-11	2017	During thalidomide treatment, a decrease in CD4/CD8 ratio (p=0.04), a decrease in CD4 count (p=0.04), an increase in cell activation calculated by the percentage of CD38 +/HLA-DR+ CD8 cells (p&lt;0.05) and an increase in US-CRP (p&lt;0.01) were observed in the Thalidomide group, with all parameters returning to baseline levels after thalidomide interruption.	Thalidomide	7-18	CD8a molecule	Homo sapiens	180-183
28822719-14	2017	CONCLUSIONS: Short-term use of thalidomide led to an intense transient increase in T cell activation and inflammation, with a decrease in the CD4+ cell count without changes to the CD8+ cell count.	Thalidomide	31-42	CD4 molecule	Homo sapiens	142-145
28822719-14	2017	CONCLUSIONS: Short-term use of thalidomide led to an intense transient increase in T cell activation and inflammation, with a decrease in the CD4+ cell count without changes to the CD8+ cell count.	Thalidomide	31-42	CD8a molecule	Homo sapiens	181-184
28500554-1	2017	PURPOSE: Circularly permuted TRAIL (CPT) has exhibited promising efficacy as a mono-therapy or in combination with thalidomide for patients with multiple myeloma (MM).	Thalidomide	115-126	TNF superfamily member 10	Homo sapiens	29-34
28737650-0	2017	Thalidomide in Transfusion Dependent Thalassemia: Hope or Hype.	Thalidomide	0-11	FIC domain protein adenylyltransferase	Homo sapiens	58-62
28665417-0	2017	VEGF, VEGFR2 and GSTM1 polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens.	Thalidomide	90-101	vascular endothelial growth factor A	Homo sapiens	0-4
28665417-0	2017	VEGF, VEGFR2 and GSTM1 polymorphisms in outcome of multiple myeloma patients treated with thalidomide-based regimens.	Thalidomide	90-101	glutathione S-transferase mu 1	Homo sapiens	17-22
27707692-1	2017	AIMS: To determine the changes in the subfoveal choroidal thickness (CT), the foveal thickness (FT) and the serum level of vascular endothelial growth factor (VEGF) after thalidomide treatment in patients with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome.	Thalidomide	171-182	vascular endothelial growth factor A	Homo sapiens	123-157
27707692-1	2017	AIMS: To determine the changes in the subfoveal choroidal thickness (CT), the foveal thickness (FT) and the serum level of vascular endothelial growth factor (VEGF) after thalidomide treatment in patients with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome.	Thalidomide	171-182	vascular endothelial growth factor A	Homo sapiens	159-163
28811745-4	2017	The results showed a role for direct and indirect TNF-alpha inhibition through agents such as thalidomide, 3,6-dithiothalidomide, etanercept, infliximab, exendin-4, sodium hydrosulfide, minocycline, imipramine, and atorvastatin.	Thalidomide	94-105	tumor necrosis factor	Rattus norvegicus	50-59
28161597-6	2017	The STRING-tool suggested nitric oxide and beta-catenin as the central angiogenesis-related molecules affected by thalidomide"s antiangiogenic property.	Thalidomide	114-125	catenin beta 1	Homo sapiens	43-55
28409562-5	2017	Interestingly, abrogation of AIM2 signalling, either in AIM2-deficient mice or by a pharmacological inhibitor such as thalidomide, significantly reduces the incidence of drug-induced diarrhoea without affecting the anticancer efficacy of CPT-11.	Thalidomide	118-129	absent in melanoma 2	Mus musculus	29-33
28422447-5	2017	We also revealed that monohydrolyzed and monohydroxylated metabolites of thalidomide were likely to generate mainly by a C-5 oxidation of thalidomide and subsequent ring opening of the hydroxylated metabolite.	Thalidomide	73-84	complement C5	Homo sapiens	121-124
28422447-5	2017	We also revealed that monohydrolyzed and monohydroxylated metabolites of thalidomide were likely to generate mainly by a C-5 oxidation of thalidomide and subsequent ring opening of the hydroxylated metabolite.	Thalidomide	138-149	complement C5	Homo sapiens	121-124
28521705-5	2017	Here we report a case of DVT induced after 8 months of use of thalidomide in a young patient of 22 years age suffering from ENL.	Thalidomide	62-73	MLLT1 super elongation complex subunit	Homo sapiens	124-127
28415757-8	2017	However, while mice injected with thalidomide displayed no increased surface expression of platelet P-selectin or alphaIIbbeta3, there was a significantly shortened tail bleeding time, thrombin time, prothrombin time together with higher levels of Factor IX and fibrinogen.	Thalidomide	34-45	coagulation factor II	Mus musculus	185-193
28469241-0	2017	A HAND to TBX5 Explains the Link Between Thalidomide and Cardiac Diseases.	Thalidomide	41-52	T-box transcription factor 5	Homo sapiens	10-14
27753513-5	2017	Furthermore, ubiquitin ligase inhibitor, thalidomide, was added in culture process, and resulted in efficient and stable secretion of HSA-HGF (R494E) in CHO cells.	Thalidomide	41-52	hepatocyte growth factor	Cricetulus griseus	138-141
28469241-4	2017	We used both in silico docking software, and in vitro molecular and biochemical methods to document a novel interaction involving Thalidomide, TBX5, and HAND2.	Thalidomide	130-141	T-box transcription factor 5	Homo sapiens	143-147
28469241-4	2017	We used both in silico docking software, and in vitro molecular and biochemical methods to document a novel interaction involving Thalidomide, TBX5, and HAND2.	Thalidomide	130-141	heart and neural crest derivatives expressed 2	Homo sapiens	153-158
28469241-5	2017	Thalidomide binds readily to TBX5 through amino acids R81, R82, and K226 all implicated in DNA binding.	Thalidomide	0-11	T-box transcription factor 5	Homo sapiens	29-33
28469241-8	2017	Similarly, thalidomide inhibited the TBX5/HAND2 physical interaction, and the in silico docking revealed that the same amino acids involved in the interaction of TBX5 with DNA are also involved in its binding to HAND2.	Thalidomide	11-22	T-box transcription factor 5	Homo sapiens	37-41
28469241-8	2017	Similarly, thalidomide inhibited the TBX5/HAND2 physical interaction, and the in silico docking revealed that the same amino acids involved in the interaction of TBX5 with DNA are also involved in its binding to HAND2.	Thalidomide	11-22	heart and neural crest derivatives expressed 2	Homo sapiens	42-47
28469241-8	2017	Similarly, thalidomide inhibited the TBX5/HAND2 physical interaction, and the in silico docking revealed that the same amino acids involved in the interaction of TBX5 with DNA are also involved in its binding to HAND2.	Thalidomide	11-22	T-box transcription factor 5	Homo sapiens	162-166
28469241-8	2017	Similarly, thalidomide inhibited the TBX5/HAND2 physical interaction, and the in silico docking revealed that the same amino acids involved in the interaction of TBX5 with DNA are also involved in its binding to HAND2.	Thalidomide	11-22	heart and neural crest derivatives expressed 2	Homo sapiens	212-217
28124585-3	2017	Pre-clinical data obtained in APP23 mice suggested that the anti-cancer drug thalidomide decreases brainBACE1 and Abeta levels.	Thalidomide	77-88	amyloid beta (A4) precursor protein	Mus musculus	114-119
28300056-7	2017	The intracerebroventricular (ICV) injection of PGRN or intraperitoneal injection of TNFalpha synthesis blocker thalidomide (25 mg/kg), prevented the memory impairment and anxiety behaviors induced by S-DEP.	Thalidomide	111-122	tumor necrosis factor	Mus musculus	84-92
28099781-4	2017	Herein we report some effects on the growth and progression of MCF-7 and MDA-MB-231 breast cancer cells by a small series of thalidomide-correlated compounds, which are very effective at inducing cancer cell death by triggering TNFalpha-mediated apoptosis.	Thalidomide	125-136	tumor necrosis factor	Homo sapiens	228-236
27889230-0	2017	Anticancer effects of novel thalidomide analogs in A549 cells through inhibition of vascular endothelial growth factor and matrix metalloproteinase-2.	Thalidomide	28-39	matrix metallopeptidase 2	Homo sapiens	123-149
28516791-8	2017	TNF-alpha levels were found statistically significantly decreased in LPS+etanercept and LPS+thalidomide+etanercept treated groups when compared with LPS group (p &lt; 0.05).	Thalidomide	92-103	tumor necrosis factor	Rattus norvegicus	0-9
28516791-9	2017	For IL-1beta and IL-6 levels a statistically significant decline was observed in the LPS+thalidomide and LPS+etanercept treated groups compared to the LPS group (p &lt; 0.05).	Thalidomide	89-100	interleukin 1 beta	Rattus norvegicus	4-12
28516791-9	2017	For IL-1beta and IL-6 levels a statistically significant decline was observed in the LPS+thalidomide and LPS+etanercept treated groups compared to the LPS group (p &lt; 0.05).	Thalidomide	89-100	interleukin 6	Rattus norvegicus	17-21
28298557-2	2017	An increased understanding of the molecular mechanism of thalidomide and its analogues following their clinical use has unlocked small-molecule modulation of the substrate specificity of the E3 ligase cereblon (CRBN), which in turn has resulted in the advancement of new immunomodulatory drugs (IMiDs) into the clinic.	Thalidomide	57-68	cereblon	Homo sapiens	211-215
27750412-2	2017	Thalidomide exerts its various pharmacological and toxic actions in primates through multiple mechanisms, including nonspecific modification of many protein networks after bioactivation by autoinduced human P450 enzymes.	Thalidomide	0-11	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	207-211
27899254-0	2017	Thalidomide attenuates the development and expression of antinociceptive tolerance to mu-opioid agonist morphine through l-arginine-iNOS and nitric oxide pathway.	Thalidomide	0-11	nitric oxide synthase 2	Homo sapiens	132-136
27899254-11	2017	In addition, thalidomide (20muM) also significantly inhibited the overexpression of iNOS gene induced by morphine (2.5muM) in T98G cell line.	Thalidomide	13-24	nitric oxide synthase 2	Homo sapiens	84-88
27899254-13	2017	It is also evident that this effect of thalidomide is induced by the inhibition of NOS enzyme predominantly iNOS.	Thalidomide	39-50	nitric oxide synthase 2	Homo sapiens	108-112
28009008-0	2016	Down-regulation of common NFkappaB-iNOS pathway by chronic Thalidomide treatment improves Hepatopulmonary Syndrome and Muscle Wasting in rats with Biliary Cirrhosis.	Thalidomide	59-70	nitric oxide synthase 2	Rattus norvegicus	35-39
28496040-6	2017	Thalidomide significantly induced P450 3A4/5, 2B6, and pregnane X receptor (PXR) mRNA levels 2 to 3-fold, but rifampicin only enhanced P450 3A5 and PXR mRNA under the modified media conditions.	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	55-74
28496040-6	2017	Thalidomide significantly induced P450 3A4/5, 2B6, and pregnane X receptor (PXR) mRNA levels 2 to 3-fold, but rifampicin only enhanced P450 3A5 and PXR mRNA under the modified media conditions.	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	76-79
28571559-3	2017	Through an increase in the degradation of TNFalpha-mRNA, thalidomide reduces the production of TNFalpha by monocytes and macrophages stimulated by lipopolysaccharide or by T lymphocytes induced by mitogenic stimuli.	Thalidomide	57-68	tumor necrosis factor	Homo sapiens	42-50
28571559-3	2017	Through an increase in the degradation of TNFalpha-mRNA, thalidomide reduces the production of TNFalpha by monocytes and macrophages stimulated by lipopolysaccharide or by T lymphocytes induced by mitogenic stimuli.	Thalidomide	57-68	tumor necrosis factor	Homo sapiens	95-103
28571559-5	2017	Furthermore, thalidomide affects VEGF levels by down-regulating its expression.	Thalidomide	13-24	vascular endothelial growth factor A	Homo sapiens	33-37
28009008-1	2016	Thalidomide can modulate the TNFalpha-NFkappaB and iNOS pathway, which involve in the pathogenesis of hepatopulmonary syndrome (HPS) and muscle wasting in cirrhosis.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	29-37
28009008-1	2016	Thalidomide can modulate the TNFalpha-NFkappaB and iNOS pathway, which involve in the pathogenesis of hepatopulmonary syndrome (HPS) and muscle wasting in cirrhosis.	Thalidomide	0-11	nitric oxide synthase 2	Rattus norvegicus	51-55
28009008-4	2016	The in vitro data demonstrated an iNOS-dependent inhibition of thalidomide on the TNFalpha-stimulated angiogenesis and myogenesis in human pulmonary artery endothelial cells (HPAECs) and C2C12 myoblasts.	Thalidomide	63-74	inositol-3-phosphate synthase 1	Homo sapiens	34-38
28009008-4	2016	The in vitro data demonstrated an iNOS-dependent inhibition of thalidomide on the TNFalpha-stimulated angiogenesis and myogenesis in human pulmonary artery endothelial cells (HPAECs) and C2C12 myoblasts.	Thalidomide	63-74	tumor necrosis factor	Rattus norvegicus	82-90
28009008-6	2016	Our findings demonstrate that TNFalpha inhibitor thalidomide markedly diminishes the severity of experimental HPS and muscle wasting by down-regulation of common peripheral and local NFkappaB-iNOS pathway.	Thalidomide	49-60	tumor necrosis factor	Rattus norvegicus	30-38
28009008-6	2016	Our findings demonstrate that TNFalpha inhibitor thalidomide markedly diminishes the severity of experimental HPS and muscle wasting by down-regulation of common peripheral and local NFkappaB-iNOS pathway.	Thalidomide	49-60	nitric oxide synthase 2	Rattus norvegicus	192-196
27991432-5	2016	The concommitant use of omeprazole/esomeprazole, therefore, could have critical clinical relevance in individualizing medications metabolized primarily by CYP2C19 such as PPI, clopidogrel, phenytoin, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, proguanil, tivantinib etc.	Thalidomide	218-229	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	155-162
27618360-6	2016	RESULTS: A treatment response (complete remission, very good partial remission, partial remission) was achieved in 83.7% of the patients and correlated with high CRBN expression (P = .006), mainly in the patients treated with thalidomide (P = .028).	Thalidomide	226-237	cereblon	Homo sapiens	162-166
27492707-5	2016	In addition, thalidomide and its analogs inhibit release of tumor necrosis factor-alpha and increase interleukin-2 (IL-2) and interferon-gamma release from T cells.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	60-87
27492707-5	2016	In addition, thalidomide and its analogs inhibit release of tumor necrosis factor-alpha and increase interleukin-2 (IL-2) and interferon-gamma release from T cells.	Thalidomide	13-24	interleukin 2	Homo sapiens	101-114
27492707-5	2016	In addition, thalidomide and its analogs inhibit release of tumor necrosis factor-alpha and increase interleukin-2 (IL-2) and interferon-gamma release from T cells.	Thalidomide	13-24	interleukin 2	Homo sapiens	116-120
27492707-5	2016	In addition, thalidomide and its analogs inhibit release of tumor necrosis factor-alpha and increase interleukin-2 (IL-2) and interferon-gamma release from T cells.	Thalidomide	13-24	interferon gamma	Homo sapiens	126-142
27492707-6	2016	The underlying molecular mechanisms for these pleiotropic effects remained obscure until the identification of the cereblon (CRBN) E3 ubiquitin ligase as the primary target of thalidomide and its analogs in 2010.	Thalidomide	176-187	cereblon	Homo sapiens	125-129
27492707-7	2016	Binding of thalidomide or lenalidomide increases the affinity of CRBN to the transcription factors IKZF1 and IKZF3 and casein kinase 1alpha (CK1alpha).	Thalidomide	11-22	cereblon	Homo sapiens	65-69
27573481-6	2016	Finally, STZ-induced diabetes promoted PKC activation and enhanced TNFalpha level in the spinal cord, which were attenuated by intrathecal administrations of thalidomide.	Thalidomide	158-169	tumor necrosis factor	Rattus norvegicus	67-75
27573481-7	2016	Taken together, these results suggested that thalidomide may potentiate morphine efficacy on diabetic neuropathy and prevent the development of morphine tolerance by suppressing PKC activation and TNFalpha level in the spinal cord.	Thalidomide	45-56	tumor necrosis factor	Rattus norvegicus	197-205
27702999-3	2016	Furthermore, human CRBN was identified as the primary target of thalidomide teratogenicity.	Thalidomide	64-75	cereblon	Homo sapiens	19-23
28083618-8	2016	The CRBN (rs711613) A allele-carriers were better responders to the treatment (P = 0.012), in particular to thalidomide including therapy (P = 0.023).	Thalidomide	108-119	cereblon	Homo sapiens	4-8
27748909-3	2016	Thalidomide was added to osteosarcoma cells and studied by cytotoxicity assay, evaluating apoptosis, cell cycle arrest, mitochondrial membrane potential (DeltaPsim), and reactive oxygen species (ROS) levels and the expression of Bcl-2, Bax, caspase-3 and NF-kappaB.	Thalidomide	0-11	BCL2 apoptosis regulator	Homo sapiens	229-234
27748909-3	2016	Thalidomide was added to osteosarcoma cells and studied by cytotoxicity assay, evaluating apoptosis, cell cycle arrest, mitochondrial membrane potential (DeltaPsim), and reactive oxygen species (ROS) levels and the expression of Bcl-2, Bax, caspase-3 and NF-kappaB.	Thalidomide	0-11	BCL2 associated X, apoptosis regulator	Homo sapiens	236-239
27748909-3	2016	Thalidomide was added to osteosarcoma cells and studied by cytotoxicity assay, evaluating apoptosis, cell cycle arrest, mitochondrial membrane potential (DeltaPsim), and reactive oxygen species (ROS) levels and the expression of Bcl-2, Bax, caspase-3 and NF-kappaB.	Thalidomide	0-11	caspase 3	Homo sapiens	241-250
27748909-3	2016	Thalidomide was added to osteosarcoma cells and studied by cytotoxicity assay, evaluating apoptosis, cell cycle arrest, mitochondrial membrane potential (DeltaPsim), and reactive oxygen species (ROS) levels and the expression of Bcl-2, Bax, caspase-3 and NF-kappaB.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	255-264
27748909-8	2016	By western blot analysis, thalidomide resulted in the decreasing expression of Bcl-2 and NF-kappaB, and the increasing expression of Bcl-2/Bax and caspase-3.	Thalidomide	26-37	BCL2 apoptosis regulator	Homo sapiens	79-84
27748909-8	2016	By western blot analysis, thalidomide resulted in the decreasing expression of Bcl-2 and NF-kappaB, and the increasing expression of Bcl-2/Bax and caspase-3.	Thalidomide	26-37	nuclear factor kappa B subunit 1	Homo sapiens	89-98
27748909-8	2016	By western blot analysis, thalidomide resulted in the decreasing expression of Bcl-2 and NF-kappaB, and the increasing expression of Bcl-2/Bax and caspase-3.	Thalidomide	26-37	BCL2 apoptosis regulator	Homo sapiens	133-138
27748909-8	2016	By western blot analysis, thalidomide resulted in the decreasing expression of Bcl-2 and NF-kappaB, and the increasing expression of Bcl-2/Bax and caspase-3.	Thalidomide	26-37	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142
27748909-8	2016	By western blot analysis, thalidomide resulted in the decreasing expression of Bcl-2 and NF-kappaB, and the increasing expression of Bcl-2/Bax and caspase-3.	Thalidomide	26-37	caspase 3	Homo sapiens	147-156
27751757-2	2016	Investigations with Cereblon, a thalidomide target protein encoded by CRBN gene, have helped to understand thalidomide therapeutic and teratogenic properties.	Thalidomide	32-43	cereblon	Homo sapiens	70-74
27751757-2	2016	Investigations with Cereblon, a thalidomide target protein encoded by CRBN gene, have helped to understand thalidomide therapeutic and teratogenic properties.	Thalidomide	107-118	cereblon	Homo sapiens	70-74
27751757-3	2016	We sequenced CRBN-thalidomide binding region in 38 TE individuals and 136 Brazilians without congenital anomalies, and performed in silico analyses.	Thalidomide	18-29	cereblon	Homo sapiens	13-17
27751757-8	2016	Comparison of the Cereblon-thalidomide binding domains in mammals demonstrated that CRBN is highly conserved across species.	Thalidomide	27-38	cereblon	Homo sapiens	84-88
27553604-8	2016	Albeit remaining within the reference ranges, erythrocytes, haematocrit, total leucocyte count, neutrophils, lymphocytes, monocytes and gamma-glutamyltranspeptidase showed significant alteration associated to thalidomide treatment.	Thalidomide	209-220	inactive glutathione hydrolase 2	Homo sapiens	136-164
27618360-8	2016	In the Cox regression model, low CRBN expression was the most important prognostic parameter that influenced PFS in the thalidomide-treated patients (P = .012).	Thalidomide	120-131	cytochrome c oxidase subunit 8A	Homo sapiens	7-10
27618360-8	2016	In the Cox regression model, low CRBN expression was the most important prognostic parameter that influenced PFS in the thalidomide-treated patients (P = .012).	Thalidomide	120-131	cereblon	Homo sapiens	33-37
27618360-9	2016	CONCLUSION: CRBN expression is of prognostic value in MM patients ineligible for ASCT treated with thalidomide as an immunomodulatory drug.	Thalidomide	99-110	cereblon	Homo sapiens	12-16
27739411-0	2016	Inhibition of Uterine Contractility by Thalidomide Analogs via Phosphodiesterase-4 Inhibition and Calcium Entry Blockade.	Thalidomide	39-50	phosphodiesterase 4A	Homo sapiens	63-82
27748917-7	2016	It was identified that treatment of cells with lenalidomide and thalidomide led to a dose-dependent inhibition of cell proliferation, and the two drugs were able to induce cells apoptosis and inhibit VEGF expression in HCC cells.	Thalidomide	64-75	vascular endothelial growth factor A	Homo sapiens	200-204
27739411-3	2016	Some thalidomide analogs are PDE-4 inhibitors.	Thalidomide	5-16	phosphodiesterase 4A	Homo sapiens	29-34
27739411-11	2016	The inhibitory effects of thalidomide analogs on the contractions of pregnant human myometrium tissue may be due to their PDE-4 inhibitory effect and novel mechanism as calcium-channel blockers.	Thalidomide	26-37	phosphodiesterase 4A	Homo sapiens	122-127
27695085-7	2016	We further analysed monocyte TLR and CD14 expression upon exposure to the IMID  immunomodulatory drug Pomalidomide (CC-4047), a Thalidomide analogue known to downregulate PU.1.	Thalidomide	128-139	Spi-1 proto-oncogene	Homo sapiens	171-175
27365142-1	2016	Cereblon (CRBN) has been identified as a primary target of immunomodulatory drugs and is considered a biomarker for the prediction of outcomes after thalidomide- or lenalidomide-based treatments.	Thalidomide	149-160	cereblon	Homo sapiens	10-14
27365142-6	2016	Among patients treated with thalidomide-based regimens, CRBN(+) patients showed a better treatment response than did CRBN-negative patients (35.0 vs. 11.8 % complete response rate, respectively; HR = 4.038, P = 0.137).	Thalidomide	28-39	cereblon	Homo sapiens	56-60
27365142-6	2016	Among patients treated with thalidomide-based regimens, CRBN(+) patients showed a better treatment response than did CRBN-negative patients (35.0 vs. 11.8 % complete response rate, respectively; HR = 4.038, P = 0.137).	Thalidomide	28-39	cereblon	Homo sapiens	117-121
27365142-9	2016	These data suggest that thalidomide-based regimens are as effective as bortezomib-based regimens in elderly patients with MM who are CRBN(+).	Thalidomide	24-35	cereblon	Homo sapiens	133-137
27422610-5	2016	Here, we modulate the permeability of tumor vessels by thalidomide (THD) in a sarcoma-bearing EPR mouse model via monitoring endogenous deoxygenated hemoglobin in circulation, and then we confirm the effect of THD on tumor vessel permeability by vessel density, vessel maturity, VEGF expression and so on.	Thalidomide	68-71	vascular endothelial growth factor A	Mus musculus	279-283
27496680-3	2016	Thalidomide suppresses VEGF and plasma cell proliferation.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	23-27
27496680-12	2016	The adjusted mean VEGF concentration reduction rate at 24 weeks was 0 39 (SD 0 34) in the thalidomide group compared with -0 02 (0 54) in the placebo group (adjusted mean difference 0 41, 95% CI 0 02-0 80; p=0 04).	Thalidomide	90-101	vascular endothelial growth factor A	Homo sapiens	18-22
27496680-18	2016	INTERPRETATION: Thalidomide reduces serum VEGF concentrations and represents a new treatment for patients with POEMS syndrome who are not eligible for stem-cell transplantation.	Thalidomide	16-27	vascular endothelial growth factor A	Homo sapiens	42-46
27343012-2	2016	Several key findings suggest diverse roles of CRBN, including its regulation of the large-conductance calcium- and voltage-activated potassium (BKCa) channels, regulation of thalidomide-binding proteins, and mediation of lenalidomide treatment in multiple myeloma.	Thalidomide	174-185	cereblon	Homo sapiens	46-50
27556927-6	2016	Several mechanisms have been proposed to explain the efficacy of thalidomide in ENL, including the inhibition of TNF production.	Thalidomide	65-76	tumor necrosis factor	Homo sapiens	113-116
27556927-12	2016	The present study demonstrated that CD64 mRNA and protein were expressed in ENL lesions and that thalidomide treatment reduced CD64 expression and neutrophil infiltrates-a hallmark of ENL.	Thalidomide	97-108	Fc gamma receptor Ia	Homo sapiens	127-131
27460676-4	2016	Although the molecular mechanism of thalidomide and IMiDs remained unclear for a long time, cereblon, a substrate receptor of the CRL4 E3 ubiquitin ligase was identified as a primary direct target by a new affinity technique.	Thalidomide	36-47	interleukin 17 receptor B	Homo sapiens	130-134
27693314-6	2016	The results demonstrated that SNAP-25 mRNA levels were increased by 49 and 66% by TBBPA and THAL, respectively, whereas VPA and NAg reduced these levels to 48 and 64% of the control, respectively.	Thalidomide	92-96	synaptosome associated protein 25	Rattus norvegicus	30-37
27693314-7	2016	The SNAP-25 protein content in CGCs was increased by 79% by TBBPA, 25% by THAL and 21% by NAg; VPA and TH reduced these levels to 73 and 69% of the control, respectively.	Thalidomide	74-78	synaptosome associated protein 25	Rattus norvegicus	4-11
27329811-7	2016	CRBN was also identified as a thalidomide-binding protein and component of the cullin-4-containing E3 ubiquitin ligase complex.	Thalidomide	30-41	cereblon	Homo sapiens	0-4
27329811-8	2016	Thalidomide has been reported to be involved in the regulation of the transcription factor Ikaros by CRBN-mediated degradation.	Thalidomide	0-11	IKAROS family zinc finger 1	Homo sapiens	91-97
27329811-8	2016	Thalidomide has been reported to be involved in the regulation of the transcription factor Ikaros by CRBN-mediated degradation.	Thalidomide	0-11	cereblon	Homo sapiens	101-105
27282278-3	2016	The present study was initiated to determine the effect of the NF-kappaB inhibitor thalidomide on the clinical manifestation of oral mucositis in the established mouse tongue model.	Thalidomide	83-94	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	63-72
27282278-10	2016	CONCLUSION: Thalidomide treatment demonstrated a significant mucositis-ameliorating effect during fractionated irradiation, which is likely to result from NF-kappaB inhibition.	Thalidomide	12-23	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	155-164
27531780-1	2016	OBJECTIVE: To investigate the expression of PIGF and its receptor Flt-1 in patients with multiple myeloma, and to analyze their correlation with the efficacy of thalidomide-based chemotherapy so as to provide further theoretical basis for individualized treatment.	Thalidomide	161-172	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	44-48
27531780-11	2016	CONCLUSION: PIGF and FLT-1 are highly expressed in patients with multiple myeloma, and their expression levels positively correlates with curative effecacy of thalidomide-based chemotherapy.	Thalidomide	159-170	phosphatidylinositol glycan anchor biosynthesis class F	Homo sapiens	12-16
27531780-11	2016	CONCLUSION: PIGF and FLT-1 are highly expressed in patients with multiple myeloma, and their expression levels positively correlates with curative effecacy of thalidomide-based chemotherapy.	Thalidomide	159-170	fms related receptor tyrosine kinase 1	Homo sapiens	21-26
27417535-3	2016	The intellectual disability-associated and thalidomide-binding protein cereblon (CRBN) contains a large, highly conserved Lon domain.	Thalidomide	43-54	cereblon	Homo sapiens	81-85
27294876-8	2016	Finally, we show that BSG (CD147) knockdown phenocopies the teratogenic effects of thalidomide exposure in zebrafish.	Thalidomide	83-94	basigin	Danio rerio	22-25
27346278-6	2016	Intra-RVM administrations of thalidomide dose-dependently attenuated mechanical allodynia and thermal hyperalgesia, and this phenomenon was associated with reduced levels of TNFalpha, IL-1beta, and NFkappaB in the RVM, without altering serum levels of TNFalpha or IL-1beta.	Thalidomide	29-40	tumor necrosis factor	Rattus norvegicus	174-182
27346278-6	2016	Intra-RVM administrations of thalidomide dose-dependently attenuated mechanical allodynia and thermal hyperalgesia, and this phenomenon was associated with reduced levels of TNFalpha, IL-1beta, and NFkappaB in the RVM, without altering serum levels of TNFalpha or IL-1beta.	Thalidomide	29-40	interleukin 1 beta	Rattus norvegicus	184-192
27346278-6	2016	Intra-RVM administrations of thalidomide dose-dependently attenuated mechanical allodynia and thermal hyperalgesia, and this phenomenon was associated with reduced levels of TNFalpha, IL-1beta, and NFkappaB in the RVM, without altering serum levels of TNFalpha or IL-1beta.	Thalidomide	29-40	tumor necrosis factor	Rattus norvegicus	252-260
27346278-6	2016	Intra-RVM administrations of thalidomide dose-dependently attenuated mechanical allodynia and thermal hyperalgesia, and this phenomenon was associated with reduced levels of TNFalpha, IL-1beta, and NFkappaB in the RVM, without altering serum levels of TNFalpha or IL-1beta.	Thalidomide	29-40	interleukin 1 beta	Rattus norvegicus	264-272
27346278-7	2016	These results suggested that supraspinal mechanisms of thalidomide play a critical role in modulations of type 2 diabetes induced neuropathic pain, which is likely mediated by TNFalpha and IL-1beta in the RVM.	Thalidomide	55-66	tumor necrosis factor	Rattus norvegicus	176-184
27346278-7	2016	These results suggested that supraspinal mechanisms of thalidomide play a critical role in modulations of type 2 diabetes induced neuropathic pain, which is likely mediated by TNFalpha and IL-1beta in the RVM.	Thalidomide	55-66	interleukin 1 beta	Rattus norvegicus	189-197
27294876-8	2016	Finally, we show that BSG (CD147) knockdown phenocopies the teratogenic effects of thalidomide exposure in zebrafish.	Thalidomide	83-94	basigin	Danio rerio	27-32
27249651-7	2016	In vivo zebrafish experiments suggested that HIF-2alpha overexpression was associated with abnormal subintestinal vascular (SIV) sprouting, which was reversed by thalidomide.	Thalidomide	162-173	hypoxia inducible factor 1 subunit alpha, like 2	Danio rerio	45-55
26865412-1	2016	Thalidomide and its derivatives, collectively referred to as immunomodulatory drugs (IMiDs), are effective inhibitors of inflammation and are known to inhibit TLR-induced TNFalpha production.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	171-179
26689580-9	2016	miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex).	Thalidomide	77-88	microRNA 202	Homo sapiens	0-7
26689580-9	2016	miR-202 over-expression sensitized MM cells to bortezomib (Bort) but less to Thalidomide (Thal) and dexamethasone (Dex).	Thalidomide	77-81	microRNA 202	Homo sapiens	0-7
27249651-8	2016	This result indicated that thalidomide regulated angiogenesis via the inhibition of HIF-1alpha and HIF-2alpha expression, which further regulated downstream factors, including VEGF, NOTCH1, DLL4, and Ang2.	Thalidomide	27-38	vascular endothelial growth factor A	Homo sapiens	176-180
27249651-8	2016	This result indicated that thalidomide regulated angiogenesis via the inhibition of HIF-1alpha and HIF-2alpha expression, which further regulated downstream factors, including VEGF, NOTCH1, DLL4, and Ang2.	Thalidomide	27-38	notch receptor 1	Homo sapiens	182-188
27249651-8	2016	This result indicated that thalidomide regulated angiogenesis via the inhibition of HIF-1alpha and HIF-2alpha expression, which further regulated downstream factors, including VEGF, NOTCH1, DLL4, and Ang2.	Thalidomide	27-38	delta like canonical Notch ligand 4	Homo sapiens	190-194
27249651-8	2016	This result indicated that thalidomide regulated angiogenesis via the inhibition of HIF-1alpha and HIF-2alpha expression, which further regulated downstream factors, including VEGF, NOTCH1, DLL4, and Ang2.	Thalidomide	27-38	angiopoietin 2	Homo sapiens	200-204
27629726-8	2016	The ELISA assay revealed that both 350 mug/mL of thalidomide and 1400 U/mL of IFN could reduce the VEGF levels in cell culture supernatants; the two-drug combination group had a further decreased VEGF concentration.	Thalidomide	49-60	vascular endothelial growth factor A	Homo sapiens	99-103
27129176-0	2016	Thalidomide enhanced the efficacy of CHOP chemotherapy in the treatment of diffuse large B cell lymphoma: A phase II study.	Thalidomide	0-11	DNA damage inducible transcript 3	Homo sapiens	37-41
27129176-11	2016	We concluded that the addition of thalidomide to the CHOP regimen significantly improved the CRR and showed a trend of improving clinical outcome in patients with DLBCL, especially for patients with Bcl-2 positive and Bcl-6 negative B-cell phenotype, without increased toxicity.	Thalidomide	34-45	DNA damage inducible transcript 3	Homo sapiens	53-57
27129176-11	2016	We concluded that the addition of thalidomide to the CHOP regimen significantly improved the CRR and showed a trend of improving clinical outcome in patients with DLBCL, especially for patients with Bcl-2 positive and Bcl-6 negative B-cell phenotype, without increased toxicity.	Thalidomide	34-45	BCL2 apoptosis regulator	Homo sapiens	199-204
27129176-11	2016	We concluded that the addition of thalidomide to the CHOP regimen significantly improved the CRR and showed a trend of improving clinical outcome in patients with DLBCL, especially for patients with Bcl-2 positive and Bcl-6 negative B-cell phenotype, without increased toxicity.	Thalidomide	34-45	BCL6 transcription repressor	Homo sapiens	218-223
27386947-13	2016	Meanwhile, we found that isoform D of vascular endothelial growth factor was elevated, which was normalized after the introduction of thalidomide.	Thalidomide	134-145	vascular endothelial growth factor A	Homo sapiens	38-72
27629726-9	2016	Forty-eighthour treatment of thalidomide 350 mug/mL and IFN 1400 U/mL could significantly decrease Bcl-2 expression and increase the expression levels of phosphor-P38, BAX, cytochrome c, and cleaved caspase-3, -8, and -9 as compared to the control group.	Thalidomide	29-40	BCL2 apoptosis regulator	Homo sapiens	99-104
27629726-9	2016	Forty-eighthour treatment of thalidomide 350 mug/mL and IFN 1400 U/mL could significantly decrease Bcl-2 expression and increase the expression levels of phosphor-P38, BAX, cytochrome c, and cleaved caspase-3, -8, and -9 as compared to the control group.	Thalidomide	29-40	BCL2 associated X, apoptosis regulator	Homo sapiens	168-171
27629726-9	2016	Forty-eighthour treatment of thalidomide 350 mug/mL and IFN 1400 U/mL could significantly decrease Bcl-2 expression and increase the expression levels of phosphor-P38, BAX, cytochrome c, and cleaved caspase-3, -8, and -9 as compared to the control group.	Thalidomide	29-40	cytochrome c, somatic	Homo sapiens	173-185
27629726-8	2016	The ELISA assay revealed that both 350 mug/mL of thalidomide and 1400 U/mL of IFN could reduce the VEGF levels in cell culture supernatants; the two-drug combination group had a further decreased VEGF concentration.	Thalidomide	49-60	vascular endothelial growth factor A	Homo sapiens	196-200
27629726-11	2016	CONCLUSIONS: Thalidomide and IFN can synergistically inhibit Kasumi-1 cell proliferation, which is possibly achieved through the mitochondrial and death receptor pathways and through the activation of the P38 signaling pathway to induce apoptosis and by inhibiting Kasumi-1 cell autocrine VEGF secretion.	Thalidomide	13-24	vascular endothelial growth factor A	Homo sapiens	289-293
27320601-0	2016	Role of Thalidomide on the Expression of OX40, 4-1BB, and GITR in T Cell Subsets.	Thalidomide	8-19	tumor necrosis factor receptor superfamily, member 4	Mus musculus	41-45
27320601-0	2016	Role of Thalidomide on the Expression of OX40, 4-1BB, and GITR in T Cell Subsets.	Thalidomide	8-19	tumor necrosis factor receptor superfamily, member 9	Mus musculus	47-52
27320601-0	2016	Role of Thalidomide on the Expression of OX40, 4-1BB, and GITR in T Cell Subsets.	Thalidomide	8-19	tumor necrosis factor receptor superfamily, member 18	Mus musculus	58-62
26990986-4	2016	Binding of acetylated degron peptides to CRBN depends on an intact thalidomide-binding pocket but is not competitive with IMiDs.	Thalidomide	67-78	cereblon	Homo sapiens	41-45
26692341-0	2016	Thalidomide analogues: Tumor necrosis factor-alpha inhibitors and their evaluation as anti-inflammatory agents.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	23-50
26990986-1	2016	Cereblon (CRBN), a substrate receptor for the cullin-RING ubiquitin ligase 4 (CRL4) complex, is a direct protein target for thalidomide teratogenicity and antitumor activity of immunomodulatory drugs (IMiDs).	Thalidomide	124-135	cereblon	Homo sapiens	0-8
26990986-1	2016	Cereblon (CRBN), a substrate receptor for the cullin-RING ubiquitin ligase 4 (CRL4) complex, is a direct protein target for thalidomide teratogenicity and antitumor activity of immunomodulatory drugs (IMiDs).	Thalidomide	124-135	cereblon	Homo sapiens	10-14
26903378-0	2016	Thalidomide-induced limb abnormalities in a humanized CYP3A mouse model.	Thalidomide	0-11	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	54-59
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-48
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-104
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	0-11	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-104
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	220-231	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-48
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	220-231	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-104
26903378-8	2016	Thalidomide-treated embryos with the human CYP3A gene cluster showed limb abnormalities, and human CYP3A was expressed in the placenta, suggesting that human CYP3A in the placenta may contribute to the teratogenicity of thalidomide.	Thalidomide	220-231	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-104
27003992-4	2016	Thalidomide, which caused severe deformities in newborn children in the 1960s, is now increasingly used after it was shown to suppress tumor necrosis factor alpha, inhibit angiogenesis and to be also effective for treatment of multiple myeloma.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	135-162
26998101-4	2016	The exact mechanism of action is not yet clear, however, we hypothesize that thalidomide may function through decreasing the secretion of interleukin-6 and affecting the growth of plasma cells.	Thalidomide	77-88	interleukin 6	Homo sapiens	138-151
26820153-1	2016	BACKGROUND AND AIMS: By blocking TNFalpha-related effects, thalidomide not only inhibits hepatic fibrogenesis but improves peripheral vasodilatation and portal hypertension in cirrhotic rats.	Thalidomide	59-70	tumor necrosis factor	Rattus norvegicus	33-41
26373954-12	2016	Co-administration of thalidomide (TNF-alpha synthesis inhibitor) and IL-1ra prevented BTZ-induced mechanical allodynia.	Thalidomide	21-32	tumor necrosis factor	Rattus norvegicus	34-43
26781879-7	2016	of the TNF-alpha synthesis inhibitor thalidomide reduced the SNI-induced mechanical hypersensitivity and inhibited the expression of CXCL12 in the DRG and spinal cord.	Thalidomide	37-48	tumor necrosis factor	Rattus norvegicus	7-16
26781879-7	2016	of the TNF-alpha synthesis inhibitor thalidomide reduced the SNI-induced mechanical hypersensitivity and inhibited the expression of CXCL12 in the DRG and spinal cord.	Thalidomide	37-48	C-X-C motif chemokine ligand 12	Rattus norvegicus	133-139
26820153-10	2016	Additionally, acute incubation with thalidomide abolished TNFalpha-augmented VEGF-mediated migration of and tube formation of human umbilical vein endothelial cells, which was accompanied by corresponding changes in inflammatory and angiogenic substances release.	Thalidomide	36-47	tumor necrosis factor	Homo sapiens	58-66
26820153-10	2016	Additionally, acute incubation with thalidomide abolished TNFalpha-augmented VEGF-mediated migration of and tube formation of human umbilical vein endothelial cells, which was accompanied by corresponding changes in inflammatory and angiogenic substances release.	Thalidomide	36-47	vascular endothelial growth factor A	Homo sapiens	77-81
26554332-5	2016	Chorioallantoic membrane assay (CAM) shows that antiangiogenic activity of latent and oxidized AT are better than thalidomide, a potent antiangiogenic drug.	Thalidomide	114-125	serpin family C member 1	Homo sapiens	95-97
26711561-0	2016	Thalidomide represses inflammatory response and reduces radiculopathic pain by inhibiting IRAK-1 and NF-kappaB/p38/JNK signaling.	Thalidomide	0-11	interleukin-1 receptor-associated kinase 1	Rattus norvegicus	90-96
26711561-0	2016	Thalidomide represses inflammatory response and reduces radiculopathic pain by inhibiting IRAK-1 and NF-kappaB/p38/JNK signaling.	Thalidomide	0-11	mitogen activated protein kinase 14	Rattus norvegicus	111-114
26711561-0	2016	Thalidomide represses inflammatory response and reduces radiculopathic pain by inhibiting IRAK-1 and NF-kappaB/p38/JNK signaling.	Thalidomide	0-11	mitogen-activated protein kinase 8	Rattus norvegicus	115-118
26711561-6	2016	Our results indicated that thalidomide significantly inhibited the expression of pro-inflammatory mediators and matrix metalloproteinases in vitro, as well as radiculopathic pain in vivo, most probably by modulation of the activity of IRAK-1 and its downstream effectors p38, JNK and NF-kappaB.	Thalidomide	27-38	interleukin-1 receptor-associated kinase 1	Rattus norvegicus	235-241
26711561-6	2016	Our results indicated that thalidomide significantly inhibited the expression of pro-inflammatory mediators and matrix metalloproteinases in vitro, as well as radiculopathic pain in vivo, most probably by modulation of the activity of IRAK-1 and its downstream effectors p38, JNK and NF-kappaB.	Thalidomide	27-38	mitogen activated protein kinase 14	Rattus norvegicus	271-274
26711561-6	2016	Our results indicated that thalidomide significantly inhibited the expression of pro-inflammatory mediators and matrix metalloproteinases in vitro, as well as radiculopathic pain in vivo, most probably by modulation of the activity of IRAK-1 and its downstream effectors p38, JNK and NF-kappaB.	Thalidomide	27-38	mitogen-activated protein kinase 8	Rattus norvegicus	276-279
29741823-8	2016	To conclude, for the management of recurrent/chronic ENL, both the combinations-prednisolone with thalidomide or clofazimine appear to be efficacious.	Thalidomide	98-109	MLLT1 super elongation complex subunit	Homo sapiens	53-56
26951036-5	2016	But because of their high cost we chose thalidomide, which also has TNF-alpha inhibiting properties to successfully treat a long-standing case of ulcerative NL, which was refractory to various treatment modalities.	Thalidomide	40-51	tumor necrosis factor	Homo sapiens	68-77
27047649-0	2016	Thalidomide is more efficient than sodium butyrate in enhancing GATA-1 and EKLF gene expression in erythroid progenitors derived from HSCs with beta-globin gene mutation.	Thalidomide	0-11	GATA binding protein 1	Homo sapiens	64-70
26440459-0	2016	LASSBio-1425, an analog of thalidomide, decreases triglyceride and increases HDL cholesterol levels by inhibition of TNF-alpha production.	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	117-126
26586093-12	2016	CONCLUSION: Metronomic capecitabine and thalidomide after RFA significantly reduced recurrence of HCC and extended PFS, especially for HCC outside the Milan criteria, perhaps via reduction of serum CECs and VEGF levels and inhibition of tumour angiogenesis.	Thalidomide	40-51	vascular endothelial growth factor A	Homo sapiens	207-211
27047649-0	2016	Thalidomide is more efficient than sodium butyrate in enhancing GATA-1 and EKLF gene expression in erythroid progenitors derived from HSCs with beta-globin gene mutation.	Thalidomide	0-11	Kruppel like factor 1	Homo sapiens	75-79
27047649-7	2016	RESULTS: Thalidomide and sodium butyrate increased GATA-1 and EKLF gene expression, compared to the non-treated control (P&lt;0.05).	Thalidomide	9-20	GATA binding protein 1	Homo sapiens	51-57
27047649-7	2016	RESULTS: Thalidomide and sodium butyrate increased GATA-1 and EKLF gene expression, compared to the non-treated control (P&lt;0.05).	Thalidomide	9-20	Kruppel like factor 1	Homo sapiens	62-66
27047649-8	2016	CONCLUSION: Thalidomide was more efficient than sodium butyrate in augmenting expression of GATA-1 and EKLF genes.	Thalidomide	12-23	GATA binding protein 1	Homo sapiens	92-98
27047649-8	2016	CONCLUSION: Thalidomide was more efficient than sodium butyrate in augmenting expression of GATA-1 and EKLF genes.	Thalidomide	12-23	Kruppel like factor 1	Homo sapiens	103-107
27047649-9	2016	It seems that GATA-1 and EKLF have crucial roles in the efficient induction of HbF by thalidomide.	Thalidomide	86-97	GATA binding protein 1	Homo sapiens	14-20
27047649-9	2016	It seems that GATA-1 and EKLF have crucial roles in the efficient induction of HbF by thalidomide.	Thalidomide	86-97	Kruppel like factor 1	Homo sapiens	25-29
27863757-4	2016	The objective of this study was to assess the number of CD34+ cells mobilized using granulocyte-colony stimulating factor with and without cyclophosphamide after induction with cyclophosphamide, thalidomide and dexamethasone.	Thalidomide	195-206	CD34 molecule	Homo sapiens	56-60
26546878-9	2015	Spot-forming cell (SFC) counts in the IFN-gamma ELISPOT assay decreased from baseline after bortezomib (p=0.011) or thalidomide (p=0.096) treatment.	Thalidomide	116-127	interferon gamma	Homo sapiens	38-47
26231201-2	2015	Thalidomide binds to cereblon (CRBN), a substrate receptor of the cullin-4 really interesting new gene (RING) E3 ligase complex.	Thalidomide	0-11	cereblon	Homo sapiens	31-35
26231201-3	2015	Here, we examine the effect of thalidomide and its analogs on CRBN ubiquitination and its functions in human cell lines.	Thalidomide	31-42	cereblon	Homo sapiens	62-66
26231201-4	2015	We find that the ubiquitin modification of CRBN includes K48-linked polyubiquitin chains and that thalidomide blocks the formation of CRBN-ubiquitin conjugates.	Thalidomide	98-109	cereblon	Homo sapiens	134-138
26231201-6	2015	Treatment of human myeloma cell lines such as MM1.S, OPM2, and U266 with thalidomide (100 muM) and its structural analog lenalidomide (10 muM) results in stabilization of CRBN and elevation of CRBN protein levels.	Thalidomide	73-84	latexin	Homo sapiens	90-93
26231201-6	2015	Treatment of human myeloma cell lines such as MM1.S, OPM2, and U266 with thalidomide (100 muM) and its structural analog lenalidomide (10 muM) results in stabilization of CRBN and elevation of CRBN protein levels.	Thalidomide	73-84	latexin	Homo sapiens	138-141
26231201-6	2015	Treatment of human myeloma cell lines such as MM1.S, OPM2, and U266 with thalidomide (100 muM) and its structural analog lenalidomide (10 muM) results in stabilization of CRBN and elevation of CRBN protein levels.	Thalidomide	73-84	cereblon	Homo sapiens	171-175
26231201-6	2015	Treatment of human myeloma cell lines such as MM1.S, OPM2, and U266 with thalidomide (100 muM) and its structural analog lenalidomide (10 muM) results in stabilization of CRBN and elevation of CRBN protein levels.	Thalidomide	73-84	cereblon	Homo sapiens	193-197
26231201-8	2015	Our results reveal a novel mechanism by which thalidomide and its analogs modulate the CRBN function in cells.	Thalidomide	46-57	cereblon	Homo sapiens	87-91
26231201-9	2015	Through inhibition of CRBN ubiquitination, thalidomide and its analogs allow CRBN to accumulate, leading to the increased cullin-4 RING E3 ligase-mediated degradation of target proteins.	Thalidomide	43-54	cereblon	Homo sapiens	22-26
26231201-9	2015	Through inhibition of CRBN ubiquitination, thalidomide and its analogs allow CRBN to accumulate, leading to the increased cullin-4 RING E3 ligase-mediated degradation of target proteins.	Thalidomide	43-54	cereblon	Homo sapiens	77-81
26503997-5	2015	Herein the signalling pathways modulated by thalidomides via the mediation of vascular endothelial growth factor, phosphoinositide-kinase/protein kinase B and nuclear factor kappa B, and mammalian target of rapamycin, which integrates these signalling systems, are discussed.	Thalidomide	44-56	vascular endothelial growth factor A	Homo sapiens	78-112
26521987-1	2015	Recent studies have suggested that cereblon (CRBN) is essential for the anti-myeloma (MM) activity of immunomodulatory drugs (IMiDs), such as thalidomide and lenalidomide, and that dysregulation of Wnt/beta-catenin pathway may be one of possible reasons of lenalidomide resistance.	Thalidomide	142-153	cereblon	Homo sapiens	45-49
26521987-6	2015	Patients carrying the CTNNB1 (rs4533622) AA genotype were better responders to the first line therapy with thalidomide containing regimens (p&lt;0.05).	Thalidomide	107-118	catenin beta 1	Homo sapiens	22-28
26481541-0	2015	Thalidomide can promote erythropoiesis by induction of STAT5 and repression of external pathway of apoptosis resulting in increased expression of GATA-1 transcription factor.	Thalidomide	0-11	signal transducer and activator of transcription 5A	Homo sapiens	55-60
26481541-0	2015	Thalidomide can promote erythropoiesis by induction of STAT5 and repression of external pathway of apoptosis resulting in increased expression of GATA-1 transcription factor.	Thalidomide	0-11	GATA binding protein 1	Homo sapiens	146-152
26481541-8	2015	CONCLUSION: Our results suggest that thalidomide enhances expression of STAT5 in response of erythroid cells to erythropoietin and as a result of caspase 3 suppression.	Thalidomide	37-48	signal transducer and activator of transcription 5A	Homo sapiens	72-77
26481541-8	2015	CONCLUSION: Our results suggest that thalidomide enhances expression of STAT5 in response of erythroid cells to erythropoietin and as a result of caspase 3 suppression.	Thalidomide	37-48	erythropoietin	Homo sapiens	112-126
26481541-8	2015	CONCLUSION: Our results suggest that thalidomide enhances expression of STAT5 in response of erythroid cells to erythropoietin and as a result of caspase 3 suppression.	Thalidomide	37-48	caspase 3	Homo sapiens	146-155
26608985-8	2015	Dynamic real-time polymerase chain reaction assay, ELISA and Western blotting from patient"s peripheral blood mononuclear cells and plasma were used to detect the expression of transforming growth factor beta 3 (TGF-beta3) messenger RNA (mRNA) and vascular endothelial growth factor (VEGF) protein before and after 6 months of thalidomide treatment.	Thalidomide	327-338	transforming growth factor beta 3	Homo sapiens	177-210
26608985-11	2015	The Fli-EGFP zebrafish model manifested discontinuous vessel development and vascular occlusion (7 of 10 fishes), and the TGF-beta3 mRNA expression of five patients was lower after thalidomide therapy.	Thalidomide	181-192	Fli-1 proto-oncogene, ETS transcription factor	Danio rerio	4-7
26608985-11	2015	The Fli-EGFP zebrafish model manifested discontinuous vessel development and vascular occlusion (7 of 10 fishes), and the TGF-beta3 mRNA expression of five patients was lower after thalidomide therapy.	Thalidomide	181-192	transforming growth factor beta 3	Homo sapiens	122-131
26608985-13	2015	CONCLUSIONS: Thalidomide reverses telangiectasia and controls nosebleeds by down-regulating the expression of TGF-beta3 and VEGF in HHT patients.	Thalidomide	13-24	transforming growth factor beta 3	Homo sapiens	110-119
26608985-13	2015	CONCLUSIONS: Thalidomide reverses telangiectasia and controls nosebleeds by down-regulating the expression of TGF-beta3 and VEGF in HHT patients.	Thalidomide	13-24	vascular endothelial growth factor A	Homo sapiens	124-128
26503997-5	2015	Herein the signalling pathways modulated by thalidomides via the mediation of vascular endothelial growth factor, phosphoinositide-kinase/protein kinase B and nuclear factor kappa B, and mammalian target of rapamycin, which integrates these signalling systems, are discussed.	Thalidomide	44-56	protein tyrosine kinase 2 beta	Homo sapiens	138-181
26503997-5	2015	Herein the signalling pathways modulated by thalidomides via the mediation of vascular endothelial growth factor, phosphoinositide-kinase/protein kinase B and nuclear factor kappa B, and mammalian target of rapamycin, which integrates these signalling systems, are discussed.	Thalidomide	44-56	mechanistic target of rapamycin kinase	Homo sapiens	187-216
26220057-5	2015	The sequential drug release of LDC and THD from the developed LDC-THD-GO nanosheets exhibited a synergistic effect on neuropathic pain in vitro and in vivo, as evidenced by the increased pain threshold in mechanical allodynia and hyperalgesic response tests, and the improved inhibition of proinflammatory cytokines TNF-alpha, IL-1beta, IL-6, and nitric oxide.	Thalidomide	39-42	tumor necrosis factor	Homo sapiens	316-325
26486925-7	2015	RESULTS: Among our 64 patients with gastrointestinal involvement of Behcet"s syndrome, we identified 13 (20%) (7 women, 6 men, mean age 27.4+-9.4) who had been treated with TNF-alpha antagonists and/or thalidomide.	Thalidomide	202-213	tumor necrosis factor	Homo sapiens	173-182
26398114-5	2015	Thalidomide-gamma-cyclodextrin complex exerted a concentration-dependent cytotoxicity in TCC cells, but was relatively less cytotoxic (with IC50 of 200 microM) in BFTC905 cells than the other 3 TCC cell lines, possibly due to upregulation of Bcl-xL and HIF-1alpha mediated carbonic anhydrase IX, and promotion of quiescence.	Thalidomide	0-11	BCL2 like 1	Homo sapiens	242-248
26398114-5	2015	Thalidomide-gamma-cyclodextrin complex exerted a concentration-dependent cytotoxicity in TCC cells, but was relatively less cytotoxic (with IC50 of 200 microM) in BFTC905 cells than the other 3 TCC cell lines, possibly due to upregulation of Bcl-xL and HIF-1alpha mediated carbonic anhydrase IX, and promotion of quiescence.	Thalidomide	0-11	hypoxia inducible factor 1 subunit alpha	Homo sapiens	253-263
26398114-5	2015	Thalidomide-gamma-cyclodextrin complex exerted a concentration-dependent cytotoxicity in TCC cells, but was relatively less cytotoxic (with IC50 of 200 microM) in BFTC905 cells than the other 3 TCC cell lines, possibly due to upregulation of Bcl-xL and HIF-1alpha mediated carbonic anhydrase IX, and promotion of quiescence.	Thalidomide	0-11	carbonic anhydrase 9	Homo sapiens	273-294
26398114-7	2015	Thalidomide induced apoptosis through downregulation of survivin and securin.	Thalidomide	0-11	PTTG1 regulator of sister chromatid separation, securin	Homo sapiens	69-76
26398114-8	2015	The secretion of VEGF and TNF-alpha was ameliorated by thalidomide, but they did not affect cell proliferation.	Thalidomide	55-66	vascular endothelial growth factor A	Homo sapiens	17-21
26398114-8	2015	The secretion of VEGF and TNF-alpha was ameliorated by thalidomide, but they did not affect cell proliferation.	Thalidomide	55-66	tumor necrosis factor	Homo sapiens	26-35
26398114-12	2015	Thalidomide also inhibited TNF-alpha induced invasion through inhibition of NF-kappaB, and downregulation of effectors, ICAM-1 and MMP-9.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	27-36
26398114-12	2015	Thalidomide also inhibited TNF-alpha induced invasion through inhibition of NF-kappaB, and downregulation of effectors, ICAM-1 and MMP-9.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	76-85
26398114-12	2015	Thalidomide also inhibited TNF-alpha induced invasion through inhibition of NF-kappaB, and downregulation of effectors, ICAM-1 and MMP-9.	Thalidomide	0-11	intercellular adhesion molecule 1	Homo sapiens	120-126
26398114-12	2015	Thalidomide also inhibited TNF-alpha induced invasion through inhibition of NF-kappaB, and downregulation of effectors, ICAM-1 and MMP-9.	Thalidomide	0-11	matrix metallopeptidase 9	Homo sapiens	131-136
26220057-5	2015	The sequential drug release of LDC and THD from the developed LDC-THD-GO nanosheets exhibited a synergistic effect on neuropathic pain in vitro and in vivo, as evidenced by the increased pain threshold in mechanical allodynia and hyperalgesic response tests, and the improved inhibition of proinflammatory cytokines TNF-alpha, IL-1beta, IL-6, and nitric oxide.	Thalidomide	39-42	interleukin 1 beta	Homo sapiens	327-335
26220057-5	2015	The sequential drug release of LDC and THD from the developed LDC-THD-GO nanosheets exhibited a synergistic effect on neuropathic pain in vitro and in vivo, as evidenced by the increased pain threshold in mechanical allodynia and hyperalgesic response tests, and the improved inhibition of proinflammatory cytokines TNF-alpha, IL-1beta, IL-6, and nitric oxide.	Thalidomide	39-42	interleukin 6	Homo sapiens	337-341
26446639-0	2015	Thalidomide Accelerates the Degradation of Extracellular Matrix in Rat Hepatic Cirrhosis via Down-Regulation of Transforming Growth Factor-beta1.	Thalidomide	0-11	transforming growth factor, beta 1	Rattus norvegicus	112-144
26446639-8	2015	The levels of TIMP-1 and TGF-beta1 mRNA and protein expressions were decreased significantly and MMP-13 mRNA and protein in the liver were significantly elevated in the thalidomide-treated group.	Thalidomide	169-180	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	14-20
26446639-8	2015	The levels of TIMP-1 and TGF-beta1 mRNA and protein expressions were decreased significantly and MMP-13 mRNA and protein in the liver were significantly elevated in the thalidomide-treated group.	Thalidomide	169-180	transforming growth factor, beta 1	Rattus norvegicus	25-34
26446639-8	2015	The levels of TIMP-1 and TGF-beta1 mRNA and protein expressions were decreased significantly and MMP-13 mRNA and protein in the liver were significantly elevated in the thalidomide-treated group.	Thalidomide	169-180	matrix metallopeptidase 13	Rattus norvegicus	97-103
26446639-9	2015	CONCLUSION: Thalidomide may exert its effects on the regulation of MMP-13 and TIMP-1 via inhibition of the TGF-beta1 signaling pathway, which enhances the degradation of extracellular matrix and accelerates the regression of hepatic cirrhosis in rats.	Thalidomide	12-23	matrix metallopeptidase 13	Rattus norvegicus	67-73
26446639-9	2015	CONCLUSION: Thalidomide may exert its effects on the regulation of MMP-13 and TIMP-1 via inhibition of the TGF-beta1 signaling pathway, which enhances the degradation of extracellular matrix and accelerates the regression of hepatic cirrhosis in rats.	Thalidomide	12-23	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	78-84
26446639-9	2015	CONCLUSION: Thalidomide may exert its effects on the regulation of MMP-13 and TIMP-1 via inhibition of the TGF-beta1 signaling pathway, which enhances the degradation of extracellular matrix and accelerates the regression of hepatic cirrhosis in rats.	Thalidomide	12-23	transforming growth factor, beta 1	Rattus norvegicus	107-116
26126925-12	2015	Treatment with fluoxetine or thalidomide reversed crush-induced mechanical hyperalgesia, depressive-like behaviors and the increased TNF-alpha levels in the sciatic nerve, prefrontal cortex and hippocampus.	Thalidomide	29-40	tumor necrosis factor	Mus musculus	133-142
26632468-12	2015	CONCLUSION: CsA combined with thalidomide regime could improve the anemia symptom in low/int-1 risk MDS patients without del(5q).	Thalidomide	30-41	Wnt family member 1	Homo sapiens	89-94
26362268-2	2015	However, RA may also induce the expression of resistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL).	Thalidomide	104-115	homeobox B7	Homo sapiens	71-76
26362268-2	2015	However, RA may also induce the expression of resistance genes such as HOXB7 which can be suppressed by Thalidomide (THAL).	Thalidomide	117-121	homeobox B7	Homo sapiens	71-76
26450624-7	2015	An important and novel finding of our study was that a thalidomide derivative lenalidomide induced 3C10-CAR PBMC proliferation and enhanced the persistent antitumor effect of the cells in vivo.	Thalidomide	55-66	nuclear receptor subfamily 1, group I, member 3	Mus musculus	104-107
25895164-9	2015	Intraperitoneal injection of an inhibitor of TNF-alpha synthesis thalidomide at 50 or 100 mg/kg dose (but not 10 mg/kg dose) significantly ameliorated the reduced paw withdrawal threshold induced by SMIR surgery.	Thalidomide	65-76	tumor necrosis factor	Rattus norvegicus	45-54
26524034-7	2015	The percentage of Th17 cells, the mRNA expression of RORgammat and the plasm IL-17 levels in patients with response to thalidomide were statistically lower than those in patients before treatment (P &lt; 0.05).	Thalidomide	119-130	interleukin 17A	Homo sapiens	77-82
26126925-14	2015	Furthermore, inhibitors of TNF-alpha synthesis, like thalidomide, have a potential to treat depressive disorders associated with neuropathic pain.	Thalidomide	53-64	tumor necrosis factor	Mus musculus	27-36
28913056-10	2015	CONCLUSION: Thalidomide provides volumetric and histopathologic recovery in implants particularly because the VEGF inhibition and anti-angiogenic effect, which suggests that it could be effective in the treatment of endometriosis.	Thalidomide	12-23	vascular endothelial growth factor A	Rattus norvegicus	110-114
26134001-6	2015	Immunohistochemistry labeling assays with CD-31 (PECAM-1) antibody showed microvascular density (MVD) was significantly reduced in thalidomide, 2a and 2b groups (30+-4.9, 64.6+-1.8 and 46.5+-19.5%, respectively) (p&lt;0.05).	Thalidomide	131-142	platelet/endothelial cell adhesion molecule 1	Mus musculus	42-47
26134001-6	2015	Immunohistochemistry labeling assays with CD-31 (PECAM-1) antibody showed microvascular density (MVD) was significantly reduced in thalidomide, 2a and 2b groups (30+-4.9, 64.6+-1.8 and 46.5+-19.5%, respectively) (p&lt;0.05).	Thalidomide	131-142	platelet/endothelial cell adhesion molecule 1	Mus musculus	49-56
26131937-5	2015	We further demonstrate that minor side chain modifications in thalidomide and a novel analogue, CC-122, can modulate the spectrum of substrates targeted by CRL4(CRBN).	Thalidomide	62-73	cereblon	Mus musculus	161-165
26462773-2	2015	METHODS: The inhibitiory effect of Kasumi- 1 cells by thalidomide, interferon or combination was detected by CCK- 8 method, the apoptosis by flow cytometry, the expression of apoptosis related proteins by Western blot, vascular endothelial growth factor (VEGF) concentration in culture supernatant by ELISA.	Thalidomide	54-65	vascular endothelial growth factor A	Homo sapiens	219-253
26462773-2	2015	METHODS: The inhibitiory effect of Kasumi- 1 cells by thalidomide, interferon or combination was detected by CCK- 8 method, the apoptosis by flow cytometry, the expression of apoptosis related proteins by Western blot, vascular endothelial growth factor (VEGF) concentration in culture supernatant by ELISA.	Thalidomide	54-65	vascular endothelial growth factor A	Homo sapiens	255-259
26462773-5	2015	The VEGF concentrations of combination group [(94.61 +- 5.46) ng/L decreased significantly, as compared to thalidomide group [(141.11 +- 3.70) ng/L and IFN group [(119.90 +- 2.00) ng/L (P &lt; 0.05).	Thalidomide	107-118	vascular endothelial growth factor A	Homo sapiens	4-8
26462773-7	2015	CONCLUSION: Thalidomide and IFN could synergistically inhibit the proliferation of Kasumi-1 cells probably through inducing apoptosis via the mitochondrial pathway, death receptor pathway and P38 MAPK pathway, as well as inhibiting VEGF secretion.	Thalidomide	12-23	vascular endothelial growth factor A	Homo sapiens	232-236
26221080-6	2015	Thalidomide treatment after PQ exposure resulted in significantly reduced serum levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1, as compared to PQ group.	Thalidomide	0-11	interleukin 6	Rattus norvegicus	90-94
26221080-6	2015	Thalidomide treatment after PQ exposure resulted in significantly reduced serum levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1, as compared to PQ group.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	96-105
26221080-6	2015	Thalidomide treatment after PQ exposure resulted in significantly reduced serum levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1, as compared to PQ group.	Thalidomide	0-11	transforming growth factor, beta 1	Rattus norvegicus	107-116
26221080-6	2015	Thalidomide treatment after PQ exposure resulted in significantly reduced serum levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1, as compared to PQ group.	Thalidomide	0-11	collagen type I alpha 1 chain	Rattus norvegicus	121-127
26221080-7	2015	PCR analysis demonstrated that expression levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1 in lung tissue were significantly increased after PQ exposure but reduced by thalidomide, which were confirmed by immunohistochemistry staining.	Thalidomide	167-178	interleukin 6	Rattus norvegicus	52-56
26221080-7	2015	PCR analysis demonstrated that expression levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1 in lung tissue were significantly increased after PQ exposure but reduced by thalidomide, which were confirmed by immunohistochemistry staining.	Thalidomide	167-178	tumor necrosis factor	Rattus norvegicus	58-67
26221080-7	2015	PCR analysis demonstrated that expression levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1 in lung tissue were significantly increased after PQ exposure but reduced by thalidomide, which were confirmed by immunohistochemistry staining.	Thalidomide	167-178	transforming growth factor, beta 1	Rattus norvegicus	69-78
26221080-7	2015	PCR analysis demonstrated that expression levels of IL-6, TNF-alpha, TGF-beta1 and COL1A1 in lung tissue were significantly increased after PQ exposure but reduced by thalidomide, which were confirmed by immunohistochemistry staining.	Thalidomide	167-178	collagen type I alpha 1 chain	Rattus norvegicus	83-89
25978432-1	2015	Immunomodulatory drugs (IMiDs) thalidomide, lenalidomide (Len) and pomalidomide trigger anti-tumor activities in multiple myeloma (MM) by targetting cereblon and thereby impacting IZF1/3, c-Myc and IRF4.	Thalidomide	31-42	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	188-193
25929448-0	2015	Involvement of peripheral TRPV1 channels in the analgesic effects of thalidomide.	Thalidomide	69-80	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	26-31
25929448-4	2015	Many studies suggest that the analgesic effect of thalidomide may be due to its immunomodulatory and anti-inflammatory properties as it suppresses the production of tumor necrosis factor alpha (TNF-alpha) selectively.	Thalidomide	50-61	tumor necrosis factor	Mus musculus	165-192
25929448-4	2015	Many studies suggest that the analgesic effect of thalidomide may be due to its immunomodulatory and anti-inflammatory properties as it suppresses the production of tumor necrosis factor alpha (TNF-alpha) selectively.	Thalidomide	50-61	tumor necrosis factor	Mus musculus	194-203
25929448-6	2015	In this study, we demonstrated that the peripheral vanilloid receptor 1 (TRPV1) channel was also involved in the analgesic effect of thalidomide in different cell and animal models.	Thalidomide	133-144	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	51-71
25929448-6	2015	In this study, we demonstrated that the peripheral vanilloid receptor 1 (TRPV1) channel was also involved in the analgesic effect of thalidomide in different cell and animal models.	Thalidomide	133-144	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	73-78
25929448-8	2015	And such attenuation in the TRPV1 activity was in a dose-dependent manner of thalidomide.	Thalidomide	77-88	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	28-33
25929448-9	2015	In an acetic acid writhing test, pre-treatment of thalidomide decreased the writhing number in the wild type mice, while it did not happen in TRPV1 knockout mice, suggesting that the TRPV1 channel was involved in the pain relief by thalidomide.	Thalidomide	50-61	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	183-188
25929448-9	2015	In an acetic acid writhing test, pre-treatment of thalidomide decreased the writhing number in the wild type mice, while it did not happen in TRPV1 knockout mice, suggesting that the TRPV1 channel was involved in the pain relief by thalidomide.	Thalidomide	232-243	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	183-188
26171197-1	2015	The objective of this study was to assess the efficacy of granulocyte-macrophage colony-stimulating factor (GM-CSF) in combination with thalidomide for prostate-specific antigen (PSA) reduction in older patients (aged &gt;=70 years, life expectancy of &gt;1 year) with castration-resistant prostate cancer (CRPC).	Thalidomide	136-147	kallikrein related peptidase 3	Homo sapiens	152-183
25929448-10	2015	Taken together, the study showed that TRPV1 channels were involved in the analgesic effects of thalidomide.	Thalidomide	95-106	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	38-43
25929448-11	2015	Such alteration in the action of TRPV1 channels by thalidomide may help understand how thalidomide takes analgesic effect in the body in addition to its selective inhibition of TNF-alpha production.	Thalidomide	51-62	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	33-38
25929448-11	2015	Such alteration in the action of TRPV1 channels by thalidomide may help understand how thalidomide takes analgesic effect in the body in addition to its selective inhibition of TNF-alpha production.	Thalidomide	87-98	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	33-38
25840743-10	2015	In contrast, Thal and Dex had a direct inhibitory effect on the expression of EPCR and TM, and this inhibitory effect was especially significant when MM serum was added.	Thalidomide	13-17	protein C receptor	Homo sapiens	78-82
25978432-1	2015	Immunomodulatory drugs (IMiDs) thalidomide, lenalidomide (Len) and pomalidomide trigger anti-tumor activities in multiple myeloma (MM) by targetting cereblon and thereby impacting IZF1/3, c-Myc and IRF4.	Thalidomide	31-42	interferon regulatory factor 4	Homo sapiens	198-202
25905462-8	2015	RESULTS: The mice with thalidomide treatment showed significantly reduced levels of allergen-induced BALF and lung inflammation, AHR, and the expression of a number of pro-inflammatory cytokines and mediators including Th2 related, IL-17 cytokines, and altered levels of allergen-specific IgG1/IgG2a.	Thalidomide	23-34	heart and neural crest derivatives expressed 2	Mus musculus	219-222
25905462-8	2015	RESULTS: The mice with thalidomide treatment showed significantly reduced levels of allergen-induced BALF and lung inflammation, AHR, and the expression of a number of pro-inflammatory cytokines and mediators including Th2 related, IL-17 cytokines, and altered levels of allergen-specific IgG1/IgG2a.	Thalidomide	23-34	interleukin 17A	Mus musculus	232-237
25905462-8	2015	RESULTS: The mice with thalidomide treatment showed significantly reduced levels of allergen-induced BALF and lung inflammation, AHR, and the expression of a number of pro-inflammatory cytokines and mediators including Th2 related, IL-17 cytokines, and altered levels of allergen-specific IgG1/IgG2a.	Thalidomide	23-34	LOC105243590	Mus musculus	289-293
25905462-8	2015	RESULTS: The mice with thalidomide treatment showed significantly reduced levels of allergen-induced BALF and lung inflammation, AHR, and the expression of a number of pro-inflammatory cytokines and mediators including Th2 related, IL-17 cytokines, and altered levels of allergen-specific IgG1/IgG2a.	Thalidomide	23-34	immunoglobulin heavy variable V1-9	Mus musculus	294-299
25905462-9	2015	Of interesting note, thalidomide treatment significantly reduced expression levels of allergen- or Th2 cytokine-stimulated alternative activation of macrophages in vivo and in vitro.	Thalidomide	21-32	heart and neural crest derivatives expressed 2	Mus musculus	99-102
25749497-5	2015	Thalidomide (Thal) has been used to treat multiple myeloma due to its inhibitory effects on IL-6-induced cell growth.	Thalidomide	0-11	interleukin 6	Mus musculus	92-96
25818676-9	2015	Thalidomide also lowered significantly the number of TUNEL-positive cells, levels of Bax, caspase-3, lipoperoxidation, and pro-inflammatory cytokines, and increased the levels of SOD1, Bcl-2 and pAkt.	Thalidomide	0-11	BCL2 associated X, apoptosis regulator	Rattus norvegicus	85-88
25818676-9	2015	Thalidomide also lowered significantly the number of TUNEL-positive cells, levels of Bax, caspase-3, lipoperoxidation, and pro-inflammatory cytokines, and increased the levels of SOD1, Bcl-2 and pAkt.	Thalidomide	0-11	caspase 3	Rattus norvegicus	90-99
25818676-9	2015	Thalidomide also lowered significantly the number of TUNEL-positive cells, levels of Bax, caspase-3, lipoperoxidation, and pro-inflammatory cytokines, and increased the levels of SOD1, Bcl-2 and pAkt.	Thalidomide	0-11	superoxide dismutase 1	Rattus norvegicus	179-183
25818676-9	2015	Thalidomide also lowered significantly the number of TUNEL-positive cells, levels of Bax, caspase-3, lipoperoxidation, and pro-inflammatory cytokines, and increased the levels of SOD1, Bcl-2 and pAkt.	Thalidomide	0-11	BCL2, apoptosis regulator	Rattus norvegicus	185-190
25892862-0	2015	Thalidomide ameliorates portal hypertension via nitric oxide synthase independent reduced systolic blood pressure.	Thalidomide	0-11	nitric oxide synthase 1, neuronal	Mus musculus	48-69
25892862-4	2015	One hypothesis is that thalidomide destabilizes tumor necrosis factor alpha (TNFalpha) mRNA and therefore diminishes TNFalpha induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO).	Thalidomide	23-34	tumor necrosis factor	Mus musculus	48-75
25892862-4	2015	One hypothesis is that thalidomide destabilizes tumor necrosis factor alpha (TNFalpha) mRNA and therefore diminishes TNFalpha induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO).	Thalidomide	23-34	tumor necrosis factor	Mus musculus	77-85
25892862-4	2015	One hypothesis is that thalidomide destabilizes tumor necrosis factor alpha (TNFalpha) mRNA and therefore diminishes TNFalpha induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO).	Thalidomide	23-34	tumor necrosis factor	Mus musculus	117-125
25892862-4	2015	One hypothesis is that thalidomide destabilizes tumor necrosis factor alpha (TNFalpha) mRNA and therefore diminishes TNFalpha induction of nitric oxide synthase (NOS) and the production of nitric oxide (NO).	Thalidomide	23-34	nitric oxide synthase 1, neuronal	Mus musculus	139-160
24950782-12	2015	Thalidomide treatment also significantly reduced tissue levels of the proinflammatory cytokines, MDA, MPO, and NO and increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	myeloperoxidase	Mus musculus	102-105
24950782-12	2015	Thalidomide treatment also significantly reduced tissue levels of the proinflammatory cytokines, MDA, MPO, and NO and increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interleukin 10	Mus musculus	155-160
25749497-5	2015	Thalidomide (Thal) has been used to treat multiple myeloma due to its inhibitory effects on IL-6-induced cell growth.	Thalidomide	0-4	interleukin 6	Mus musculus	92-96
25749497-12	2015	In vitro studies revealed that Thal decreased 1) the expression of IL-1beta and IL-6 in human lung epithelial cells, and 2) CSE-induced apoptosis and the inhibition of cell growth, which may be the underlying mechanisms for the preventative effects of Thal on emphysema.	Thalidomide	31-35	interleukin 1 beta	Homo sapiens	67-75
25596877-15	2015	Our findings are in line with the findings reported in the literature and encourage further studies with TNF-alpha antagonists, in particular Thalidomide.	Thalidomide	142-153	tumor necrosis factor	Rattus norvegicus	105-114
25749497-12	2015	In vitro studies revealed that Thal decreased 1) the expression of IL-1beta and IL-6 in human lung epithelial cells, and 2) CSE-induced apoptosis and the inhibition of cell growth, which may be the underlying mechanisms for the preventative effects of Thal on emphysema.	Thalidomide	31-35	interleukin 6	Homo sapiens	80-84
25617013-3	2015	Thalidomide has immunomodulatory and anti-tumor necrosis factor-alpha effects as well as antiangiogenic properties, making it useful for a broad spectrum of inflammatory disorders.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	42-69
25617013-8	2015	We review the mechanism of action and propose that thalidomide is an alternative treatment for patients who fail or have contraindications to anti-tumor necrosis factor-alpha biologics.	Thalidomide	51-62	tumor necrosis factor	Homo sapiens	147-174
25596877-3	2015	Recent reports indicate a protective role of Thalidomide, Etanercept, and Infliximab, all of which have anti-TNF-alpha activity, against cognitive and neuropathological changes in experimental and clinical studies.	Thalidomide	45-56	tumor necrosis factor	Rattus norvegicus	109-118
25891732-10	2015	RESULTS: Thalidomide significantly decreased the proliferation of CD4(+) Teffs in a dose-dependent manner (P &lt; .01).	Thalidomide	9-20	CD4 antigen	Mus musculus	66-69
25891732-11	2015	In contrast, conversion to CD4(+)FoxP3(+) Tregs tended to increase by thalidomide treatment, although the increase was not statistically significant.	Thalidomide	70-81	CD4 antigen	Mus musculus	27-30
25891732-11	2015	In contrast, conversion to CD4(+)FoxP3(+) Tregs tended to increase by thalidomide treatment, although the increase was not statistically significant.	Thalidomide	70-81	forkhead box P3	Mus musculus	33-38
25891732-12	2015	CONCLUSION: These findings suggest that thalidomide may have an immune modulatory effect by selectively suppressing CD4(+) Teff proliferation.	Thalidomide	40-51	CD4 antigen	Mus musculus	116-119
25886177-3	2015	In a 2012 case report, we described our breakthrough finding in two advanced HCC patients, of whom one achieved complete remission of liver tumors and the other a normalized alpha-fetoprotein level, along with complete remission of their lung metastases, after the concomitant use of thalidomide and cyproheptadine.	Thalidomide	284-295	alpha fetoprotein	Homo sapiens	174-191
25584775-9	2015	The combined treatment with pentoxifylline or thalidomide with morphine, at doses that are ineffective as single treatment, diminished G-CSF-induced hyperalgesia through inhibiting cytokine production.	Thalidomide	46-57	colony stimulating factor 3 (granulocyte)	Mus musculus	135-140
25584775-8	2015	G-CSF-induced hyperalgesia was dose-dependently inhibited by thalidomide (5-45mg/kg) and pentoxifylline (0.5-13.5mg/kg), and treatment with these drugs inhibited G-CSF-induced TNFalpha, IL-1beta and IL-10 production.	Thalidomide	61-72	colony stimulating factor 3 (granulocyte)	Mus musculus	0-5
25724264-4	2015	In both circumstances thalidomide improved the neurotoxicity induced by MPTP as seen by a significant raise of the striatal contents of dopamine and simultaneous decrease of monoamine-oxidase-B (MAO-B).	Thalidomide	22-33	monoamine oxidase B	Mus musculus	174-193
25724264-4	2015	In both circumstances thalidomide improved the neurotoxicity induced by MPTP as seen by a significant raise of the striatal contents of dopamine and simultaneous decrease of monoamine-oxidase-B (MAO-B).	Thalidomide	22-33	monoamine oxidase B	Mus musculus	195-200
25741973-1	2015	Neurologic tuberculous pseudoabscesses that clinically progress despite conventional antituberculosis therapy may be responsive to adjuvant thalidomide, a potent tumor necrosis factor-alpha inhibitor.	Thalidomide	140-151	tumor necrosis factor	Homo sapiens	162-189
25302852-0	2015	Thalidomide-prednisone maintenance following autologous stem cell transplant for multiple myeloma: effect on thrombin generation and procoagulant markers in NCIC CTG MY.10.	Thalidomide	0-11	coagulation factor II, thrombin	Homo sapiens	109-117
25370353-3	2015	Thalidomide (40 microg/ml) exerted differing effects on the activities of ADAM10 and NEP enzymes.	Thalidomide	0-11	a disintegrin and metallopeptidase domain 10	Mus musculus	74-80
25370353-3	2015	Thalidomide (40 microg/ml) exerted differing effects on the activities of ADAM10 and NEP enzymes.	Thalidomide	0-11	membrane metallo endopeptidase	Mus musculus	85-88
25370353-6	2015	By contrast, in the 4THMpc cell line, 40 microg/ml thalidomide alone induced a 66.6% increase in ADAM10 enzyme activity.	Thalidomide	51-62	a disintegrin and metallopeptidase domain 10	Mus musculus	97-103
25370353-7	2015	Radiotherapy alone and thalidomide with 60Co combined therapy caused a 33.3 and 40% inhibition of ADAM10 activity, respectively.	Thalidomide	23-34	a disintegrin and metallopeptidase domain 10	Mus musculus	98-104
25370353-8	2015	In 4T1 cells, thalidomide alone caused a 40.9% increase in NEP activity.	Thalidomide	14-25	membrane metallo endopeptidase	Mus musculus	59-62
25370353-10	2015	In more aggressive 4THMpc cells, thalidomide alone caused a 26.6% increase in NEP activity.	Thalidomide	33-44	membrane metallo endopeptidase	Mus musculus	78-81
25370353-12	2015	To the best of our knowledge, the present study is the first to demonstrate that thalidomide alone or in combination with radiotherapy exhibits significant cytotoxic effects on 4T1 and 4THMpc mouse breast cancer cell lines indicating that this drug affects the enzymatic activity of ADAM10 and NEP in vitro.	Thalidomide	81-92	a disintegrin and metallopeptidase domain 10	Mus musculus	283-289
25370353-12	2015	To the best of our knowledge, the present study is the first to demonstrate that thalidomide alone or in combination with radiotherapy exhibits significant cytotoxic effects on 4T1 and 4THMpc mouse breast cancer cell lines indicating that this drug affects the enzymatic activity of ADAM10 and NEP in vitro.	Thalidomide	81-92	membrane metallo endopeptidase	Mus musculus	294-297
25222109-8	2015	In addition, significant decreases of NAG release, TNF-alpha concentrations and p22(phox) protein levels in HK2 cells were observed in high glucose-treated group with thalidomide.	Thalidomide	167-178	tumor necrosis factor	Homo sapiens	51-60
25222109-8	2015	In addition, significant decreases of NAG release, TNF-alpha concentrations and p22(phox) protein levels in HK2 cells were observed in high glucose-treated group with thalidomide.	Thalidomide	167-178	O-GlcNAcase	Homo sapiens	38-41
25222109-8	2015	In addition, significant decreases of NAG release, TNF-alpha concentrations and p22(phox) protein levels in HK2 cells were observed in high glucose-treated group with thalidomide.	Thalidomide	167-178	calcineurin like EF-hand protein 1	Homo sapiens	80-83
25687062-6	2015	Meanwhile, the level of plasma TM in the group of thalidomide combined with chemotherapy was higer than that in newly diagnosed patients (P &lt; 0.05).	Thalidomide	50-61	thrombomodulin	Homo sapiens	31-33
25687062-12	2015	The level of plasma TM and D-Dimer can be elevated when thalidomide used, which indirectly suggested the tendency for thrombosis in MM patients.	Thalidomide	56-67	thrombomodulin	Homo sapiens	20-22
25569776-2	2015	The protein cereblon, which forms an E3 ubiquitin ligase compex together with damaged DNA-binding protein 1 (DDB1) and cullin 4A, has been recently indentified as a primary target of thalidomide and its C-terminal part as responsible for binding thalidomide within a domain carrying several invariant cysteine and tryptophan residues.	Thalidomide	183-194	damage specific DNA binding protein 1	Homo sapiens	78-107
25569776-2	2015	The protein cereblon, which forms an E3 ubiquitin ligase compex together with damaged DNA-binding protein 1 (DDB1) and cullin 4A, has been recently indentified as a primary target of thalidomide and its C-terminal part as responsible for binding thalidomide within a domain carrying several invariant cysteine and tryptophan residues.	Thalidomide	183-194	damage specific DNA binding protein 1	Homo sapiens	109-113
25569776-2	2015	The protein cereblon, which forms an E3 ubiquitin ligase compex together with damaged DNA-binding protein 1 (DDB1) and cullin 4A, has been recently indentified as a primary target of thalidomide and its C-terminal part as responsible for binding thalidomide within a domain carrying several invariant cysteine and tryptophan residues.	Thalidomide	183-194	cullin 4A	Homo sapiens	119-128
25441253-9	2015	RESULTS: In obese mice, thalidomide administration induced a reduction in adiposity accompanied by a reduction of tumor necrosis factor-alpha (TNF-alpha), leptin and MCP-1 adipose tissue production, macrophage infiltration and JNK activation.	Thalidomide	24-35	tumor necrosis factor	Mus musculus	114-141
25478868-7	2015	Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	89-122
25478868-7	2015	Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity.	Thalidomide	0-11	interleukin 1 beta	Mus musculus	124-146
25478868-7	2015	Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity.	Thalidomide	0-11	interleukin 6	Mus musculus	148-152
25478868-7	2015	Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity.	Thalidomide	0-11	myeloperoxidase	Mus musculus	181-196
25478868-7	2015	Thalidomide pretreatment significantly reduced the levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6], malondialdehyde (MDA) and myeloperoxidase (MPO) activity.	Thalidomide	0-11	myeloperoxidase	Mus musculus	198-201
25441253-9	2015	RESULTS: In obese mice, thalidomide administration induced a reduction in adiposity accompanied by a reduction of tumor necrosis factor-alpha (TNF-alpha), leptin and MCP-1 adipose tissue production, macrophage infiltration and JNK activation.	Thalidomide	24-35	tumor necrosis factor	Mus musculus	143-152
25441253-9	2015	RESULTS: In obese mice, thalidomide administration induced a reduction in adiposity accompanied by a reduction of tumor necrosis factor-alpha (TNF-alpha), leptin and MCP-1 adipose tissue production, macrophage infiltration and JNK activation.	Thalidomide	24-35	chemokine (C-C motif) ligand 2	Mus musculus	166-171
25441253-9	2015	RESULTS: In obese mice, thalidomide administration induced a reduction in adiposity accompanied by a reduction of tumor necrosis factor-alpha (TNF-alpha), leptin and MCP-1 adipose tissue production, macrophage infiltration and JNK activation.	Thalidomide	24-35	mitogen-activated protein kinase 8	Mus musculus	227-230
25441253-10	2015	TNF-alpha and leptin serum levels were also reduced by thalidomide treatment in obese mice.	Thalidomide	55-66	tumor necrosis factor	Mus musculus	0-9
26763359-0	2015	CD200 Expression on Plasma Cell Myeloma Cells is Associated with the Efficacies of Bortezomib, Lenalidomide and Thalidomide.	Thalidomide	112-123	CD200 molecule	Homo sapiens	0-5
23634876-1	2015	A 61-year-old man with newly diagnosed INT-1 risk myelodysplastic syndrome--refractory cytopenia with multilineage dysplasia (MDS-RCMD) was not responsive to treatment, such as androgen, thalidomide, granulocyte--colony stimulating factor (G-CSF) combined with erythropoietin (EPO), interleukin-11 (IL-11) and thrombopoietin (TPO), and became transfusion dependent.	Thalidomide	187-198	Wnt family member 1	Homo sapiens	39-44
25186973-9	2014	Interestingly, an anti-inflammatory drug, such as a corticosteroid or thalidomide, but not anti-bacterial or anti-fungal drugs, improved CT image findings and reduced their KL-6 levels.	Thalidomide	70-81	mucin 1, cell surface associated	Homo sapiens	173-177
25326112-0	2014	Inhibition of endothelial Slit2/Robo1 signaling by thalidomide restrains angiogenesis by blocking the PI3K/Akt pathway.	Thalidomide	51-62	slit guidance ligand 2	Homo sapiens	26-31
25326112-0	2014	Inhibition of endothelial Slit2/Robo1 signaling by thalidomide restrains angiogenesis by blocking the PI3K/Akt pathway.	Thalidomide	51-62	roundabout guidance receptor 1	Homo sapiens	32-37
25326112-0	2014	Inhibition of endothelial Slit2/Robo1 signaling by thalidomide restrains angiogenesis by blocking the PI3K/Akt pathway.	Thalidomide	51-62	AKT serine/threonine kinase 1	Homo sapiens	107-110
25326112-4	2014	PURPOSE: The aim of this study was to explore the expression and effects of Robo1 and Slit2 in angiodysplasia and to identify the possible therapeutic mechanisms of thalidomide.	Thalidomide	165-176	roundabout guidance receptor 1	Homo sapiens	76-81
25326112-10	2014	High concentrations of Slit2 increased the levels of VEGF in HUVECs via signaling through the PI3K/Akt pathway-an effect that could be inhibited by thalidomide.	Thalidomide	148-159	slit guidance ligand 2	Homo sapiens	23-28
25326112-10	2014	High concentrations of Slit2 increased the levels of VEGF in HUVECs via signaling through the PI3K/Akt pathway-an effect that could be inhibited by thalidomide.	Thalidomide	148-159	vascular endothelial growth factor A	Homo sapiens	53-57
25326112-10	2014	High concentrations of Slit2 increased the levels of VEGF in HUVECs via signaling through the PI3K/Akt pathway-an effect that could be inhibited by thalidomide.	Thalidomide	148-159	AKT serine/threonine kinase 1	Homo sapiens	99-102
24912813-4	2014	The results showed that Thd significantly improved the survival rate, reduced the infiltration of inflammatory cells and cytokine (e.g., IL-6, TNF-alpha) and chemokine (e.g., RANTES, IP-10) levels, and inhibited activated p-NFkappaB p65 in infected mice.	Thalidomide	24-27	interleukin 6	Mus musculus	137-141
24912813-4	2014	The results showed that Thd significantly improved the survival rate, reduced the infiltration of inflammatory cells and cytokine (e.g., IL-6, TNF-alpha) and chemokine (e.g., RANTES, IP-10) levels, and inhibited activated p-NFkappaB p65 in infected mice.	Thalidomide	24-27	tumor necrosis factor	Mus musculus	143-152
24912813-4	2014	The results showed that Thd significantly improved the survival rate, reduced the infiltration of inflammatory cells and cytokine (e.g., IL-6, TNF-alpha) and chemokine (e.g., RANTES, IP-10) levels, and inhibited activated p-NFkappaB p65 in infected mice.	Thalidomide	24-27	chemokine (C-C motif) ligand 5	Mus musculus	175-181
24912813-4	2014	The results showed that Thd significantly improved the survival rate, reduced the infiltration of inflammatory cells and cytokine (e.g., IL-6, TNF-alpha) and chemokine (e.g., RANTES, IP-10) levels, and inhibited activated p-NFkappaB p65 in infected mice.	Thalidomide	24-27	chemokine (C-X-C motif) ligand 10	Mus musculus	183-188
24912813-4	2014	The results showed that Thd significantly improved the survival rate, reduced the infiltration of inflammatory cells and cytokine (e.g., IL-6, TNF-alpha) and chemokine (e.g., RANTES, IP-10) levels, and inhibited activated p-NFkappaB p65 in infected mice.	Thalidomide	24-27	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	233-236
25579023-10	2014	CONCLUSIONS: Lipid peroxide damage was one of the mechanisms of paraquat poisioning, thalidomide could attenuate paraquat-induced acute lung injury and its mechanism may be activating the Nrf2-ARE signaling pathway to protect mouse from Lipid peroxide damage.	Thalidomide	85-96	nuclear factor, erythroid derived 2, like 2	Mus musculus	188-192
24392952-11	2014	Compared with BOR and DEX (minimum 72 and 56%, respectively), the PBF of THA (37%) was significantly lower (P &lt; 0.001).	Thalidomide	73-76	PTTG1 interacting protein	Homo sapiens	66-69
24859059-9	2014	Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-alpha, VEGF165, and MMP-2 than thalidomide.	Thalidomide	0-11	interleukin 6	Homo sapiens	95-99
25015938-6	2014	Moreover, a detrimental effect of thalidomide, even when administered in association with bortezomib, was observed in patients with abnormal chromosome 1 as well as in those with 17p deletion, while the benefit of adding thalidomide to the bortezomib-melphalan-prednisone regimen was noted in patients carrying an aggressive CD19(+)/CD117(-) bone marrow plasma cell immunophenotype.	Thalidomide	34-45	CD19 molecule	Homo sapiens	325-329
24718779-8	2014	Further, levels of NK-1R in the cisplatin, thalidomide, and granisetron group were significantly increased at both 5 and 33 h (p &lt; 0.05 vs. control group), with no obvious difference among these three groups.	Thalidomide	43-54	tachykinin receptor 1	Rattus norvegicus	19-24
25108355-0	2014	Structure of the human Cereblon-DDB1-lenalidomide complex reveals basis for responsiveness to thalidomide analogs.	Thalidomide	94-105	damage specific DNA binding protein 1	Homo sapiens	32-36
25108355-1	2014	The Cul4-Rbx1-DDB1-Cereblon E3 ubiquitin ligase complex is the target of thalidomide, lenalidomide and pomalidomide, therapeutically important drugs for multiple myeloma and other B-cell malignancies.	Thalidomide	73-84	ring-box 1	Homo sapiens	9-13
25108355-1	2014	The Cul4-Rbx1-DDB1-Cereblon E3 ubiquitin ligase complex is the target of thalidomide, lenalidomide and pomalidomide, therapeutically important drugs for multiple myeloma and other B-cell malignancies.	Thalidomide	73-84	damage specific DNA binding protein 1	Homo sapiens	14-18
25108355-4	2014	A hydrophobic pocket in the thalidomide-binding domain (TBD) of CRBN accommodates the glutarimide moiety of lenalidomide, whereas the isoindolinone ring is exposed to solvent.	Thalidomide	28-39	cereblon	Homo sapiens	64-68
24939146-0	2014	Thalidomide alleviates acute pancreatitis-associated lung injury via down-regulation of NFkappaB induced TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	105-114
24939146-1	2014	AIMS: We studied the effect of thalidomide on NFkappaB-induced TNF-alpha in acute pancreatitis-associated lung injury in the rat.	Thalidomide	31-42	tumor necrosis factor	Rattus norvegicus	63-72
24939146-6	2014	CONCLUSION: Thalidomide may inhibit TNF-alpha expression via down-regulation of the NFkappaB signaling pathway to alleviate acute pancreatitis-associated lung injury in rats.	Thalidomide	12-23	tumor necrosis factor	Rattus norvegicus	36-45
24687382-1	2014	Cereblon (CRBN) is essential for the anti-myeloma (MM) activity of immunomodulatory drugs (IMiDs), such as thalidomide and lenalidomide.	Thalidomide	107-118	cereblon	Homo sapiens	10-14
24687382-3	2014	Using immunohistochemical (IHC) staining on paraffin-embedded bone marrow sections, the expression of CRBN protein in myeloma cells (MCs) was assessed in 40 relapsed/refractory MM (RRMM) patients who received lenalidomide/dexamethasone (LD) and 45 and 22 newly diagnosed MM (NDMM) patients who received thalidomide/dexamethasone (TD) and melphalan/bortezomib/prednisolone (MVP), respectively.	Thalidomide	303-314	cereblon	Homo sapiens	102-106
25141548-4	2014	Extracts (25, 50 and 100 microg) were screened in the vascular endothelial growth factor (VEGF) induced angiogenesis in inovo chick chorioallontoic membrane assay (CAM) at various concentrations using thalidomide and normal saline as positive and untreated control groups respectively.	Thalidomide	201-212	vascular endothelial growth factor A	Gallus gallus	54-88
25141548-4	2014	Extracts (25, 50 and 100 microg) were screened in the vascular endothelial growth factor (VEGF) induced angiogenesis in inovo chick chorioallontoic membrane assay (CAM) at various concentrations using thalidomide and normal saline as positive and untreated control groups respectively.	Thalidomide	201-212	vascular endothelial growth factor A	Gallus gallus	90-94
24893330-5	2014	Inhibiting the synthesis of tumor necrosis factor-alpha (TNF-alpha) by thalidomide prevented DN, accompanied by strongly blocking the up-regulation of Nav1.7, TNF-alpha and p-nucleus factor-kappa B (p-NF-kappaB) in DRG.	Thalidomide	71-82	tumor necrosis factor	Rattus norvegicus	28-55
24893330-5	2014	Inhibiting the synthesis of tumor necrosis factor-alpha (TNF-alpha) by thalidomide prevented DN, accompanied by strongly blocking the up-regulation of Nav1.7, TNF-alpha and p-nucleus factor-kappa B (p-NF-kappaB) in DRG.	Thalidomide	71-82	tumor necrosis factor	Rattus norvegicus	57-66
24893330-5	2014	Inhibiting the synthesis of tumor necrosis factor-alpha (TNF-alpha) by thalidomide prevented DN, accompanied by strongly blocking the up-regulation of Nav1.7, TNF-alpha and p-nucleus factor-kappa B (p-NF-kappaB) in DRG.	Thalidomide	71-82	tumor necrosis factor	Rattus norvegicus	159-168
25043012-0	2014	Structure of the DDB1-CRBN E3 ubiquitin ligase in complex with thalidomide.	Thalidomide	63-74	damage specific DNA binding protein 1	Homo sapiens	17-21
25043012-0	2014	Structure of the DDB1-CRBN E3 ubiquitin ligase in complex with thalidomide.	Thalidomide	63-74	cereblon	Homo sapiens	22-26
25043012-0	2014	Structure of the DDB1-CRBN E3 ubiquitin ligase in complex with thalidomide.	Thalidomide	63-74	Cbl proto-oncogene like 2	Homo sapiens	27-46
25043012-4	2014	Here we present crystal structures of the DDB1-CRBN complex bound to thalidomide, lenalidomide and pomalidomide.	Thalidomide	69-80	damage specific DNA binding protein 1	Homo sapiens	42-46
25043012-4	2014	Here we present crystal structures of the DDB1-CRBN complex bound to thalidomide, lenalidomide and pomalidomide.	Thalidomide	69-80	cereblon	Homo sapiens	47-51
24840055-3	2014	However, the exact mechanism of action has been difficult to quantify until recently when it was shown that another IMiD, thalidomide, binds to an E3 ubiquitin ligase complex constituent, CRBN.	Thalidomide	122-133	cereblon	Homo sapiens	188-192
24859059-9	2014	Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-alpha, VEGF165, and MMP-2 than thalidomide.	Thalidomide	0-11	matrix metallopeptidase 2	Homo sapiens	131-136
24859059-9	2014	Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-alpha, VEGF165, and MMP-2 than thalidomide.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	101-105
24859059-9	2014	Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-alpha, VEGF165, and MMP-2 than thalidomide.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	107-116
24754268-0	2014	Behavioural, metabolic, and endothelial effects of the TNF-alpha suppressor thalidomide on rats subjected to chronic mild stress and fed an atherogenic diet.	Thalidomide	76-87	tumor necrosis factor	Rattus norvegicus	55-64
25610725-1	2014	Lenalidomide and its analogs, thalidomide and pomalidomide, specifically inhibit growth of mature B-cell lymphomas, including multiple myeloma, and induce interleukin-2 (IL-2) release from T cells.	Thalidomide	30-41	interleukin 2	Homo sapiens	155-168
25610725-1	2014	Lenalidomide and its analogs, thalidomide and pomalidomide, specifically inhibit growth of mature B-cell lymphomas, including multiple myeloma, and induce interleukin-2 (IL-2) release from T cells.	Thalidomide	30-41	interleukin 2	Homo sapiens	170-174
24739012-1	2014	Lenalidomide (Revlimid; Selleck Chemicals, Houston, TX, USA), an analogue of thalidomide, possesses potent cytokine modulatory capacity through inhibition of cytokines such as tumour necrosis factor (TNF)-alpha, a cytokine pivotal for the onset and development of complications in obesity and diabetes mellitus.	Thalidomide	77-88	tumor necrosis factor	Mus musculus	176-210
24667589-1	2014	Thalidomide is an oral immunomodulatory and anti-inflammatory drug with antitumor necrosis factor-alpha (TNF-alpha) activity.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	105-114
24667589-3	2014	We report the effect and tolerability of thalidomide in 3 patients with moderate-to-severe CD who were not responsive to anti-TNF-alpha therapies, and review the relevant literature.	Thalidomide	41-52	tumor necrosis factor	Homo sapiens	126-135
24667589-8	2014	In our CD patients who experienced loss of response or were unable to tolerate anti-TNF-alpha drugs, thalidomide was an effective and well-tolerated therapy for inducing and maintaining long-term remission.	Thalidomide	101-112	tumor necrosis factor	Homo sapiens	84-93
24803825-10	2014	CONCLUSION: Thalidomide can down-regulate serum VEGF level in EC patients, and combined with radiotherapy may improve treatment outcome.	Thalidomide	12-23	vascular endothelial growth factor A	Homo sapiens	48-52
24530998-4	2014	Furthermore, the TNF-alpha synthesis inhibitor thalidomide significantly blocked the activation of both isoforms JNK1 and JNK2 in the DRG and attenuated mechanical allodynia following BTZ treatment.	Thalidomide	47-58	tumor necrosis factor	Mus musculus	17-26
24530998-4	2014	Furthermore, the TNF-alpha synthesis inhibitor thalidomide significantly blocked the activation of both isoforms JNK1 and JNK2 in the DRG and attenuated mechanical allodynia following BTZ treatment.	Thalidomide	47-58	mitogen-activated protein kinase 8	Mus musculus	113-117
24530998-4	2014	Furthermore, the TNF-alpha synthesis inhibitor thalidomide significantly blocked the activation of both isoforms JNK1 and JNK2 in the DRG and attenuated mechanical allodynia following BTZ treatment.	Thalidomide	47-58	mitogen-activated protein kinase 9	Mus musculus	122-126
24735834-5	2014	Some investigations revealed that thalidomide could elicit immunomodulatory or neuromodulatory properties by affecting different targets, including cytokines (such as TNF alpha), neurotransmitters, and nitric oxide (NO).	Thalidomide	34-45	tumor necrosis factor	Mus musculus	167-176
24361040-2	2014	We hypothesized that because thalidomide inhibits secretion of tumor necrosis factor alpha (TNF-alpha), survival of animals that received thalidomide would be significantly prolonged.	Thalidomide	29-40	tumor necrosis factor	Oryctolagus cuniculus	63-90
24361040-2	2014	We hypothesized that because thalidomide inhibits secretion of tumor necrosis factor alpha (TNF-alpha), survival of animals that received thalidomide would be significantly prolonged.	Thalidomide	29-40	tumor necrosis factor	Oryctolagus cuniculus	92-101
24361040-2	2014	We hypothesized that because thalidomide inhibits secretion of tumor necrosis factor alpha (TNF-alpha), survival of animals that received thalidomide would be significantly prolonged.	Thalidomide	138-149	tumor necrosis factor	Oryctolagus cuniculus	63-90
24361040-2	2014	We hypothesized that because thalidomide inhibits secretion of tumor necrosis factor alpha (TNF-alpha), survival of animals that received thalidomide would be significantly prolonged.	Thalidomide	138-149	tumor necrosis factor	Oryctolagus cuniculus	92-101
24769540-3	2014	Total three studies were finally included, indicating that docetaxel plus thalidomide exhibited better survival prognosis and greater prostate-specific antigen (PSA) decline than docetaxel alone.	Thalidomide	74-85	kallikrein related peptidase 3	Homo sapiens	134-165
24134145-11	2014	Thalidomide is the drug of choice for severe atypical lepra reactions because of its anti-tumor necrosis factor-alpha action.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	90-117
24692723-5	2014	RESULTS: RA up-regulated FGF2 gene expression, which was abrogated by thalidomide.	Thalidomide	70-81	fibroblast growth factor 2	Homo sapiens	25-29
24520265-16	2014	Thus, thalidomide eased the degree of BLM-induced pulmonary fibrosis in rats by downregulating p-JNK and alpha-SMA expression.	Thalidomide	6-17	actin gamma 2, smooth muscle	Rattus norvegicus	105-114
24487918-0	2014	Thalidomide influences atherogenesis in aortas of ApoE(-/-)/LDLR (-/-) double knockout mice: a nano-CT study.	Thalidomide	0-11	apolipoprotein E	Mus musculus	50-54
24487918-0	2014	Thalidomide influences atherogenesis in aortas of ApoE(-/-)/LDLR (-/-) double knockout mice: a nano-CT study.	Thalidomide	0-11	low density lipoprotein receptor	Mus musculus	60-64
25053990-0	2014	Internal ribosome entry site of bFGF is the target of thalidomide for IMiDs development in multiple myeloma.	Thalidomide	54-65	fibroblast growth factor 2	Homo sapiens	32-36
24460184-0	2014	Thalidomide increases human hepatic cytochrome P450 3A enzymes by direct activation of the pregnane X receptor.	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	91-110
25053990-4	2014	Interestingly, we further demonstrated that although thalidomide down-regulated bFGF translation through the inhibition of IRES even at 0.1 mug/ml, pomalidomide did not have a similar affect bFGF levels.	Thalidomide	53-64	fibroblast growth factor 2	Homo sapiens	80-84
25053990-5	2014	A colony formation assay demonstrated that thalidomide and the bFGF knock-down clones caused a significant reduction in the clonogenic ability of MM cells, and treatment with exogenous bFGF can recover the clonogenic ability of thalidomide-treated cells and knock-down clones, but not that of pomalidomide-treated cells.	Thalidomide	228-239	fibroblast growth factor 2	Homo sapiens	63-67
25053990-5	2014	A colony formation assay demonstrated that thalidomide and the bFGF knock-down clones caused a significant reduction in the clonogenic ability of MM cells, and treatment with exogenous bFGF can recover the clonogenic ability of thalidomide-treated cells and knock-down clones, but not that of pomalidomide-treated cells.	Thalidomide	228-239	fibroblast growth factor 2	Homo sapiens	185-189
25053990-6	2014	This implies that thalidomide, but not pomalidomide, targets the IRES of FGF-2.	Thalidomide	18-29	fibroblast growth factor 2	Homo sapiens	73-78
24460184-8	2014	Thalidomide enhanced levels of P450 3A4 and 2B6 mRNA, protein expression, and/or oxidation activity in human hepatocytes, indirectly suggesting the activation of upstream transcription factors involved in detoxication, e.g., the nuclear receptors pregnane X receptor (PXR) and constitutive androstane receptor (CAR).	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	247-266
24460184-8	2014	Thalidomide enhanced levels of P450 3A4 and 2B6 mRNA, protein expression, and/or oxidation activity in human hepatocytes, indirectly suggesting the activation of upstream transcription factors involved in detoxication, e.g., the nuclear receptors pregnane X receptor (PXR) and constitutive androstane receptor (CAR).	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	268-271
24460184-8	2014	Thalidomide enhanced levels of P450 3A4 and 2B6 mRNA, protein expression, and/or oxidation activity in human hepatocytes, indirectly suggesting the activation of upstream transcription factors involved in detoxication, e.g., the nuclear receptors pregnane X receptor (PXR) and constitutive androstane receptor (CAR).	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 3	Homo sapiens	277-309
24460184-8	2014	Thalidomide enhanced levels of P450 3A4 and 2B6 mRNA, protein expression, and/or oxidation activity in human hepatocytes, indirectly suggesting the activation of upstream transcription factors involved in detoxication, e.g., the nuclear receptors pregnane X receptor (PXR) and constitutive androstane receptor (CAR).	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 3	Homo sapiens	311-314
24460184-10	2014	To investigate direct engagement and functional alteration of PXR and CAR by thalidomide, we utilized a peptide microarray with 154 coregulator-derived nuclear receptor-interaction motifs and coregulator and nuclear receptor boxes, which serves as a sensor for nuclear receptor conformation and activity status as a function of ligand.	Thalidomide	77-88	nuclear receptor subfamily 1 group I member 2	Homo sapiens	62-65
24460184-10	2014	To investigate direct engagement and functional alteration of PXR and CAR by thalidomide, we utilized a peptide microarray with 154 coregulator-derived nuclear receptor-interaction motifs and coregulator and nuclear receptor boxes, which serves as a sensor for nuclear receptor conformation and activity status as a function of ligand.	Thalidomide	77-88	nuclear receptor subfamily 1 group I member 3	Homo sapiens	70-73
24460184-11	2014	Thalidomide and its human proximate metabolite 5-hydroxythalidomide displayed significant modulation of coregulator interaction with PXR and CAR ligand-binding domains, similar to established agonists for these receptors.	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 2	Homo sapiens	133-136
24460184-11	2014	Thalidomide and its human proximate metabolite 5-hydroxythalidomide displayed significant modulation of coregulator interaction with PXR and CAR ligand-binding domains, similar to established agonists for these receptors.	Thalidomide	0-11	nuclear receptor subfamily 1 group I member 3	Homo sapiens	141-144
24460184-12	2014	These results collectively suggest that thalidomide acts as a ligand for PXR and CAR and causes enzyme induction leading to increased P450 enzyme activity.	Thalidomide	40-51	nuclear receptor subfamily 1 group I member 2	Homo sapiens	73-76
24460184-12	2014	These results collectively suggest that thalidomide acts as a ligand for PXR and CAR and causes enzyme induction leading to increased P450 enzyme activity.	Thalidomide	40-51	nuclear receptor subfamily 1 group I member 3	Homo sapiens	81-84
24219762-4	2014	In addition, in vitro effect of thalidomide on Ang2, Notch1 and Dll4 in human umbilical vein endothelial cells (HUVEC) and on HUVEC proliferation was also investigated during normoxic and hypoxic conditions.	Thalidomide	32-43	angiopoietin 2	Homo sapiens	47-51
24219762-4	2014	In addition, in vitro effect of thalidomide on Ang2, Notch1 and Dll4 in human umbilical vein endothelial cells (HUVEC) and on HUVEC proliferation was also investigated during normoxic and hypoxic conditions.	Thalidomide	32-43	notch receptor 1	Homo sapiens	53-59
24219762-0	2014	Thalidomide-induced angiopoietin 2, Notch1 and Dll4 downregulation under hypoxic condition in tissues with gastrointestinal vascular malformation and human umbilical vein endothelial cells.	Thalidomide	0-11	angiopoietin 2	Homo sapiens	20-34
24219762-4	2014	In addition, in vitro effect of thalidomide on Ang2, Notch1 and Dll4 in human umbilical vein endothelial cells (HUVEC) and on HUVEC proliferation was also investigated during normoxic and hypoxic conditions.	Thalidomide	32-43	delta like canonical Notch ligand 4	Homo sapiens	64-68
24219762-0	2014	Thalidomide-induced angiopoietin 2, Notch1 and Dll4 downregulation under hypoxic condition in tissues with gastrointestinal vascular malformation and human umbilical vein endothelial cells.	Thalidomide	0-11	notch receptor 1	Homo sapiens	36-42
24219762-0	2014	Thalidomide-induced angiopoietin 2, Notch1 and Dll4 downregulation under hypoxic condition in tissues with gastrointestinal vascular malformation and human umbilical vein endothelial cells.	Thalidomide	0-11	delta like canonical Notch ligand 4	Homo sapiens	47-51
24219762-9	2014	CONCLUSION: Ang2, Notch1, Dll4 and Hif-1alpha may play an important role in the pathogenesis of GIVM and may be potential targets of thalidomide in the treatment of the disease.	Thalidomide	133-144	angiopoietin 2	Homo sapiens	12-16
24219762-9	2014	CONCLUSION: Ang2, Notch1, Dll4 and Hif-1alpha may play an important role in the pathogenesis of GIVM and may be potential targets of thalidomide in the treatment of the disease.	Thalidomide	133-144	notch receptor 1	Homo sapiens	18-24
24219762-9	2014	CONCLUSION: Ang2, Notch1, Dll4 and Hif-1alpha may play an important role in the pathogenesis of GIVM and may be potential targets of thalidomide in the treatment of the disease.	Thalidomide	133-144	delta like canonical Notch ligand 4	Homo sapiens	26-30
24219762-9	2014	CONCLUSION: Ang2, Notch1, Dll4 and Hif-1alpha may play an important role in the pathogenesis of GIVM and may be potential targets of thalidomide in the treatment of the disease.	Thalidomide	133-144	hypoxia inducible factor 1 subunit alpha	Homo sapiens	35-45
24596000-0	2014	Thalidomide regulation of NF-kappaB proteins limits Tregs activity in chronic lymphocytic leukemia.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	26-35
24292623-6	2014	Analysis of myeloma cell lines revealed that loss of IKZF1 and IKZF3 is both necessary and sufficient for lenalidomide"s therapeutic effect, suggesting that the antitumor and teratogenic activities of thalidomide-like drugs are dissociable.	Thalidomide	201-212	IKAROS family zinc finger 1	Homo sapiens	53-58
24292623-6	2014	Analysis of myeloma cell lines revealed that loss of IKZF1 and IKZF3 is both necessary and sufficient for lenalidomide"s therapeutic effect, suggesting that the antitumor and teratogenic activities of thalidomide-like drugs are dissociable.	Thalidomide	201-212	IKAROS family zinc finger 3	Homo sapiens	63-68
24596000-4	2014	Thalidomide"s influence on NF-kappaB proteins and on regulatory T cells (Treg) in CLL was investigated.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	27-36
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	nuclear factor kappa B subunit 1	Homo sapiens	49-58
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	nuclear factor kappa B subunit 1	Homo sapiens	112-121
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	149-152
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	CD4 molecule	Homo sapiens	183-186
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	interleukin 2 receptor subunit alpha	Homo sapiens	189-193
24596000-10	2014	RESULTS: It was found that thalidomide regulates NF-kappaB activity differentially, and the activity of certain NF-kappaB components correlated with TNF levels and T regulatory cell (CD4 + CD25 high GITR + ).	Thalidomide	27-38	TNF receptor superfamily member 18	Homo sapiens	199-203
24596000-11	2014	CONCLUSIONS: These results might indicate that thalidomide not only regulates TNF but also directly interferes with NF-kappaB components.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	78-81
24596000-11	2014	CONCLUSIONS: These results might indicate that thalidomide not only regulates TNF but also directly interferes with NF-kappaB components.	Thalidomide	47-58	nuclear factor kappa B subunit 1	Homo sapiens	116-125
24451995-6	2014	Similar to valproate, thalidomide was classified as a Class 2 agent, with weak embryotoxicity, by the mEST criteria, and was classified as Category 3 embryotoxic based on our criteria.	Thalidomide	22-33	sulfotransferase family 1E, member 1	Mus musculus	102-106
25531359-9	2014	In patients not responding to anti-TNF therapy, thalidomide or tacrolimus may be considered.	Thalidomide	48-59	tumor necrosis factor	Homo sapiens	35-38
24118365-0	2014	Do baseline Cereblon gene expression and IL-6 receptor expression determine the response to thalidomide-dexamethasone treatment in multiple myeloma patients?	Thalidomide	92-103	cereblon	Homo sapiens	12-20
24118365-2	2014	Cereblon (CRBN) expression was described to be essential for the activity of thalidomide.	Thalidomide	77-88	cereblon	Homo sapiens	0-8
24118365-2	2014	Cereblon (CRBN) expression was described to be essential for the activity of thalidomide.	Thalidomide	77-88	cereblon	Homo sapiens	10-14
24118365-6	2014	The aim of the study was to evaluate CRBN and IL-6R expressions and their impact on clinical efficacy of dexamethasone-thalidomide therapy in multiple myeloma (MM) patients, in addition to their association with other clinical and prognostic parameters.	Thalidomide	119-130	cereblon	Homo sapiens	37-41
24118365-6	2014	The aim of the study was to evaluate CRBN and IL-6R expressions and their impact on clinical efficacy of dexamethasone-thalidomide therapy in multiple myeloma (MM) patients, in addition to their association with other clinical and prognostic parameters.	Thalidomide	119-130	interleukin 6 receptor	Homo sapiens	46-51
24931258-21	2014	On day 7 the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were lower than in the TNBS model group.	Thalidomide	58-69	tumor necrosis factor	Rattus norvegicus	28-37
24931258-21	2014	On day 7 the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were lower than in the TNBS model group.	Thalidomide	58-69	interleukin 1 beta	Rattus norvegicus	42-50
24931258-22	2014	On day 14, the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were significantly lower than in the TNBS model group (P &lt; 0.05).	Thalidomide	60-71	tumor necrosis factor	Rattus norvegicus	30-39
24931258-22	2014	On day 14, the expressions of TNF-alpha and IL-1beta in the thalidomide treatment group were significantly lower than in the TNBS model group (P &lt; 0.05).	Thalidomide	60-71	interleukin 1 beta	Rattus norvegicus	44-52
24931258-23	2014	On day 4, the IL-10 levels of the thalidomide treatment group became significantly elevated.	Thalidomide	34-45	interleukin 10	Rattus norvegicus	14-19
23510862-3	2014	GM-CSF in combination with thalidomide induces prostate-specific antigen (PSA) responses in 20% to 25% of patients with castration-resistant prostate cancer (CRPC).	Thalidomide	27-38	kallikrein related peptidase 3	Homo sapiens	47-78
24275522-7	2014	In cancer cell lines, thalidomide is antiangiogenic and antiproliferative via suppression of tumor necrosis factor-alpha (TNF-alpha) and downstream effects on the nuclear factor (NFkappaB) cascade.	Thalidomide	22-33	tumor necrosis factor	Homo sapiens	93-120
24275522-7	2014	In cancer cell lines, thalidomide is antiangiogenic and antiproliferative via suppression of tumor necrosis factor-alpha (TNF-alpha) and downstream effects on the nuclear factor (NFkappaB) cascade.	Thalidomide	22-33	tumor necrosis factor	Homo sapiens	122-131
24275522-7	2014	In cancer cell lines, thalidomide is antiangiogenic and antiproliferative via suppression of tumor necrosis factor-alpha (TNF-alpha) and downstream effects on the nuclear factor (NFkappaB) cascade.	Thalidomide	22-33	nuclear factor kappa B subunit 1	Homo sapiens	179-187
24154490-7	2014	Specifically, 71 drug-like compounds with known in vivo effects, including thalidomide, were examined in the hPST.	Thalidomide	75-86	sulfotransferase family 1A member 1	Homo sapiens	109-113
23810410-10	2013	Thalidomide decreased production of inflammatory and fibrogenic cytokine tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and transforming growth factor (TGF)-beta1.	Thalidomide	0-11	interleukin 1 beta	Mus musculus	108-130
24030118-0	2013	Increased PAC-1 expression among patients with multiple myeloma on concurrent thalidomide and warfarin.	Thalidomide	78-89	dual specificity phosphatase 2	Homo sapiens	10-15
24030118-7	2013	Increased expression marker for PAC-1 was observed after 4 weeks of thalidomide treatment (P &lt; 0.05) indicating one aspect of platelet activation activity seen in these patients.	Thalidomide	68-79	dual specificity phosphatase 2	Homo sapiens	32-37
24210217-6	2013	Bortezomib, thalidomide or lenalidomide extended OS of FGFR3 and/or c-MAF-positive patients.	Thalidomide	12-23	fibroblast growth factor receptor 3	Homo sapiens	55-60
24210217-6	2013	Bortezomib, thalidomide or lenalidomide extended OS of FGFR3 and/or c-MAF-positive patients.	Thalidomide	12-23	MAF bZIP transcription factor	Homo sapiens	68-73
24055736-0	2013	Polymorphisms in the endothelial nitric oxide synthase gene in thalidomide embryopathy.	Thalidomide	63-74	nitric oxide synthase 3	Homo sapiens	21-54
24187103-7	2013	Treatment with meloxicam, thalidomide, and etanercept for 1 month significantly reduced percentages of IL-21+CXCR5+CD4+ T cells and concentrations of serum IL-21 (p &lt; 0.001, p &lt; 0.001, respectively), accompanied by significantly minimized disease activity in drug responders, but not in the drug nonresponders.	Thalidomide	26-37	interleukin 21	Homo sapiens	103-108
24187103-7	2013	Treatment with meloxicam, thalidomide, and etanercept for 1 month significantly reduced percentages of IL-21+CXCR5+CD4+ T cells and concentrations of serum IL-21 (p &lt; 0.001, p &lt; 0.001, respectively), accompanied by significantly minimized disease activity in drug responders, but not in the drug nonresponders.	Thalidomide	26-37	C-X-C motif chemokine receptor 5	Homo sapiens	109-114
24187103-7	2013	Treatment with meloxicam, thalidomide, and etanercept for 1 month significantly reduced percentages of IL-21+CXCR5+CD4+ T cells and concentrations of serum IL-21 (p &lt; 0.001, p &lt; 0.001, respectively), accompanied by significantly minimized disease activity in drug responders, but not in the drug nonresponders.	Thalidomide	26-37	interleukin 21	Homo sapiens	156-161
23952807-9	2013	There was significant regression of vessels in CAM incubated with thalidomide dispersion, thalidomide-loaded implants and vitreous samples from group I when compared to control.	Thalidomide	66-77	calmodulin	Oryctolagus cuniculus	47-50
23952807-9	2013	There was significant regression of vessels in CAM incubated with thalidomide dispersion, thalidomide-loaded implants and vitreous samples from group I when compared to control.	Thalidomide	90-101	calmodulin	Oryctolagus cuniculus	47-50
23810410-10	2013	Thalidomide decreased production of inflammatory and fibrogenic cytokine tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and transforming growth factor (TGF)-beta1.	Thalidomide	0-11	interleukin 6	Mus musculus	132-136
23810410-10	2013	Thalidomide decreased production of inflammatory and fibrogenic cytokine tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and transforming growth factor (TGF)-beta1.	Thalidomide	0-11	transforming growth factor, beta 1	Mus musculus	142-180
23810410-11	2013	In addition thalidomide reduced myeloperoxidase (MPO), nitric oxide (NO), and hydroxyproline content in lung tissue.	Thalidomide	12-23	myeloperoxidase	Mus musculus	32-47
23810410-11	2013	In addition thalidomide reduced myeloperoxidase (MPO), nitric oxide (NO), and hydroxyproline content in lung tissue.	Thalidomide	12-23	myeloperoxidase	Mus musculus	49-52
23926306-4	2013	According to the gene profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, may be associated with THD modulation.	Thalidomide	144-147	caspase 8	Homo sapiens	53-62
23926306-4	2013	According to the gene profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, may be associated with THD modulation.	Thalidomide	144-147	caspase 10	Homo sapiens	67-77
23926306-4	2013	According to the gene profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, may be associated with THD modulation.	Thalidomide	144-147	POU class 5 homeobox 1	Homo sapiens	99-105
23926306-4	2013	According to the gene profile, the downregulation of caspase-8 and caspase-10, and upregulation of oct3/4 and tgf-beta1, may be associated with THD modulation.	Thalidomide	144-147	transforming growth factor beta 1	Homo sapiens	110-119
23767831-2	2013	Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results.	Thalidomide	96-107	vascular endothelial growth factor A	Homo sapiens	24-58
23447383-8	2013	Now we observe the reduction of the NRP1 expression on Tregs in vitro, thereby suggesting a possible target of thalidomide action.	Thalidomide	111-122	neuropilin 1	Homo sapiens	36-40
23767831-2	2013	Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results.	Thalidomide	96-107	vascular endothelial growth factor A	Homo sapiens	60-64
23500539-7	2013	Furthermore, pretreatment with thalidomide inhibited the TGF-beta1-induced phosphorylation of p38 and Smad3, but not that of ERK1/2, JNK, and Smad2.	Thalidomide	31-42	transforming growth factor beta 1	Homo sapiens	57-66
23722461-5	2013	RESULTS: Thalidomide (20 muM) not only inhibited cell proliferation after 24 h [fold increase of cell number, 0.85 +- 0.09 vs. 1.47 +- 0.14 (treatment vs. control group); P &lt; 0.01] and 48 h of incubation (0.85 +- 0.10 vs. 1.97 +- 0.12; P &lt; 0.001), it also inhibited cell migration and slowed wound closure at 24 h (P &lt; 0.001).	Thalidomide	9-20	latexin	Homo sapiens	25-28
23722461-6	2013	Thalidomide significantly attenuated TGF-beta1-induced VEGF expression at both the mRNA and protein levels.	Thalidomide	0-11	transforming growth factor beta 1	Homo sapiens	37-46
23722461-6	2013	Thalidomide significantly attenuated TGF-beta1-induced VEGF expression at both the mRNA and protein levels.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	55-59
23722461-7	2013	Incubation of thalidomide with cells stimulated with TGF-beta1 significantly inhibited their production of collagen.	Thalidomide	14-25	transforming growth factor beta 1	Homo sapiens	53-62
23722461-8	2013	Thalidomide inhibited Smad3, STAT3, and subsequent p44/42 kinase phosphorylation.	Thalidomide	0-11	SMAD family member 3	Homo sapiens	22-27
23722461-8	2013	Thalidomide inhibited Smad3, STAT3, and subsequent p44/42 kinase phosphorylation.	Thalidomide	0-11	signal transducer and activator of transcription 3	Homo sapiens	29-34
23722461-8	2013	Thalidomide inhibited Smad3, STAT3, and subsequent p44/42 kinase phosphorylation.	Thalidomide	0-11	interferon induced protein 44	Homo sapiens	51-54
23500539-0	2013	Thalidomide inhibits fibronectin production in TGF-beta1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway.	Thalidomide	0-11	fibronectin 1	Homo sapiens	21-32
23500539-0	2013	Thalidomide inhibits fibronectin production in TGF-beta1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway.	Thalidomide	0-11	transforming growth factor beta 1	Homo sapiens	47-56
24284039-0	2013	Thalidomide distinctly affected TNF-alpha, IL-6 and MMP secretion by an ovarian cancer cell line (SKOV-3) and primary ovarian cancer cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	32-41
24284039-0	2013	Thalidomide distinctly affected TNF-alpha, IL-6 and MMP secretion by an ovarian cancer cell line (SKOV-3) and primary ovarian cancer cells.	Thalidomide	0-11	interleukin 6	Homo sapiens	43-47
24284039-1	2013	BACKGROUND: Thalidomide inhibits TNF-alpha production in lipopolysaccharide-stimulated monocytes.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	33-42
24284039-2	2013	The aim of this study was to evaluate the effect of thalidomide on TNF-alpha, IL-6 and MMP secretion in epithelial ovarian carcinoma cells.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	67-76
24284039-2	2013	The aim of this study was to evaluate the effect of thalidomide on TNF-alpha, IL-6 and MMP secretion in epithelial ovarian carcinoma cells.	Thalidomide	52-63	interleukin 6	Homo sapiens	78-82
24284039-8	2013	Thalidomide also significantly decreased the capacity of SKOV-3 cells, but not primary epithelial ovarian carcinoma cells, to secrete MMP-9 and MMP-2.	Thalidomide	0-11	matrix metallopeptidase 9	Homo sapiens	134-139
24284039-8	2013	Thalidomide also significantly decreased the capacity of SKOV-3 cells, but not primary epithelial ovarian carcinoma cells, to secrete MMP-9 and MMP-2.	Thalidomide	0-11	matrix metallopeptidase 2	Homo sapiens	144-149
24284039-10	2013	CONCLUSION: Our study suggests that thalidomide distinctly affected TNF-alpha, IL-6 and MMPs secretion by an ovarian carcinoma cell line (SKOV-3) and primary ovarian cancer cells.	Thalidomide	36-47	tumor necrosis factor	Homo sapiens	68-77
24284039-10	2013	CONCLUSION: Our study suggests that thalidomide distinctly affected TNF-alpha, IL-6 and MMPs secretion by an ovarian carcinoma cell line (SKOV-3) and primary ovarian cancer cells.	Thalidomide	36-47	interleukin 6	Homo sapiens	79-83
24284039-10	2013	CONCLUSION: Our study suggests that thalidomide distinctly affected TNF-alpha, IL-6 and MMPs secretion by an ovarian carcinoma cell line (SKOV-3) and primary ovarian cancer cells.	Thalidomide	36-47	matrix metallopeptidase 2	Homo sapiens	88-92
23500539-0	2013	Thalidomide inhibits fibronectin production in TGF-beta1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway.	Thalidomide	0-11	mitogen-activated protein kinase 1	Homo sapiens	117-120
23500539-0	2013	Thalidomide inhibits fibronectin production in TGF-beta1-treated normal and keloid fibroblasts via inhibition of the p38/Smad3 pathway.	Thalidomide	0-11	SMAD family member 3	Homo sapiens	121-126
23500539-3	2013	The aims were to examine possible therapeutic effects of thalidomide on fibronectin expression in transforming growth factor-beta1 (TGF-beta1)-treated normal fibroblasts (NFs) and keloid-derived fibroblasts (KFs) and the underlying mechanism of action, especially the involvement of mitogen-activated protein kinase (MAPKs) and Sma- and Mad-related family (Smads) pathways.	Thalidomide	57-68	fibronectin 1	Homo sapiens	72-83
23500539-3	2013	The aims were to examine possible therapeutic effects of thalidomide on fibronectin expression in transforming growth factor-beta1 (TGF-beta1)-treated normal fibroblasts (NFs) and keloid-derived fibroblasts (KFs) and the underlying mechanism of action, especially the involvement of mitogen-activated protein kinase (MAPKs) and Sma- and Mad-related family (Smads) pathways.	Thalidomide	57-68	transforming growth factor beta 1	Homo sapiens	98-130
23500539-7	2013	Furthermore, pretreatment with thalidomide inhibited the TGF-beta1-induced phosphorylation of p38 and Smad3, but not that of ERK1/2, JNK, and Smad2.	Thalidomide	31-42	mitogen-activated protein kinase 1	Homo sapiens	94-97
23500539-5	2013	TGF-beta1 induced significant fibronectin expression in NFs and KFs and the effect was inhibited by pretreatment with thalidomide.	Thalidomide	118-129	transforming growth factor beta 1	Homo sapiens	0-9
23500539-5	2013	TGF-beta1 induced significant fibronectin expression in NFs and KFs and the effect was inhibited by pretreatment with thalidomide.	Thalidomide	118-129	fibronectin 1	Homo sapiens	30-41
23500539-7	2013	Furthermore, pretreatment with thalidomide inhibited the TGF-beta1-induced phosphorylation of p38 and Smad3, but not that of ERK1/2, JNK, and Smad2.	Thalidomide	31-42	SMAD family member 3	Homo sapiens	102-107
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	transforming growth factor beta 1	Homo sapiens	52-60
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	SMAD family member 3	Homo sapiens	102-107
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	fibronectin 1	Homo sapiens	118-129
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	matrix metallopeptidase 9	Homo sapiens	172-198
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	transforming growth factor beta 1	Homo sapiens	228-237
23500539-8	2013	In addition, thalidomide pretreatment inhibited the TGF-beta-induced DNA binding activity of AP-1 and Smad3/4, caused fibronectin degradation by increasing the activity of matrix metalloproteinase 9, and decreased production of TGF-beta1 and fibronectin and the number of fibroblasts in an in vivo keloid model.	Thalidomide	13-24	fibronectin 1	Homo sapiens	242-253
23500539-9	2013	These results show that thalidomide has an antifibrotic effect on keloid fibroblasts that is caused by suppression of TGF-beta1-induced p38 and Smad3 signaling.	Thalidomide	24-35	transforming growth factor beta 1	Homo sapiens	118-127
23500539-9	2013	These results show that thalidomide has an antifibrotic effect on keloid fibroblasts that is caused by suppression of TGF-beta1-induced p38 and Smad3 signaling.	Thalidomide	24-35	mitogen-activated protein kinase 1	Homo sapiens	136-139
23500539-9	2013	These results show that thalidomide has an antifibrotic effect on keloid fibroblasts that is caused by suppression of TGF-beta1-induced p38 and Smad3 signaling.	Thalidomide	24-35	SMAD family member 3	Homo sapiens	144-149
23531412-10	2013	We show that thalidomide activity on organizer formation in hydra depends on the activity of casein kinase1 and the abundance of beta-catenin.	Thalidomide	13-24	catenin beta 1	Homo sapiens	129-141
23686003-0	2013	A myeloma cell line established from a patient refractory to thalidomide therapy revealed high-risk cytogenetic abnormalities and produced vascular endothelial growth factor.	Thalidomide	61-72	vascular endothelial growth factor A	Homo sapiens	139-173
23737889-0	2013	Effect of thalidomide on the proliferation of hepatoma cells assessed by osteopontin levels in nude mice.	Thalidomide	10-21	secreted phosphoprotein 1	Mus musculus	73-84
23717811-15	2013	An analog of thalidomide, CC-5103 increases the secretion of critical cytokines of the tumor microenvironment, including IL-2, IFN-gamma, TNF-alpha, and IL-10, and is currently being evaluated in clinical trials for the treatment of recurrent or refractory pediatric central nervous system tumors.	Thalidomide	13-24	interleukin 2	Homo sapiens	121-125
23717811-15	2013	An analog of thalidomide, CC-5103 increases the secretion of critical cytokines of the tumor microenvironment, including IL-2, IFN-gamma, TNF-alpha, and IL-10, and is currently being evaluated in clinical trials for the treatment of recurrent or refractory pediatric central nervous system tumors.	Thalidomide	13-24	interferon gamma	Homo sapiens	127-136
23717811-15	2013	An analog of thalidomide, CC-5103 increases the secretion of critical cytokines of the tumor microenvironment, including IL-2, IFN-gamma, TNF-alpha, and IL-10, and is currently being evaluated in clinical trials for the treatment of recurrent or refractory pediatric central nervous system tumors.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	138-147
23717811-15	2013	An analog of thalidomide, CC-5103 increases the secretion of critical cytokines of the tumor microenvironment, including IL-2, IFN-gamma, TNF-alpha, and IL-10, and is currently being evaluated in clinical trials for the treatment of recurrent or refractory pediatric central nervous system tumors.	Thalidomide	13-24	interleukin 10	Homo sapiens	153-158
23244235-2	2013	Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-alpha, which plays role in Abeta neurotoxicity.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	69-78
23583898-4	2013	Here, we show that thalidomide suppressed TNF-alpha-induced NF-kappaB activation and ATP-induced IL-1beta secretion, but did not interrupt the production of IL-1beta, IL-6, IL-8, and TNF-alpha in response to lipopolysaccharide in CGD monocytes.	Thalidomide	19-30	tumor necrosis factor	Homo sapiens	42-51
23583898-4	2013	Here, we show that thalidomide suppressed TNF-alpha-induced NF-kappaB activation and ATP-induced IL-1beta secretion, but did not interrupt the production of IL-1beta, IL-6, IL-8, and TNF-alpha in response to lipopolysaccharide in CGD monocytes.	Thalidomide	19-30	interleukin 1 beta	Homo sapiens	97-105
23737889-11	2013	Thalidomide may inhibit the generation of OPN and thereby inhibit the infiltration and metastasis of tumors; the immediate use of thalidomide following hepatectomy in the present study may block the invasion and metasis for liver cancer more effectively.	Thalidomide	0-11	secreted phosphoprotein 1	Mus musculus	42-45
23345625-15	2013	Thalidomide treatment significantly reduced gene expression of these cytokines and the activation of the NF-kappaB in the renal tissue and the circulating levels of cytokines.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	105-114
23434428-0	2013	Induction of apoptosis in multiple myeloma cells by a statin-thalidomide combination can be enhanced by p38 MAPK inhibition.	Thalidomide	61-72	mitogen-activated protein kinase 14	Homo sapiens	104-107
23434428-4	2013	What is more, the combination of thalidomide with statins inhibited cell migration and decreased the production of VEGF and MMP-9 in MM cells more effectively than each of these drugs used separately.	Thalidomide	33-44	vascular endothelial growth factor A	Homo sapiens	115-119
23434428-4	2013	What is more, the combination of thalidomide with statins inhibited cell migration and decreased the production of VEGF and MMP-9 in MM cells more effectively than each of these drugs used separately.	Thalidomide	33-44	matrix metallopeptidase 9	Homo sapiens	124-129
23434428-5	2013	The combination of simvastatin and thalidomide augmented caspase 8 and 3 activation, and the additional application of p38 MAPK inhibitor resulted in enhanced apoptosis of MM cells concomitant with increased caspase 9 and 3 activation, as well as JNK phosphorylation.	Thalidomide	35-46	caspase 8	Homo sapiens	57-66
23404341-2	2013	It was recently reported that the thalidomide analog 3,6"-dithiothalidomide (3,6"-DT) can selectively inhibit the synthesis of TNF in cultured cells.	Thalidomide	34-45	tumor necrosis factor	Mus musculus	127-130
23279849-7	2013	Suppression of STAT3 correlated with the down-regulation of various gene products linked to tumor survival, proliferation, and angiogenesis and led to sensitization of tumor cells to thalidomide and bortezomib.	Thalidomide	183-194	signal transducer and activator of transcription 3	Homo sapiens	15-20
23538327-8	2013	FINDINGS: Compared to other treatment groups, CD133+ cells treated with thalidomide alone produced more hematopoietic colonies.	Thalidomide	72-83	prominin 1	Homo sapiens	46-51
23442845-12	2013	We concluded that fluoxetine, anti-TNF-alpha antibody and thalidomide were effective in preventing depressive-like behaviour and the increase in TNF-alpha levels in the hippocampus of mice induced by an i.c.v.	Thalidomide	58-69	tumor necrosis factor	Mus musculus	145-154
22966948-2	2013	A landmark study recently identified cereblon (CRBN) as a primary target of thalidomide teratogenicity.	Thalidomide	76-87	cereblon	Homo sapiens	47-51
22966948-3	2013	Subsequently it was demonstrated that CRBN is also required for the anti-myeloma activity of thalidomide and related drugs, the so-called immune-modulatory drugs (IMiDs).	Thalidomide	93-104	cereblon	Homo sapiens	38-42
23614289-16	2013	In animals administered thalidomide in the dose of 60 mg/kg p.o., reduction mass of tibia, femur, and L-4 vertebra has been observed.	Thalidomide	24-35	ribosomal protein L3	Rattus norvegicus	102-105
23142220-8	2013	Importantly, after cessation of Thalidomide therapy, this effect was reversible in the CD8 compartment.	Thalidomide	32-43	CD8a molecule	Homo sapiens	87-90
23261764-6	2013	Furthermore, inhibition of TNF-alpha synthesis by intraperitoneal thalidomide prevented both mechanical allodynia and the up-regulation of IL-6 in DRGs following L5-VRT.	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	27-36
23261764-6	2013	Furthermore, inhibition of TNF-alpha synthesis by intraperitoneal thalidomide prevented both mechanical allodynia and the up-regulation of IL-6 in DRGs following L5-VRT.	Thalidomide	66-77	interleukin 6	Homo sapiens	139-143
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	tumor necrosis factor	Mus musculus	115-124
23426142-0	2013	Effect of thalidomide on the expression of vascular endothelial growth factor in a rat model of liver regeneration.	Thalidomide	10-21	vascular endothelial growth factor A	Rattus norvegicus	43-77
23426142-2	2013	The present study investigated the influence of thalidomide, an antiangiogenic agent, on vascular endothelial growth factor (VEGF) expression and liver regeneration after 70% partial hepatectomy (PH) in rats.	Thalidomide	48-59	vascular endothelial growth factor A	Rattus norvegicus	89-123
23426142-2	2013	The present study investigated the influence of thalidomide, an antiangiogenic agent, on vascular endothelial growth factor (VEGF) expression and liver regeneration after 70% partial hepatectomy (PH) in rats.	Thalidomide	48-59	vascular endothelial growth factor A	Rattus norvegicus	125-129
23426142-10	2013	The immunohistochemical staining revealed a waved pattern of VEGF expression which advanced from the periportal to pericentral area in both groups, but a slower advancement was detected in thalidomide-treated rats.	Thalidomide	189-200	vascular endothelial growth factor A	Rattus norvegicus	61-65
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	interleukin 1 beta	Mus musculus	126-134
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	interleukin 6	Mus musculus	136-140
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	142-151
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	170-179
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	180-183
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	tumor necrosis factor	Mus musculus	330-339
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	interleukin 1 beta	Mus musculus	341-349
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	interleukin 6	Mus musculus	351-355
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	170-179
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	170-179
23510834-8	2013	Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65 and wet/dry ratios of the lung (P &lt; 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-alpha, IL-1beta, IL-6, NF-kappaB mRNA, and nuclear NF-kappaB p65.	Thalidomide	48-59	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	395-398
22710762-7	2013	Exposure to thalidomide (100 microg/ml) reduced the intracytoplasmic pro-inflammatory cytokine production of neonatal monocytes and the IFN-gamma production of neonatal lymphocytes.	Thalidomide	12-23	interferon gamma	Homo sapiens	136-145
22710762-8	2013	In supernatants, the addition of thalidomide resulted in reduction of TNF-alpha, IL-6, IL-10 and, by trend, IFN-gamma.	Thalidomide	33-44	tumor necrosis factor	Homo sapiens	70-79
22710762-8	2013	In supernatants, the addition of thalidomide resulted in reduction of TNF-alpha, IL-6, IL-10 and, by trend, IFN-gamma.	Thalidomide	33-44	interleukin 6	Homo sapiens	81-85
22710762-8	2013	In supernatants, the addition of thalidomide resulted in reduction of TNF-alpha, IL-6, IL-10 and, by trend, IFN-gamma.	Thalidomide	33-44	interleukin 10	Homo sapiens	87-92
22710762-8	2013	In supernatants, the addition of thalidomide resulted in reduction of TNF-alpha, IL-6, IL-10 and, by trend, IFN-gamma.	Thalidomide	33-44	interferon gamma	Homo sapiens	108-117
22710762-10	2013	Bcl-2 expression tended to be increased after addition of thalidomide.	Thalidomide	58-69	BCL2 apoptosis regulator	Homo sapiens	0-5
23233657-1	2013	Recently, cereblon (CRBN) expression was found to be essential for the activity of thalidomide and lenalidomide.	Thalidomide	83-94	cereblon	Homo sapiens	20-24
23233657-2	2013	In the present study, we investigated whether the clinical efficacy of thalidomide in multiple myeloma is associated with CRBN expression in myeloma cells.	Thalidomide	71-82	cereblon	Homo sapiens	122-126
23233657-7	2013	We conclude that CRBN expression may be associated with the clinical efficacy of thalidomide.	Thalidomide	81-92	cereblon	Homo sapiens	17-21
23405115-1	2013	Thalidomide is a tumor necrosis factor alpha (TNFalpha) inhibitor which has been found to have abilities against tumor growth, angiogenesis and inflammation.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	17-44
23165864-8	2013	Genetic factors including single nucleotide polymorphisms (SNPs) that change cytochrome P450 (CYP) activity and epigenetic regulation that modifies CYP expression levels may contribute to the changes in pharmacokinetics and adverse drug reactions (ADRs) of thalidomide.	Thalidomide	257-268	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	94-97
23165864-8	2013	Genetic factors including single nucleotide polymorphisms (SNPs) that change cytochrome P450 (CYP) activity and epigenetic regulation that modifies CYP expression levels may contribute to the changes in pharmacokinetics and adverse drug reactions (ADRs) of thalidomide.	Thalidomide	257-268	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	148-151
23233155-1	2013	The CTD (cyclophosphamide, thalidomide, and dexamethasone) regimen is known to be an effective primary therapy in patients with newly diagnosed multiple myeloma (MM).	Thalidomide	27-38	CTD	Homo sapiens	4-7
23405115-1	2013	Thalidomide is a tumor necrosis factor alpha (TNFalpha) inhibitor which has been found to have abilities against tumor growth, angiogenesis and inflammation.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	46-54
23405115-9	2013	We found that, in addition of dramatic decrease in the activation of both astrocytes and microglia, thalidomide significantly reduces Abeta load and plaque formation.	Thalidomide	100-111	amyloid beta (A4) precursor protein	Mus musculus	134-139
23405115-10	2013	Furthermore, we found a significant decrease in BACE1 level and activity with long-term thalidomide application.	Thalidomide	88-99	beta-site APP cleaving enzyme 1	Mus musculus	48-53
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	123-156
22923758-2	2012	Moreover, thalidomide modulates the activity of NF-kappaB, which can up-regulate the expression of downstream genes involved in the pathophysiology of LN.	Thalidomide	10-21	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	48-57
22923758-9	2012	Also, treatment with 10 mg/kg of thalidomide significantly decreased immune complex accumulation, reduced the serum concentration of anti-dsDNA, IgG2a and IgG2b and inhibited nuclear translocation of NF-kappaB in kidney tissues, comparable to standard therapy for LN.	Thalidomide	33-44	immunoglobulin heavy variable V1-9	Mus musculus	145-150
22923758-9	2012	Also, treatment with 10 mg/kg of thalidomide significantly decreased immune complex accumulation, reduced the serum concentration of anti-dsDNA, IgG2a and IgG2b and inhibited nuclear translocation of NF-kappaB in kidney tissues, comparable to standard therapy for LN.	Thalidomide	33-44	immunoglobulin heavy constant gamma 2B	Mus musculus	155-160
22923758-9	2012	Also, treatment with 10 mg/kg of thalidomide significantly decreased immune complex accumulation, reduced the serum concentration of anti-dsDNA, IgG2a and IgG2b and inhibited nuclear translocation of NF-kappaB in kidney tissues, comparable to standard therapy for LN.	Thalidomide	33-44	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	200-209
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interleukin 1 beta	Mus musculus	158-180
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interleukin 6	Mus musculus	182-186
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interleukin 17A	Mus musculus	195-200
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interferon gamma	Mus musculus	205-227
22901832-9	2012	Thalidomide treatment also significantly decreased plasma levels of nitric oxide and pancreatic proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-12, IL-17 and interferon (IFN)-gamma)] while increased anti-inflammatory cytokine IL-10.	Thalidomide	0-11	interleukin 10	Mus musculus	273-278
22855579-0	2012	Thalidomide in total therapy 2 overcomes inferior prognosis of myeloma with low expression of the glucocorticoid receptor gene NR3C1.	Thalidomide	0-11	nuclear receptor subfamily 3 group C member 1	Homo sapiens	98-121
22552008-2	2012	The ubiquitously expressed E3 ligase protein cereblon (CRBN) has been identified as the primary teratogenic target of thalidomide.	Thalidomide	118-129	cereblon	Homo sapiens	45-53
22552008-2	2012	The ubiquitously expressed E3 ligase protein cereblon (CRBN) has been identified as the primary teratogenic target of thalidomide.	Thalidomide	118-129	cereblon	Homo sapiens	55-59
22552008-3	2012	Our studies demonstrate that thalidomide, lenalidomide and another immunomodulatory drug, pomalidomide, bound endogenous CRBN and recombinant CRBN-DNA damage binding protein-1 (DDB1) complexes.	Thalidomide	29-40	cereblon	Homo sapiens	121-125
22552008-3	2012	Our studies demonstrate that thalidomide, lenalidomide and another immunomodulatory drug, pomalidomide, bound endogenous CRBN and recombinant CRBN-DNA damage binding protein-1 (DDB1) complexes.	Thalidomide	29-40	damage specific DNA binding protein 1	Homo sapiens	142-175
22552008-3	2012	Our studies demonstrate that thalidomide, lenalidomide and another immunomodulatory drug, pomalidomide, bound endogenous CRBN and recombinant CRBN-DNA damage binding protein-1 (DDB1) complexes.	Thalidomide	29-40	damage specific DNA binding protein 1	Homo sapiens	177-181
22552008-5	2012	Lenalidomide and pomalidomide inhibited autoubiquitination of CRBN in HEK293T cells expressing thalidomide-binding competent wild-type CRBN, but not thalidomide-binding defective CRBN(YW/AA).	Thalidomide	95-106	cereblon	Homo sapiens	62-66
23076705-0	2012	Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study.	Thalidomide	106-117	HCC	Homo sapiens	50-53
23076705-0	2012	Unexpected remission of hepatocellular carcinoma (HCC) with lung metastasis to the combination therapy of thalidomide and cyproheptadine: report of two cases and a preliminary HCC cell line study.	Thalidomide	106-117	HCC	Homo sapiens	176-179
23076705-1	2012	We reported two cases of hepatocellular carcinoma (HCC) with lung metastases who were treated with a combination of thalidomide and cyproheptadine.	Thalidomide	116-127	HCC	Homo sapiens	51-54
22705333-10	2012	Likewise, the expression of FGF-1 showed weaker cytoplasmic positivity in the group treated with thalidomide compared with the control group.	Thalidomide	97-108	fibroblast growth factor 1	Mus musculus	28-33
22705333-11	2012	The levels of two cytokines, VEGF (pro-angiogenic) and TNF-alpha (pro-inflammatory) were decreased in tumor samples of thalidomide-treated group compared with the control group.	Thalidomide	119-130	vascular endothelial growth factor A	Mus musculus	29-33
22705333-11	2012	The levels of two cytokines, VEGF (pro-angiogenic) and TNF-alpha (pro-inflammatory) were decreased in tumor samples of thalidomide-treated group compared with the control group.	Thalidomide	119-130	tumor necrosis factor	Mus musculus	55-64
22855579-0	2012	Thalidomide in total therapy 2 overcomes inferior prognosis of myeloma with low expression of the glucocorticoid receptor gene NR3C1.	Thalidomide	0-11	nuclear receptor subfamily 3 group C member 1	Homo sapiens	127-132
22855579-3	2012	RESULTS: Low NR3C1 expression levels had a negative impact on progression-free survival (PFS; HR, 1.47; P = 0.030) and overall survival (OS; HR, 1.90; P = 0.002) in the no-thalidomide arm.	Thalidomide	172-183	nuclear receptor subfamily 3 group C member 1	Homo sapiens	13-18
22855579-4	2012	Conversely, there was a significant clinical benefit of thalidomide for patients with low receptor levels (OS: HR, 0.54; P = 0.015; PFS: HR, 0.54; P = 0.004), mediated most likely by thalidomide"s upregulation of NR3C1.	Thalidomide	56-67	nuclear receptor subfamily 3 group C member 1	Homo sapiens	213-218
22855579-7	2012	The identification of an interaction term between thalidomide and NR3C1 underscores the importance of pharmacogenomic studies in the systematic study of new drugs.	Thalidomide	50-61	nuclear receptor subfamily 3 group C member 1	Homo sapiens	66-71
22843924-9	2012	Net reduced levels of vascular endothelial growth factor and basic fibroblast growth factor cytokines were observed in the peripheral blood and the bone marrow of thalidomide-treated patients.	Thalidomide	163-174	vascular endothelial growth factor A	Homo sapiens	22-56
22880820-9	2012	Tumor necrosis factor (TNF)-alpha (p=0.04) and its receptors TNFR1 (p=0.04), TNFR2 (p=0.04), and interleukin (IL)-8 (p=0.04) were statistically significant in the thalidomide group.	Thalidomide	163-174	tumor necrosis factor	Homo sapiens	0-33
22880820-9	2012	Tumor necrosis factor (TNF)-alpha (p=0.04) and its receptors TNFR1 (p=0.04), TNFR2 (p=0.04), and interleukin (IL)-8 (p=0.04) were statistically significant in the thalidomide group.	Thalidomide	163-174	TNF receptor superfamily member 1A	Homo sapiens	61-66
22139971-0	2012	Vascular endothelial growth factor (VEGF) gene polymorphisms may influence the efficacy of thalidomide in multiple myeloma.	Thalidomide	91-102	vascular endothelial growth factor A	Homo sapiens	0-34
22139971-0	2012	Vascular endothelial growth factor (VEGF) gene polymorphisms may influence the efficacy of thalidomide in multiple myeloma.	Thalidomide	91-102	vascular endothelial growth factor A	Homo sapiens	36-40
22139971-4	2012	In this study, we evaluated the association between genetic variations in the VEGF gene in patients with multiple myeloma and time to treatment failure (TTF) after high-dose melphalan and stem cell support (HDT), overall survival (OS) and efficacy of the anti-angiogenic drug thalidomide.	Thalidomide	276-287	vascular endothelial growth factor A	Homo sapiens	78-82
22139971-9	2012	In conclusion, the haplotype ACG in the VEGF gene may influence the efficacy of thalidomide in multiple myeloma.	Thalidomide	80-91	vascular endothelial growth factor A	Homo sapiens	40-44
22329352-5	2012	Consolidation thalidomide conferred an improved PFS in patients with normal FGFR3 expression (41 vs. 19 months, p =0.02), but there was no improvement in patients with up-regulated FGFR3 (31 vs. 29 months, p =0.76).	Thalidomide	14-25	fibroblast growth factor receptor 3	Homo sapiens	76-81
23094815-4	2012	Greater success was achieved with thalidomide regimen (CTD: cyclophosphamide, thalidomide, dexamethasone, 10 cycles, 3/2009-1/2010) leading to reduction in the size of the hypervascularized lymph nodes (almost by 50%) as well as their radiopharmaceutical (fluorodeoxyglucose) uptake as seen on a combined positron emission tomography and computed tomography (PET/CT) scan imaging.	Thalidomide	34-45	CTD	Homo sapiens	55-58
23094815-4	2012	Greater success was achieved with thalidomide regimen (CTD: cyclophosphamide, thalidomide, dexamethasone, 10 cycles, 3/2009-1/2010) leading to reduction in the size of the hypervascularized lymph nodes (almost by 50%) as well as their radiopharmaceutical (fluorodeoxyglucose) uptake as seen on a combined positron emission tomography and computed tomography (PET/CT) scan imaging.	Thalidomide	78-89	CTD	Homo sapiens	55-58
22422151-0	2012	Oncogenic CUL4A determines the response to thalidomide treatment in prostate cancer.	Thalidomide	43-54	cullin 4A	Homo sapiens	10-15
22422151-2	2012	Here we demonstrate that CUL4A plays an oncogenic role in prostate cancer development and prostate cancer cells with higher level of CUL4A are particularly sensitive to thalidomide treatment.	Thalidomide	169-180	cullin 4A	Homo sapiens	25-30
22422151-2	2012	Here we demonstrate that CUL4A plays an oncogenic role in prostate cancer development and prostate cancer cells with higher level of CUL4A are particularly sensitive to thalidomide treatment.	Thalidomide	169-180	cullin 4A	Homo sapiens	133-138
22422151-6	2012	We further show that the sensitivity to thalidomide is positively correlated with CUL4A expression in a panel of prostate cell lines.	Thalidomide	40-51	cullin 4A	Homo sapiens	82-87
22422151-7	2012	Ectopic CUL4A expression greatly enhanced sensitivity to thalidomide, while its downregulation conferred resistance to this drug.	Thalidomide	57-68	cullin 4A	Homo sapiens	8-13
22422151-8	2012	Mechanistically, thalidomide decreased CUL4A in a time- and dose-dependent manner, consequently leading to inaction of ERK pathway.	Thalidomide	17-28	cullin 4A	Homo sapiens	39-44
22422151-8	2012	Mechanistically, thalidomide decreased CUL4A in a time- and dose-dependent manner, consequently leading to inaction of ERK pathway.	Thalidomide	17-28	mitogen-activated protein kinase 1	Homo sapiens	119-122
22422151-10	2012	Our results offer the first evidence that CUL4A is a potential therapeutic target for prostate cancer and may serve as a biomarker for assessing prognosis of human prostate cancer and response to thalidomide treatment.	Thalidomide	196-207	cullin 4A	Homo sapiens	42-47
22731394-4	2012	In this study, we investigated the effects of a novel thalidomide-based TNF-alpha lowering drug, 3,6"-dithiothalidomide, on hippocampal progenitor cell proliferation, neurogenesis and, memory tasks after intracerebroventricular injection of beta-amyloid (Ass)(1-42) peptide.	Thalidomide	54-65	tumor necrosis factor	Homo sapiens	72-81
22527432-4	2012	RESULTS: IL17A, the hallmark of TH17, was consistently seen before and after thalidomide treatment, confirming the TH17 subset to be involved in ENL and potentially up-regulated by thalidomide.	Thalidomide	181-192	interleukin 17A	Homo sapiens	9-14
22498745-1	2012	In a randomized, phase 3 study, superior complete/near-complete response (CR/nCR) rates and extended progression-free survival were demonstrated with bortezomib-thalidomide-dexamethasone (VTD) versus thalidomide-dexamethasone (TD) as induction therapy before, and consolidation after, double autologous stem cell transplantation for newly diagnosed myeloma patients (intention-to-treat analysis; VTD, n = 236; TD, n = 238).	Thalidomide	161-172	Neutrophil migration (granulocyte glycoprotein)	Homo sapiens	77-80
22770990-0	2012	Novel thalidomide analogues from diamines inhibit pro-inflammatory cytokine production and CD80 expression while enhancing IL-10.	Thalidomide	6-17	CD80 molecule	Homo sapiens	91-95
22770990-0	2012	Novel thalidomide analogues from diamines inhibit pro-inflammatory cytokine production and CD80 expression while enhancing IL-10.	Thalidomide	6-17	interleukin 10	Homo sapiens	123-128
22488443-5	2012	Given the high serum and plasma levels of VEGF observed in POEMS patients, the use of anti-angiogenetic drugs such as thalidomide and lenalidomide and other drugs with anti-VEGF and anti-TNF effect such as bortezomib have been considered to treat this syndrome.	Thalidomide	118-129	vascular endothelial growth factor A	Homo sapiens	42-46
22488443-5	2012	Given the high serum and plasma levels of VEGF observed in POEMS patients, the use of anti-angiogenetic drugs such as thalidomide and lenalidomide and other drugs with anti-VEGF and anti-TNF effect such as bortezomib have been considered to treat this syndrome.	Thalidomide	118-129	vascular endothelial growth factor A	Homo sapiens	173-177
22488443-5	2012	Given the high serum and plasma levels of VEGF observed in POEMS patients, the use of anti-angiogenetic drugs such as thalidomide and lenalidomide and other drugs with anti-VEGF and anti-TNF effect such as bortezomib have been considered to treat this syndrome.	Thalidomide	118-129	tumor necrosis factor	Homo sapiens	187-190
22098296-14	2012	Thalidomide suppressed bFGF-induced proliferation significantly and decreased VEGF expression, both at the protein and mRNA levels.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	23-27
22098296-14	2012	Thalidomide suppressed bFGF-induced proliferation significantly and decreased VEGF expression, both at the protein and mRNA levels.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	78-82
22098296-15	2012	Thalidomide also inhibited HIF-1alpha in a dose-dependent manner (P &lt; 0.05).	Thalidomide	0-11	hypoxia inducible factor 1 subunit alpha	Homo sapiens	27-37
22098296-17	2012	Thalidomide can suppress VEGF, either induced by HIF-1alpha or bFGF.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	25-29
22098296-17	2012	Thalidomide can suppress VEGF, either induced by HIF-1alpha or bFGF.	Thalidomide	0-11	hypoxia inducible factor 1 subunit alpha	Homo sapiens	49-59
22098296-17	2012	Thalidomide can suppress VEGF, either induced by HIF-1alpha or bFGF.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	63-67
22855035-6	2012	RESULTS: The VEGF expressions in brucine- or thalidomide-treated mice were significantly reduced as compared with mice in the model group (P &lt;0.01).	Thalidomide	45-56	vascular endothelial growth factor A	Mus musculus	13-17
22855035-9	2012	Further, VEGF expression was significantly increased in the low- and medium-dose brucine groups compared with the thalidomide group (P &lt;0.05).	Thalidomide	114-125	vascular endothelial growth factor A	Mus musculus	9-13
21833519-0	2012	Clinical response to thalidomide and colchicine in two siblings with Behcet"s disease carrying a single mutated MEFV allele.	Thalidomide	21-32	MEFV innate immuity regulator, pyrin	Homo sapiens	112-116
22237514-8	2012	We discovered that the mechanism for thalidomide inhibiting adipogenesis was the down-regulation of PPARgamma, rather than C/EBPbeta and C/EBPdelta.	Thalidomide	37-48	peroxisome proliferator activated receptor gamma	Homo sapiens	100-109
22249337-15	2012	The combination of thalidomide (TNF-alpha inhibitor) and dipyrone (COX inhibitor) may be used as a potential therapeutic agent for the treatment of diabetic neuropathy.	Thalidomide	19-30	tumor necrosis factor	Rattus norvegicus	32-41
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	85-96	angiopoietin 2	Homo sapiens	159-163
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	85-96	notch receptor 1	Homo sapiens	165-171
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	85-96	delta like canonical Notch ligand 4	Homo sapiens	176-180
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	221-232	angiopoietin 2	Homo sapiens	159-163
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	221-232	notch receptor 1	Homo sapiens	165-171
22883339-8	2012	CONCLUSION: Ang2, Notch1 and Dll4 may correlate with the pathogenesis of GIVM, while thalidomide can concentration-dependently down-regulate the expression of Ang2, Notch1 and Dll4, which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.	Thalidomide	221-232	delta like canonical Notch ligand 4	Homo sapiens	176-180
22425187-0	2012	The thalidomide analgesic effect is associated with differential TNF-alpha receptor expression in the dorsal horn of the spinal cord as studied in a rat model of neuropathic pain.	Thalidomide	4-15	tumor necrosis factor	Rattus norvegicus	65-74
22826791-2	2012	The common expression of vascular endothelial growth factor (VEGF) and its receptor in HEH provide a rationale for the reported use of antiangiogenic drugs, including bevacizumab, lenalidomide and thalidomide.	Thalidomide	197-208	vascular endothelial growth factor A	Homo sapiens	25-59
22826791-2	2012	The common expression of vascular endothelial growth factor (VEGF) and its receptor in HEH provide a rationale for the reported use of antiangiogenic drugs, including bevacizumab, lenalidomide and thalidomide.	Thalidomide	197-208	vascular endothelial growth factor A	Homo sapiens	61-65
22277195-3	2012	Our study was aimed to evaluate the therapeutic potential of a novel analog of thalidomide, 3,6"-dithiothalidomide (DT), an agent with anti-TNF-alpha activity, in a model of chronic neuroinflammation.	Thalidomide	79-90	tumor necrosis factor	Homo sapiens	140-149
22179948-12	2012	Administration of thalidomide (25 and 50 mg/kg, i.p), a TNF-alpha inhibitor, significantly prevented hyperglycemia-induced thermal hyperalgesia and mechanical allodynia and also attenuated the increase in serum and urinary nitrite concentration, as compared with untreated diabetic rats.	Thalidomide	18-29	tumor necrosis factor	Rattus norvegicus	56-65
22179948-14	2012	CONCLUSION: It may be concluded that thalidomide has a beneficial effect in neuropathic pain by decreasing cytokines (TNF-alpha) and nitric oxide level and may provide a novel promising therapeutic approach for managing painful diabetic neuropathy.	Thalidomide	37-48	tumor necrosis factor	Rattus norvegicus	118-127
22741020-7	2012	Treatment with thalidomide resulted in apoptosis of mouse breast cancer cells in a time- and dose-dependent manner as demonstrated by caspase-3 enzyme activity.	Thalidomide	15-26	caspase 3	Mus musculus	134-143
21757252-0	2012	The predictive role of serum VEGF in an advanced malignant mesothelioma patient cohort treated with thalidomide alone or combined with cisplatin/gemcitabine.	Thalidomide	100-111	vascular endothelial growth factor A	Homo sapiens	29-33
22348778-10	2012	This suggests that thalidomide downregulates fibroblast growth factor 8 expression and induces limb malformation by binding to wild-type cereblon, inhibiting the function of the associated E3 ubiquitin ligase.	Thalidomide	19-30	fibroblast growth factor 8	Homo sapiens	45-71
22348778-10	2012	This suggests that thalidomide downregulates fibroblast growth factor 8 expression and induces limb malformation by binding to wild-type cereblon, inhibiting the function of the associated E3 ubiquitin ligase.	Thalidomide	19-30	Cbl proto-oncogene like 2	Homo sapiens	189-208
21638302-0	2012	Metabolism of thalidomide by human liver microsome cytochrome CYP2C19 is required for its antimyeloma and antiangiogenic activities in vitro.	Thalidomide	14-25	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	62-69
21638302-7	2012	These effects were partially reversed by omeprazole (10 micromol/l), a potent inhibitor of CYP2C19, suggesting that CYP2C19 is required for thalidomide to exhibit its antimyeloma and antiangiogenic activities.	Thalidomide	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	91-98
21638302-7	2012	These effects were partially reversed by omeprazole (10 micromol/l), a potent inhibitor of CYP2C19, suggesting that CYP2C19 is required for thalidomide to exhibit its antimyeloma and antiangiogenic activities.	Thalidomide	140-151	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	116-123
22346253-15	2012	CONCLUSION: Thalidomide was found to be safe for advanced HCC patients, demonstrating anti-tumor activity including response, survival, and AFP decreases of greater than 50% from baseline.	Thalidomide	12-23	alpha fetoprotein	Homo sapiens	140-143
21883476-4	2012	In thalidomide- and bortezomid-based therapy, candidate genes include TNFA and genes involved in the nuclear factor kappa B pathway (NFKB2 and TRAF3), respectively.	Thalidomide	3-14	tumor necrosis factor	Homo sapiens	70-74
21883476-4	2012	In thalidomide- and bortezomid-based therapy, candidate genes include TNFA and genes involved in the nuclear factor kappa B pathway (NFKB2 and TRAF3), respectively.	Thalidomide	3-14	nuclear factor kappa B subunit 2	Homo sapiens	133-138
21883476-4	2012	In thalidomide- and bortezomid-based therapy, candidate genes include TNFA and genes involved in the nuclear factor kappa B pathway (NFKB2 and TRAF3), respectively.	Thalidomide	3-14	TNF receptor associated factor 3	Homo sapiens	143-148
22239529-5	2012	Results revealed that while thalidomide reduced IL-8 and nuclear factor kappa B (NF-kappaB) activity by 95% and 46% in Huh-7 cells, increasing concentrations of thalidomide correlated with a linear rise in HCV replication (17-fold at 200 mum).	Thalidomide	28-39	C-X-C motif chemokine ligand 8	Homo sapiens	48-52
22239529-5	2012	Results revealed that while thalidomide reduced IL-8 and nuclear factor kappa B (NF-kappaB) activity by 95% and 46% in Huh-7 cells, increasing concentrations of thalidomide correlated with a linear rise in HCV replication (17-fold at 200 mum).	Thalidomide	28-39	nuclear factor kappa B subunit 1	Homo sapiens	57-79
22239529-5	2012	Results revealed that while thalidomide reduced IL-8 and nuclear factor kappa B (NF-kappaB) activity by 95% and 46% in Huh-7 cells, increasing concentrations of thalidomide correlated with a linear rise in HCV replication (17-fold at 200 mum).	Thalidomide	28-39	nuclear factor kappa B subunit 1	Homo sapiens	81-90
22239529-6	2012	The NF-kappaB inhibitors, wedelolactone and NF-kappaB activation inhibitor-1, which mimic the actions of thalidomide by preventing phosphorylation and activation of IkappaB kinase (IKK) and hence block NF-kappaB activity, increased HCV RNA by 18- and 19-fold, respectively.	Thalidomide	105-116	nuclear factor kappa B subunit 1	Homo sapiens	4-13
22239529-6	2012	The NF-kappaB inhibitors, wedelolactone and NF-kappaB activation inhibitor-1, which mimic the actions of thalidomide by preventing phosphorylation and activation of IkappaB kinase (IKK) and hence block NF-kappaB activity, increased HCV RNA by 18- and 19-fold, respectively.	Thalidomide	105-116	nuclear factor kappa B subunit 1	Homo sapiens	44-53
22239529-6	2012	The NF-kappaB inhibitors, wedelolactone and NF-kappaB activation inhibitor-1, which mimic the actions of thalidomide by preventing phosphorylation and activation of IkappaB kinase (IKK) and hence block NF-kappaB activity, increased HCV RNA by 18- and 19-fold, respectively.	Thalidomide	105-116	nuclear factor kappa B subunit 1	Homo sapiens	44-53
22463096-8	2012	Thalidomide therapy (100 mg/day) provided reduction in the median D-dimer levels to 6.07 (4.71-10.21) mug/ml and increase in median fibrinogen concentration to 1.9 g/L; soluble fibrin monomers were unidentifiable.	Thalidomide	0-11	fibrinogen beta chain	Homo sapiens	132-142
22382316-0	2012	Influence of cytochrome P450 2C19 gene variations on pharmacokinetic parameters of thalidomide in Japanese patients.	Thalidomide	83-94	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	13-33
21685944-6	2012	While the anti-angiogenic drug thalidomide inhibits HIF-1-dependent VEGF transcription in breast carcinoma cells, it does not prevent HIF-1alpha stabilization, but leads to aberrant localization of HIF-1alpha to the perinuclear compartments and surprisingly stimulates nuclear export of beta-arrestin1.	Thalidomide	31-42	hypoxia inducible factor 1 subunit alpha	Homo sapiens	52-57
21685944-6	2012	While the anti-angiogenic drug thalidomide inhibits HIF-1-dependent VEGF transcription in breast carcinoma cells, it does not prevent HIF-1alpha stabilization, but leads to aberrant localization of HIF-1alpha to the perinuclear compartments and surprisingly stimulates nuclear export of beta-arrestin1.	Thalidomide	31-42	vascular endothelial growth factor A	Homo sapiens	68-72
21685944-6	2012	While the anti-angiogenic drug thalidomide inhibits HIF-1-dependent VEGF transcription in breast carcinoma cells, it does not prevent HIF-1alpha stabilization, but leads to aberrant localization of HIF-1alpha to the perinuclear compartments and surprisingly stimulates nuclear export of beta-arrestin1.	Thalidomide	31-42	hypoxia inducible factor 1 subunit alpha	Homo sapiens	198-208
21685944-6	2012	While the anti-angiogenic drug thalidomide inhibits HIF-1-dependent VEGF transcription in breast carcinoma cells, it does not prevent HIF-1alpha stabilization, but leads to aberrant localization of HIF-1alpha to the perinuclear compartments and surprisingly stimulates nuclear export of beta-arrestin1.	Thalidomide	31-42	arrestin beta 1	Homo sapiens	287-301
22382316-3	2012	MATERIALS AND METHODS: Variations in the CYP2C19 gene in 6 patients treated with thalidomide were analyzed.	Thalidomide	81-92	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	41-48
22382316-6	2012	RESULTS: The frequencies of CYP2C19 PM and hetero EM (hetEM) genotypes in Japanese patients taking thalidomide were 2 (33.3%) and 4 (66.7%), respectively.	Thalidomide	99-110	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-35
22382316-8	2012	CONCLUSIONS: This study provided new insights regarding the contribution of CYP2C19 gene variations to adverse responses to thalidomide.	Thalidomide	124-135	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	76-83
22382316-9	2012	Genotyping of CYP2C19*2 and *3 can be considerably simplified by using KOD FX as a polymerase for prediction of adverse effects to thalidomide by the PCR-RFLP method.	Thalidomide	131-142	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	14-21
22382316-10	2012	CYP2C19 PM patients tend to have high serum thalidomide concentrations.	Thalidomide	44-55	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
21681114-14	2012	CONCLUSIONS: Thalidomide is a potentially effective rescue therapy for severe refractory CD in children who fail to respond to anti-TNF medications.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	132-135
21733935-4	2012	In this in vitro study, MM by itself alters the profibrinolytic potential of ECs decreasing the tissue plasminogen activator (t-PA) and increasing the plasminogen activator inhibitor 1 (PAI-1) levels which is potentiated by thalidomide.	Thalidomide	224-235	serpin family E member 1	Homo sapiens	151-184
21733935-6	2012	Additionally, DF upregulated the t-PA and downregulated PAI-1 gene expression modulated by thalidomide.	Thalidomide	91-102	serpin family E member 1	Homo sapiens	56-61
22650376-7	2012	In particular, thalidomide was reevaluated and attracted significant attention due to its selective inhibitory activity of tumor necrosis factor-alpha (TNF-alpha), which is a clinically important activity against serious diseases such as rheumatoid arthritis, Crohn"s disease, leprosy, AIDS, and various cancers.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	123-150
22650376-7	2012	In particular, thalidomide was reevaluated and attracted significant attention due to its selective inhibitory activity of tumor necrosis factor-alpha (TNF-alpha), which is a clinically important activity against serious diseases such as rheumatoid arthritis, Crohn"s disease, leprosy, AIDS, and various cancers.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	152-161
22650377-0	2012	TNF alpha signaling beholds thalidomide saga: a review of mechanistic role of TNF-alpha signaling under thalidomide.	Thalidomide	28-39	tumor necrosis factor	Homo sapiens	0-9
22650377-0	2012	TNF alpha signaling beholds thalidomide saga: a review of mechanistic role of TNF-alpha signaling under thalidomide.	Thalidomide	28-39	tumor necrosis factor	Homo sapiens	78-87
22650377-0	2012	TNF alpha signaling beholds thalidomide saga: a review of mechanistic role of TNF-alpha signaling under thalidomide.	Thalidomide	104-115	tumor necrosis factor	Homo sapiens	0-9
22650377-0	2012	TNF alpha signaling beholds thalidomide saga: a review of mechanistic role of TNF-alpha signaling under thalidomide.	Thalidomide	104-115	tumor necrosis factor	Homo sapiens	78-87
22650377-4	2012	Thalidomide, an inhibitor of TNF-alpha protein synthesis is readily capable of crossing the blood-brain barrier and thus thalidomide and its analogs are excellent candidates for use in determining the potential value of anti-TNF-alpha therapies in a variety of diseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	29-38
22650377-4	2012	Thalidomide, an inhibitor of TNF-alpha protein synthesis is readily capable of crossing the blood-brain barrier and thus thalidomide and its analogs are excellent candidates for use in determining the potential value of anti-TNF-alpha therapies in a variety of diseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	225-234
22650377-5	2012	Thalidomide blocks TNF-alpha expression by different possible mechanisms.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	19-28
22650377-6	2012	Down regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), an essential transcription factor for TNF and other cytokines under thalidomide treatment leads to reduction in the TNF-alpha expression.	Thalidomide	159-170	tumor necrosis factor	Homo sapiens	129-132
22650377-6	2012	Down regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), an essential transcription factor for TNF and other cytokines under thalidomide treatment leads to reduction in the TNF-alpha expression.	Thalidomide	159-170	tumor necrosis factor	Homo sapiens	207-216
22650377-7	2012	Additionally, myeloid differentiation factor 88 (MyD88), an adapter protein regulates the expression of TNF under thalidomide treatment.	Thalidomide	114-125	MYD88 innate immune signal transduction adaptor	Homo sapiens	14-47
22650377-7	2012	Additionally, myeloid differentiation factor 88 (MyD88), an adapter protein regulates the expression of TNF under thalidomide treatment.	Thalidomide	114-125	MYD88 innate immune signal transduction adaptor	Homo sapiens	49-54
22650377-7	2012	Additionally, myeloid differentiation factor 88 (MyD88), an adapter protein regulates the expression of TNF under thalidomide treatment.	Thalidomide	114-125	tumor necrosis factor	Homo sapiens	104-107
22650377-8	2012	Thalidomide treatment also leads to destruction of TNF-alpha mRNA thus, reducing the total expression of TNF-alpha protein.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	51-60
22650377-8	2012	Thalidomide treatment also leads to destruction of TNF-alpha mRNA thus, reducing the total expression of TNF-alpha protein.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	105-114
22650377-9	2012	Thalidomide also targets reactive oxygen species (ROS) and alpha(1)-acid glycoprotein (AGP) to regulate TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	104-113
22650377-10	2012	In the present review, we discuss different possible mechanism that regulates TNF-alpha under thalidomide treatment.	Thalidomide	94-105	tumor necrosis factor	Homo sapiens	78-87
22650377-11	2012	Additionally, we suggest novel strategies for the future targeting combination therapies of thalidomide and its analogs with different other anti-inflammatory drug to curb TNF-alpha associated diseases.	Thalidomide	92-103	tumor necrosis factor	Homo sapiens	172-181
22949932-13	2012	This coincides with the clinical evidence of a response to thalidomide in patients with osteolytic LCH, given its reported ability to reduce TGF-beta 1 and FoxP3 cells.	Thalidomide	59-70	transforming growth factor beta 1	Homo sapiens	141-151
22949932-13	2012	This coincides with the clinical evidence of a response to thalidomide in patients with osteolytic LCH, given its reported ability to reduce TGF-beta 1 and FoxP3 cells.	Thalidomide	59-70	forkhead box P3	Homo sapiens	156-161
21876693-4	2012	Research on angiogenesis in general, and vascular endothelial growth factor in particular, is a major focus in biomedicine and has led to the clinical approval of several antiangiogenic agents including thalidomide, bevacizumab, sorafenib, sunitinib, pazopanib, temesirolimus, and everolimus.	Thalidomide	203-214	vascular endothelial growth factor A	Homo sapiens	41-75
22571700-2	2012	For a long period of time, the standard therapy for MDS was hematopoietic stem cell transplantation, however DNA methyltransferase inhibitors (DNMT inhibitors) including decitabine (DAC) and azacitidine (AZA), and lenalidomide, a derivative of thalidomide have been highlighted as new chemotherapeutic agents for MDS.	Thalidomide	244-255	DNA methyltransferase 1	Homo sapiens	143-147
21860026-2	2011	We investigated the role of cereblon (CRBN), a primary teratogenic target of thalidomide, in the antimyeloma activity of IMiDs.	Thalidomide	77-88	cereblon	Homo sapiens	28-36
20800319-4	2011	Because of severe side effects or high costs, other agents, such as thalidomide or high-dose intravenous immunoglobulins, are reserved for severe recalcitrant CLE.	Thalidomide	68-79	RNA transcription, translation and transport factor	Homo sapiens	159-162
22333255-8	2011	However, in the thalidomide group, PFS and OS were extended only in MM of immunoglobulin G (IgG) and immunoglobulin A (IgA) but not in light-chain patients.	Thalidomide	16-27	CD79a molecule	Homo sapiens	101-117
22333255-8	2011	However, in the thalidomide group, PFS and OS were extended only in MM of immunoglobulin G (IgG) and immunoglobulin A (IgA) but not in light-chain patients.	Thalidomide	16-27	CD79a molecule	Homo sapiens	119-122
21465313-2	2011	Thalidomide is an anti-angiogenic agent with anti-TNF-alpha and anti-NF-kappaB activity.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	50-59
21465313-2	2011	Thalidomide is an anti-angiogenic agent with anti-TNF-alpha and anti-NF-kappaB activity.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	69-78
21465313-12	2011	Thalidomide treatment was associated with significant down-regulation of nuclear NF-kappaB expression levels in residual neoplastic cells and microenvironments of responsive tumors, but not in t(11;18)(q21;q21)-positive, thalidomide-refractory tumors.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	81-90
21860026-2	2011	We investigated the role of cereblon (CRBN), a primary teratogenic target of thalidomide, in the antimyeloma activity of IMiDs.	Thalidomide	77-88	cereblon	Homo sapiens	38-42
22011961-5	2011	The aim of this study was to evaluate the ability of pentoxifylline, forskolin, rolipram, and thalidomide to decrease in vitro production of TNF-alpha and IFN-gamma in cells of HTLV-1-infected subjects.	Thalidomide	94-105	tumor necrosis factor	Homo sapiens	141-150
22011961-5	2011	The aim of this study was to evaluate the ability of pentoxifylline, forskolin, rolipram, and thalidomide to decrease in vitro production of TNF-alpha and IFN-gamma in cells of HTLV-1-infected subjects.	Thalidomide	94-105	interferon gamma	Homo sapiens	155-164
22011961-11	2011	The minimum dose of thalidomide used (1 microM) inhibited TNF-alpha production but thalidomide did not inhibit IFN-gamma production even when the maximum dose (50 microM) was used.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	58-67
22011961-12	2011	All drugs had an in vitro inhibitory effect on TNF-alpha production and, with the exception of thalidomide, all of them also decreased IFN-gamma production.	Thalidomide	95-106	interferon gamma	Homo sapiens	135-144
21955427-10	2011	The reduction degree of Ang-2 after a 4-month treatment of thalidomide may offer values for evaluating its prognosis and efficacy.	Thalidomide	59-70	angiopoietin 2	Homo sapiens	24-29
21784047-8	2011	Plasma levels of vascular endothelial growth factor were measured in the group given thalidomide.	Thalidomide	85-96	vascular endothelial growth factor A	Homo sapiens	17-51
21784047-12	2011	Levels of vascular endothelial growth factor were significantly reduced by thalidomide (P &lt; .001).	Thalidomide	75-86	vascular endothelial growth factor A	Homo sapiens	10-44
21784047-14	2011	Mechanisms of thalidomide activity might involve vascular endothelial growth factor.	Thalidomide	14-25	vascular endothelial growth factor A	Homo sapiens	49-83
21347685-0	2011	Single nucleotide polymorphisms in the promoter region of the IL1B gene influence outcome in multiple myeloma patients treated with high-dose chemotherapy independently of relapse treatment with thalidomide and bortezomib.	Thalidomide	195-206	interleukin 1 beta	Homo sapiens	62-66
21702058-4	2011	A morphometric analysis showed that systemic administration of thalidomide protects neural cells in the ganglion cell layer (GCL) in a dose-dependent manner and significantly decreases the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in GCL and in the inner nuclear layer (INL).	Thalidomide	63-74	germ cell-less 1, spermatogenesis associated	Rattus norvegicus	295-298
21702058-5	2011	ELISA showed that thalidomide significantly suppressed the elevation of TNF-alpha 6 and 24 hr after an NMDA injection.	Thalidomide	18-29	tumor necrosis factor	Rattus norvegicus	72-81
21702058-1	2011	Thalidomide, an inhibitor of tumor necrosis factor-alpha (TNF-alpha) production, has been indicated to be useful for many inflammatory and oncogenic diseases.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	29-56
21702058-1	2011	Thalidomide, an inhibitor of tumor necrosis factor-alpha (TNF-alpha) production, has been indicated to be useful for many inflammatory and oncogenic diseases.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	58-67
21702058-8	2011	Thalidomide suppressed the increased expressions of NF-kappaB p65, p-JNK, and p-p38 after NMDA injection.	Thalidomide	0-11	synaptotagmin 1	Rattus norvegicus	62-65
21702058-4	2011	A morphometric analysis showed that systemic administration of thalidomide protects neural cells in the ganglion cell layer (GCL) in a dose-dependent manner and significantly decreases the number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in GCL and in the inner nuclear layer (INL).	Thalidomide	63-74	germ cell-less 1, spermatogenesis associated	Rattus norvegicus	125-128
21702058-9	2011	Immunohistochemical analysis showed that thalidomide attenuated NF-kappaB p65 immunoreactivity in the GCL induced by NMDA treatment.	Thalidomide	41-52	synaptotagmin 1	Rattus norvegicus	74-77
21702058-9	2011	Immunohistochemical analysis showed that thalidomide attenuated NF-kappaB p65 immunoreactivity in the GCL induced by NMDA treatment.	Thalidomide	41-52	germ cell-less 1, spermatogenesis associated	Rattus norvegicus	102-105
21670663-12	2011	When Thal is given in combination with chemotherapies or Dex, endothelial cell and monocyte PCA may be induced through phosphatidylserine exposure, or TF expression.	Thalidomide	5-9	coagulation factor III, tissue factor	Homo sapiens	151-153
21890654-7	2011	Of note, in our study, combination therapy of bortezomib and thalidomide successfully improved the condition of the patient with polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome associated with multicentric Castleman"s disease, suggesting that the combination therapy may be an effective therapeutic strategy for the intractable polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome associated with multicentric Castleman"s disease.	Thalidomide	61-72	myomesin 2	Homo sapiens	175-184
21890654-7	2011	Of note, in our study, combination therapy of bortezomib and thalidomide successfully improved the condition of the patient with polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome associated with multicentric Castleman"s disease, suggesting that the combination therapy may be an effective therapeutic strategy for the intractable polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes syndrome associated with multicentric Castleman"s disease.	Thalidomide	61-72	myomesin 2	Homo sapiens	408-417
21400110-5	2011	RESULTS: alpha,beta-Amyrin and thalidomide significantly attenuated the cerulein-induced increase in tumor necrosis factor (TNF)-alpha, interleukin-6, lipase, amylase, MPO, and TBARS.	Thalidomide	31-42	tumor necrosis factor	Mus musculus	101-134
21941940-3	2011	Combination therapy showed additive effect of thalidomide which restored lipid peroxidation as well as reduced myeloperoxidase and TNF-a towards the normal levels.	Thalidomide	46-57	myeloperoxidase	Rattus norvegicus	111-126
21941940-3	2011	Combination therapy showed additive effect of thalidomide which restored lipid peroxidation as well as reduced myeloperoxidase and TNF-a towards the normal levels.	Thalidomide	46-57	tumor necrosis factor	Rattus norvegicus	131-136
21435719-4	2011	Finally, polymorphism in GSTT1 (rs4630) was associated with a lower frequency of thalidomide-induced peripheral neuropathy (p=0.04).	Thalidomide	81-92	glutathione S-transferase theta 1	Homo sapiens	25-30
21724449-0	2011	Thalidomide induces apoptosis in human oral squamous cell carcinoma cell line with altered expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Thalidomide	0-11	TNF superfamily member 10	Homo sapiens	105-160
21724449-0	2011	Thalidomide induces apoptosis in human oral squamous cell carcinoma cell line with altered expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Thalidomide	0-11	TNF superfamily member 10	Homo sapiens	162-167
21913886-8	2011	The repression of the tumor necrosis factor-a (TNF-alpha) expression is the crucial factor of many of the anti-inflammatory properties of thalidomide.	Thalidomide	138-149	tumor necrosis factor	Homo sapiens	22-45
21913886-8	2011	The repression of the tumor necrosis factor-a (TNF-alpha) expression is the crucial factor of many of the anti-inflammatory properties of thalidomide.	Thalidomide	138-149	tumor necrosis factor	Homo sapiens	47-56
21511336-0	2011	Effects of thalidomide on long-term bone marrow cultures from patients with myelodysplastic syndromes: induction of IL-10 expression in the stromal layers.	Thalidomide	11-22	interleukin 10	Homo sapiens	116-121
21511336-2	2011	We demonstrated that thalidomide induced an increase in granulocyte-macrophage colony forming unit numbers and in IL-10 expression.	Thalidomide	21-32	interleukin 10	Homo sapiens	114-119
21511336-3	2011	Thalidomide also promoted a slight increase in IL-6, IL-1beta and TNF-alpha expression in the stromal layers.	Thalidomide	0-11	interleukin 6	Homo sapiens	47-51
21511336-3	2011	Thalidomide also promoted a slight increase in IL-6, IL-1beta and TNF-alpha expression in the stromal layers.	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	53-61
21511336-3	2011	Thalidomide also promoted a slight increase in IL-6, IL-1beta and TNF-alpha expression in the stromal layers.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	66-75
21511336-5	2011	Our results indicate a participation of thalidomide upon the hematopoietic microenvironment of patients with myelodysplastic syndromes, especially in the up regulation of IL-10.	Thalidomide	40-51	interleukin 10	Homo sapiens	171-176
21400110-5	2011	RESULTS: alpha,beta-Amyrin and thalidomide significantly attenuated the cerulein-induced increase in tumor necrosis factor (TNF)-alpha, interleukin-6, lipase, amylase, MPO, and TBARS.	Thalidomide	31-42	interleukin 6	Mus musculus	136-149
21400110-5	2011	RESULTS: alpha,beta-Amyrin and thalidomide significantly attenuated the cerulein-induced increase in tumor necrosis factor (TNF)-alpha, interleukin-6, lipase, amylase, MPO, and TBARS.	Thalidomide	31-42	lipase, endothelial	Mus musculus	151-157
21400110-5	2011	RESULTS: alpha,beta-Amyrin and thalidomide significantly attenuated the cerulein-induced increase in tumor necrosis factor (TNF)-alpha, interleukin-6, lipase, amylase, MPO, and TBARS.	Thalidomide	31-42	myeloperoxidase	Mus musculus	168-171
21693319-9	2011	Moreover, thalidomide significantly inhibited the production of VEGF and ICAM-1 in serum (P &lt; .05).	Thalidomide	10-21	vascular endothelial growth factor A	Rattus norvegicus	64-68
21046104-2	2011	Here, we analyse the association between genetic variation in the genes RAI and CD3EAP and outcome of 348 myeloma patients treated with high-dose treatment (HDT), 146 patients treated with interferon-alpha (INF-alpha) as maintenance treatment, 177 patients treated with thalidomide, and 74 patients treated with bortezomib at relapse and address if the effects of polymorphisms in CD3EAP and RAI are modified by a functional polymorphism in NFKB1.	Thalidomide	270-281	growth differentiation factor 1	Homo sapiens	72-75
21693319-9	2011	Moreover, thalidomide significantly inhibited the production of VEGF and ICAM-1 in serum (P &lt; .05).	Thalidomide	10-21	intercellular adhesion molecule 1	Rattus norvegicus	73-79
21514830-0	2011	Peroxisome proliferator-activated receptor agonists with phenethylphenylphthalimide skeleton derived from thalidomide-related liver X receptor antagonists: relationship between absolute configuration and subtype selectivity.	Thalidomide	106-117	peroxisome proliferator activated receptor alpha	Homo sapiens	0-42
21478015-0	2011	Non-competitive and selective dipeptidyl peptidase IV inhibitors with phenethylphenylphthalimide skeleton derived from thalidomide-related alpha-glucosidase inhibitors and liver X receptor antagonists.	Thalidomide	119-130	sucrase-isomaltase	Homo sapiens	139-156
21478015-1	2011	Novel dipeptidyl peptidase IV (DPP-IV) inhibitors with a phenethylphenylphthalimide skeleton were prepared based on alpha-glucosidase inhibitors and liver X receptor (LXR) antagonists derived from thalidomide.	Thalidomide	197-208	dipeptidyl peptidase 4	Homo sapiens	6-29
21478015-1	2011	Novel dipeptidyl peptidase IV (DPP-IV) inhibitors with a phenethylphenylphthalimide skeleton were prepared based on alpha-glucosidase inhibitors and liver X receptor (LXR) antagonists derived from thalidomide.	Thalidomide	197-208	dipeptidyl peptidase 4	Homo sapiens	31-37
21478015-0	2011	Non-competitive and selective dipeptidyl peptidase IV inhibitors with phenethylphenylphthalimide skeleton derived from thalidomide-related alpha-glucosidase inhibitors and liver X receptor antagonists.	Thalidomide	119-130	dipeptidyl peptidase 4	Homo sapiens	30-53
22977536-0	2011	Thalidomide and irradiation combination therapy increases substance P levels in vitro.	Thalidomide	0-11	tachykinin 1	Mus musculus	58-69
21207098-8	2011	We identified a thalidomide-binding protein, cereblon (CRBN), as a primary target for thalidomide teratogenicity.	Thalidomide	16-27	cereblon	Homo sapiens	45-53
21207098-8	2011	We identified a thalidomide-binding protein, cereblon (CRBN), as a primary target for thalidomide teratogenicity.	Thalidomide	16-27	cereblon	Homo sapiens	55-59
21207098-8	2011	We identified a thalidomide-binding protein, cereblon (CRBN), as a primary target for thalidomide teratogenicity.	Thalidomide	86-97	cereblon	Homo sapiens	45-53
21207098-8	2011	We identified a thalidomide-binding protein, cereblon (CRBN), as a primary target for thalidomide teratogenicity.	Thalidomide	86-97	cereblon	Homo sapiens	55-59
21207098-9	2011	Our data suggest that thalidomide initiates its teratogenic effects by binding to CRBN and inhibiting its ubiquitin ligase activity.	Thalidomide	22-33	cereblon	Homo sapiens	82-86
21207214-8	2011	The patient was treated according to the CTD protocol (cyclophosphamide, thalidomide, and dexamethasone) which was effective against the myeloma as well as the systemic sclerosis and patient achieved complete remission.	Thalidomide	73-84	CTD	Homo sapiens	41-44
21539454-8	2011	The expression of vascular endothelial growth factor (VEGF) mRNA and protein was suppressed after treatment with thalidomide alone in a dose-dependent manner.	Thalidomide	113-124	vascular endothelial growth factor A	Homo sapiens	18-52
21539454-8	2011	The expression of vascular endothelial growth factor (VEGF) mRNA and protein was suppressed after treatment with thalidomide alone in a dose-dependent manner.	Thalidomide	113-124	vascular endothelial growth factor A	Homo sapiens	54-58
21539454-9	2011	Synergistic suppressive effects on VEGF expression were observed after administration of thalidomide and X-ray exposure.	Thalidomide	89-100	vascular endothelial growth factor A	Homo sapiens	35-39
21539454-10	2011	In conclusion, thalidomide was able to enhance the radiosensitivity of TE1 cells in vitro, which could be closely related to its suppressive effects on the expression of VEGF in TE1 cells, but had no obvious effects on the cell cycle.	Thalidomide	15-26	vascular endothelial growth factor A	Homo sapiens	170-174
21614166-9	2011	Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-beta-positive cells.	Thalidomide	0-11	proliferating cell nuclear antigen	Mus musculus	117-121
21614166-9	2011	Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-beta-positive cells.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	127-131
21614166-9	2011	Thalidomide treatment significantly ameliorated submesothelial thickening and angiogenesis, and decreased numbers of PCNA- and VEGF-expressing cells, myofibroblasts, and TGF-beta-positive cells.	Thalidomide	0-11	transforming growth factor, beta 1	Mus musculus	170-178
21159364-6	2011	RESULTS: At THL and LEN concentrations resembling those observed in myeloma patients in vivo and in the presence of tumor necrosis factor-alpha (TNFalpha) we observed significantly increased TF activity in human umbilical vein endothelial cells in vitro.	Thalidomide	12-15	coagulation factor III, tissue factor	Homo sapiens	191-193
21159364-10	2011	CONCLUSIONS: Our in vitro data support the hypothesis that THL and LEN induce a hypercoagulable state through increased endothelial TF expression.	Thalidomide	59-62	coagulation factor III, tissue factor	Homo sapiens	132-134
21215621-0	2011	Design, synthesis and biological evaluation of new thalidomide analogues as TNF-alpha and IL-6 production inhibitors.	Thalidomide	51-62	tumor necrosis factor	Homo sapiens	76-85
21215621-0	2011	Design, synthesis and biological evaluation of new thalidomide analogues as TNF-alpha and IL-6 production inhibitors.	Thalidomide	51-62	interleukin 6	Homo sapiens	90-94
21215621-1	2011	Several thalidomide analogues were synthesized and compared to thalidomide and its more active analogue, lenalidomide, for their ability to inhibit the production of the pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 by LPS-activated peripheral blood mononuclear cells (PBMCs).	Thalidomide	8-19	tumor necrosis factor	Homo sapiens	196-230
21215621-1	2011	Several thalidomide analogues were synthesized and compared to thalidomide and its more active analogue, lenalidomide, for their ability to inhibit the production of the pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 by LPS-activated peripheral blood mononuclear cells (PBMCs).	Thalidomide	8-19	interleukin 6	Homo sapiens	235-253
21215621-1	2011	Several thalidomide analogues were synthesized and compared to thalidomide and its more active analogue, lenalidomide, for their ability to inhibit the production of the pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 by LPS-activated peripheral blood mononuclear cells (PBMCs).	Thalidomide	63-74	tumor necrosis factor	Homo sapiens	196-230
21215621-1	2011	Several thalidomide analogues were synthesized and compared to thalidomide and its more active analogue, lenalidomide, for their ability to inhibit the production of the pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 by LPS-activated peripheral blood mononuclear cells (PBMCs).	Thalidomide	63-74	interleukin 6	Homo sapiens	235-253
20846163-4	2010	We reported recently that two substances (ATRA and thalidomide) have preventive effects on pulmonary fibrosis by inhibiting IL-6-dependent proliferation and TGF-beta1-dependent transdifferentiation of lung fibroblasts.	Thalidomide	51-62	interleukin 6	Mus musculus	124-128
21276247-3	2011	In the present study, we examined the effects of prednisone, thalidomide, cyclosporine A, and amitriptyline, drugs used in a variety of clinical conditions, on the production of TNF-alpha, IL-10, and IL-12 by purified epidermal Langerhans cells and peritoneal macrophages in BALB/c mice.	Thalidomide	61-72	tumor necrosis factor	Mus musculus	178-187
22003441-7	2011	Intriguingly, a new role for CRBN has been identified, i.e, the binding of immunomodulatory drugs (IMiDs), e.g. thalidomide, to CRBN has now been associated with teratogenicity and also the cytotoxicity of IMiDs, including lenalidomide, which are widely used to treat multiple myeloma patients.	Thalidomide	112-123	cereblon	Homo sapiens	29-33
22003441-7	2011	Intriguingly, a new role for CRBN has been identified, i.e, the binding of immunomodulatory drugs (IMiDs), e.g. thalidomide, to CRBN has now been associated with teratogenicity and also the cytotoxicity of IMiDs, including lenalidomide, which are widely used to treat multiple myeloma patients.	Thalidomide	112-123	cereblon	Homo sapiens	128-132
21792375-0	2011	Thalidomide Analogues Suppress Lipopolysaccharide-Induced Synthesis of TNF-alpha and Nitrite, an Intermediate of Nitric Oxide, in a Cellular Model of Inflammation.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	71-80
21792375-8	2011	Utilizing a RAW 264.7 cellular model of lipopolysaccharide-induced inflammation that induces high levels of TNF-alpha protein accompanied by a robust generation of nitrite, the properties of a series of thalidomide-based TNF-alpha synthesis inhibitors were evaluated to reduce the levels of both.	Thalidomide	203-214	tumor necrosis factor	Homo sapiens	108-117
21792375-8	2011	Utilizing a RAW 264.7 cellular model of lipopolysaccharide-induced inflammation that induces high levels of TNF-alpha protein accompanied by a robust generation of nitrite, the properties of a series of thalidomide-based TNF-alpha synthesis inhibitors were evaluated to reduce the levels of both.	Thalidomide	203-214	tumor necrosis factor	Homo sapiens	221-230
21792375-9	2011	Specific analogues of thalidomide effectively suppressed the generation of both TNF-alpha and nitrite at well-tolerated doses.	Thalidomide	22-33	tumor necrosis factor	Homo sapiens	80-89
21477797-0	2011	Thalidomide inhibits interferon-gamma-mediated nitric oxide production in mouse vascular endothelial cells.	Thalidomide	0-11	interferon gamma	Mus musculus	21-37
21477797-2	2011	The effect of thalidomide on interferon (IFN)-gamma induced nitric oxide (NO) production in mouse vascular endothelial cells was examined in order to elucidate the anti-angiogenic or anti-inflammatory action.	Thalidomide	14-25	interferon gamma	Mus musculus	29-51
21477797-3	2011	Thalidomide inhibited IFN-gamma-induced NO production in mouse END-D cells via reduced expression of an inducible type of NO synthase (iNOS) protein and mRNA.	Thalidomide	0-11	interferon gamma	Mus musculus	22-31
21477797-3	2011	Thalidomide inhibited IFN-gamma-induced NO production in mouse END-D cells via reduced expression of an inducible type of NO synthase (iNOS) protein and mRNA.	Thalidomide	0-11	nitric oxide synthase 2, inducible	Mus musculus	135-139
21477797-4	2011	Since thalidomide did not alter the cell surface expression of IFN-gamma receptor, the NO inhibition was suggested to be due to the impairment of IFN-gamma-induced intracellular event by thalidomide.	Thalidomide	187-198	interferon gamma	Mus musculus	146-155
21477797-5	2011	Thalidomide inhibited the phosphorylation of IRF1, which was required for the iNOS expression.	Thalidomide	0-11	interferon regulatory factor 1	Mus musculus	45-49
21477797-5	2011	Thalidomide inhibited the phosphorylation of IRF1, which was required for the iNOS expression.	Thalidomide	0-11	nitric oxide synthase 2, inducible	Mus musculus	78-82
21477797-9	2011	Therefore, thalidomide was suggested to inhibit IFN-gamma-induced NO production via impaired STAT1 phosphorylation.	Thalidomide	11-22	interferon gamma	Mus musculus	48-57
21477797-9	2011	Therefore, thalidomide was suggested to inhibit IFN-gamma-induced NO production via impaired STAT1 phosphorylation.	Thalidomide	11-22	signal transducer and activator of transcription 1	Mus musculus	93-98
20958261-6	2011	We then summarize data showing how thalidomide interferes with this signaling network: thalidomide inhibits the activity of the redox-sensitive transcription factor NF-kappaB, shifts the balance of fibroblast growth factors and bone morphogenetic proteins (Bmps) towards pro-apoptotic Bmps, and suppresses Wnt/beta-catenin- and Akt-dependent survival signaling in the limb bud.	Thalidomide	35-46	nuclear factor kappa B subunit 1	Homo sapiens	165-174
20958261-6	2011	We then summarize data showing how thalidomide interferes with this signaling network: thalidomide inhibits the activity of the redox-sensitive transcription factor NF-kappaB, shifts the balance of fibroblast growth factors and bone morphogenetic proteins (Bmps) towards pro-apoptotic Bmps, and suppresses Wnt/beta-catenin- and Akt-dependent survival signaling in the limb bud.	Thalidomide	35-46	catenin beta 1	Homo sapiens	310-331
20958261-6	2011	We then summarize data showing how thalidomide interferes with this signaling network: thalidomide inhibits the activity of the redox-sensitive transcription factor NF-kappaB, shifts the balance of fibroblast growth factors and bone morphogenetic proteins (Bmps) towards pro-apoptotic Bmps, and suppresses Wnt/beta-catenin- and Akt-dependent survival signaling in the limb bud.	Thalidomide	87-98	nuclear factor kappa B subunit 1	Homo sapiens	165-174
20958261-6	2011	We then summarize data showing how thalidomide interferes with this signaling network: thalidomide inhibits the activity of the redox-sensitive transcription factor NF-kappaB, shifts the balance of fibroblast growth factors and bone morphogenetic proteins (Bmps) towards pro-apoptotic Bmps, and suppresses Wnt/beta-catenin- and Akt-dependent survival signaling in the limb bud.	Thalidomide	87-98	catenin beta 1	Homo sapiens	310-331
20846163-4	2010	We reported recently that two substances (ATRA and thalidomide) have preventive effects on pulmonary fibrosis by inhibiting IL-6-dependent proliferation and TGF-beta1-dependent transdifferentiation of lung fibroblasts.	Thalidomide	51-62	transforming growth factor, beta 1	Mus musculus	157-166
20594187-6	2010	Several drugs effective for the treatment of MM, including proteasome inhibitors, thalidomide, lenalidomide and arsenic trioxide, block NF-kappaB activation.	Thalidomide	82-93	nuclear factor kappa B subunit 1	Homo sapiens	136-145
21211317-1	2010	OBJECTIVE: To investigate the influences of VEGF expression through the intervention of thalidomide in malignant transformation of hepatocytes.	Thalidomide	88-99	vascular endothelial growth factor A	Rattus norvegicus	44-48
21211317-12	2010	And the VEGF level of thalidomide group was lower than those in 2-FAA group.	Thalidomide	22-33	vascular endothelial growth factor A	Rattus norvegicus	8-12
21211317-13	2010	CONCLUSION: Thalidomide can inhibit the hepatic VEGF expression and arrest the development of rat hepatoma.	Thalidomide	12-23	vascular endothelial growth factor A	Rattus norvegicus	48-52
20858096-0	2010	High expression levels of the mammalian target of rapamycin inhibitor DEPTOR are predictive of response to thalidomide in myeloma.	Thalidomide	107-118	DEP domain containing MTOR interacting protein	Homo sapiens	70-76
20122728-0	2010	Role of the TNF-alpha promoter polymorphisms for development of multiple myeloma and clinical outcome in thalidomide plus dexamethasone.	Thalidomide	105-116	tumor necrosis factor	Homo sapiens	12-21
20858096-0	2010	High expression levels of the mammalian target of rapamycin inhibitor DEPTOR are predictive of response to thalidomide in myeloma.	Thalidomide	107-118	mechanistic target of rapamycin kinase	Homo sapiens	30-59
20709454-7	2010	Furthermore, systemic pre-treatment with the classically used drugs indomethacin, celecoxib, guanetidine, morphine, thalidomide or dexamethasone, also prevented IL-6-induced muscle pain.	Thalidomide	116-127	interleukin 6	Mus musculus	161-165
20837031-1	2010	AIMS: Thalidomide is thought to prevent TNF-alpha production, and such mechanism could be useful in a spinally delivered drug approach for the control of peripheral inflammation.	Thalidomide	6-17	tumor necrosis factor	Rattus norvegicus	40-49
20705061-0	2010	PI3K/Akt signaling pathway is required for neuroprotection of thalidomide on hypoxic-ischemic cortical neurons in vitro.	Thalidomide	62-73	AKT serine/threonine kinase 1	Rattus norvegicus	5-8
20705061-1	2010	Thalidomide, a derivative of glutamic acid, is used for immunomodulatory therapy in various diseases through inhibition of tumor necrotic factor-alpha (TNF-alpha) release.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	152-161
20705061-9	2010	Furthermore, we found that thalidomide protected neurons against apoptosis by decreasing CC3 and increasing Bcl-2 expression in a dose-dependent manner.	Thalidomide	27-38	BCL2, apoptosis regulator	Rattus norvegicus	108-113
20705061-10	2010	Meanwhile, we found that thalidomide induced p-Akt expression, which could be inhibited by PI3K specific inhibitor, LY294002.	Thalidomide	25-36	AKT serine/threonine kinase 1	Rattus norvegicus	47-50
20705061-12	2010	In summary, thalidomide has anti-apoptotic effects on cortical neurons after OGD by modulating CC3 and Bcl-2 expression through activation of PI3K/Akt pathway.	Thalidomide	12-23	BCL2, apoptosis regulator	Rattus norvegicus	103-108
20705061-12	2010	In summary, thalidomide has anti-apoptotic effects on cortical neurons after OGD by modulating CC3 and Bcl-2 expression through activation of PI3K/Akt pathway.	Thalidomide	12-23	AKT serine/threonine kinase 1	Rattus norvegicus	147-150
20837031-12	2010	thalidomide reduced the expression of CD11b/c and GFAP markers in the lumbar spinal cord.	Thalidomide	0-11	integrin subunit alpha M	Rattus norvegicus	38-43
20837031-12	2010	thalidomide reduced the expression of CD11b/c and GFAP markers in the lumbar spinal cord.	Thalidomide	0-11	glial fibrillary acidic protein	Rattus norvegicus	50-54
20601373-9	2010	On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-alpha, IL-1beta, ICAM-1, and VCAM-1.	Thalidomide	26-37	intercellular adhesion molecule 1	Rattus norvegicus	133-139
20923560-0	2010	Intraperitoneal injection of thalidomide attenuates bone cancer pain and decreases spinal tumor necrosis factor-alpha expression in a mouse model.	Thalidomide	29-40	tumor necrosis factor	Mus musculus	90-117
20923560-2	2010	Thalidomide has been shown to selectively inhibit TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	50-59
20923560-4	2010	Therefore, in the present study, we investigated the effect of thalidomide on bone cancer-induced hyperalgesia and up-regulated expression of spinal TNF-alpha in a mouse model.	Thalidomide	63-74	tumor necrosis factor	Mus musculus	149-158
20923560-7	2010	Intraperitoneal injection of thalidomide (50 mg/kg), started at day 1 after surgery and once daily thereafter until day 7, attenuated bone cancer-evoked mechanical allodynia and thermal hyperalgesia as well as the up-regulation of TNF-alpha in the spinal cord.	Thalidomide	29-40	tumor necrosis factor	Mus musculus	231-240
20601373-9	2010	On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-alpha, IL-1beta, ICAM-1, and VCAM-1.	Thalidomide	26-37	tumor necrosis factor	Rattus norvegicus	112-121
20601373-9	2010	On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-alpha, IL-1beta, ICAM-1, and VCAM-1.	Thalidomide	26-37	vascular cell adhesion molecule 1	Rattus norvegicus	145-151
20601373-9	2010	On histological analysis, thalidomide treatment lowered total myocardial collagen content and the expression of TNF-alpha, IL-1beta, ICAM-1, and VCAM-1.	Thalidomide	26-37	interleukin 1 beta	Rattus norvegicus	123-131
21222370-10	2010	Thalidomide is a drug with pleiotropic effects: it appears to downregulate production of TNF-alpha and other proinflammatory cytokines.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	89-98
20857659-0	2010	[Thalidomide--coverage by health insurance when used for treatment of ENL].	Thalidomide	1-12	MLLT1 super elongation complex subunit	Homo sapiens	70-73
20627385-0	2010	The efficacy and safety of the low-thalidomide dose CTD (cyclophosphamide, thalidomide, dexamethasone) regimen in patients with multiple myeloma--a report by the Polish Myeloma Study Group.	Thalidomide	35-46	CTD	Homo sapiens	52-55
20627385-0	2010	The efficacy and safety of the low-thalidomide dose CTD (cyclophosphamide, thalidomide, dexamethasone) regimen in patients with multiple myeloma--a report by the Polish Myeloma Study Group.	Thalidomide	75-86	CTD	Homo sapiens	52-55
20627385-8	2010	The outpatient low-thalidomide dose CTD regimen is well tolerated and produces a significant response rate both in untreated and relapsing/resistant MM patients.	Thalidomide	19-30	CTD	Homo sapiens	36-39
20538468-4	2010	We identified potential novel anti-influenza agents from a screen of 34 synthesized phenethylphenylphthalimide analogs derived from thalidomide (PPT analogs).	Thalidomide	132-143	tachykinin precursor 1	Homo sapiens	145-148
20421453-0	2010	XBP1s levels are implicated in the biology and outcome of myeloma mediating different clinical outcomes to thalidomide-based treatments.	Thalidomide	107-118	X-box binding protein 1	Homo sapiens	0-4
20421453-6	2010	Furthermore, we show the beneficial therapeutic effects of thalidomide in patients with low XBP1s/u ratios.	Thalidomide	59-70	X-box binding protein 1	Homo sapiens	92-96
20346742-1	2010	We document an EGFR mutation in a patient with papillary renal cell cancer with a history of multiple therapies, including interferon-alpha, interleukin-2, 5-fluorouracil, and interferon-alpha together with 13-cis-retinoic acid, to which floxuridine was later added, and thalidomide maintenance therapy for six years.	Thalidomide	271-282	epidermal growth factor receptor	Homo sapiens	15-19
20346742-1	2010	We document an EGFR mutation in a patient with papillary renal cell cancer with a history of multiple therapies, including interferon-alpha, interleukin-2, 5-fluorouracil, and interferon-alpha together with 13-cis-retinoic acid, to which floxuridine was later added, and thalidomide maintenance therapy for six years.	Thalidomide	271-282	interleukin 2	Homo sapiens	141-154
20399910-6	2010	Remarkably, the levels of pro-inflammatory cytokines (IL-1alpha and TNF-alpha) were found to be decreased significantly (p&lt;0.05) in thalidomide treated group but the levels of IL-10 were found to be significantly (p&lt;0.05) elevated.	Thalidomide	135-146	interleukin 1 alpha	Mus musculus	54-63
20421453-7	2010	This study highlights the importance of XBP1 in myeloma and its significance as an independent prognostic marker and as a predictor of thalidomide response.	Thalidomide	135-146	X-box binding protein 1	Homo sapiens	40-44
20438868-5	2010	As shown in our results, treatment of solid tumor-bearing mice with thalidomide 1 resulted in a significant reduction in tumor volume with 75.4% inhibition, a significant decrease in lactate dehydrogenase (LDH), ICAM-1 expression and NO.	Thalidomide	68-79	intercellular adhesion molecule 1	Mus musculus	212-218
20399910-6	2010	Remarkably, the levels of pro-inflammatory cytokines (IL-1alpha and TNF-alpha) were found to be decreased significantly (p&lt;0.05) in thalidomide treated group but the levels of IL-10 were found to be significantly (p&lt;0.05) elevated.	Thalidomide	135-146	tumor necrosis factor	Mus musculus	68-77
20399910-6	2010	Remarkably, the levels of pro-inflammatory cytokines (IL-1alpha and TNF-alpha) were found to be decreased significantly (p&lt;0.05) in thalidomide treated group but the levels of IL-10 were found to be significantly (p&lt;0.05) elevated.	Thalidomide	135-146	interleukin 10	Mus musculus	179-184
20616958-8	2010	Thalidomide inhibits the activity of basic fibroblast growth factor-2 (bFGF).	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	37-69
22966360-0	2010	Effect of thalidomide and arsenic trioxide on the release of tumor necrosis factor-alpha and vascular endothelial growth factor from the KG-1a human acute myelogenous leukemia cell line.	Thalidomide	10-21	tumor necrosis factor	Homo sapiens	61-88
22966360-0	2010	Effect of thalidomide and arsenic trioxide on the release of tumor necrosis factor-alpha and vascular endothelial growth factor from the KG-1a human acute myelogenous leukemia cell line.	Thalidomide	10-21	vascular endothelial growth factor A	Homo sapiens	93-127
22966360-2	2010	The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) from this cell line in an attempt to clarify its possible cytotoxic mechanism(s).	Thalidomide	75-86	tumor necrosis factor	Homo sapiens	158-185
22966360-2	2010	The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) from this cell line in an attempt to clarify its possible cytotoxic mechanism(s).	Thalidomide	75-86	tumor necrosis factor	Homo sapiens	187-196
22966360-2	2010	The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) from this cell line in an attempt to clarify its possible cytotoxic mechanism(s).	Thalidomide	75-86	vascular endothelial growth factor A	Homo sapiens	202-236
22966360-2	2010	The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in combination with arsenic trioxide on the release of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor (VEGF) from this cell line in an attempt to clarify its possible cytotoxic mechanism(s).	Thalidomide	75-86	vascular endothelial growth factor A	Homo sapiens	238-242
22966360-6	2010	Results obtained indicate that the levels of TNF-alpha in the supernatant of KG-1a cell cultures incubated with thalidomide, arsenic trioxide, or combination were statistically lower than those observed in the supernatant of control cells (2.89, 5.07, 4.15 and 16.88 pg/ml, respectively).	Thalidomide	112-123	tumor necrosis factor	Homo sapiens	45-54
22966360-7	2010	However, the levels of VEGF in the supernatant of thalidomide-treated cells were statistically higher than those in the supernatant of control cells (69.61 vs. 11.48 pg/l).	Thalidomide	50-61	vascular endothelial growth factor A	Homo sapiens	23-27
20616958-8	2010	Thalidomide inhibits the activity of basic fibroblast growth factor-2 (bFGF).	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	71-75
20620488-9	2010	Both thalidomide and pentoxyphylline effectively reduced AST, LDH, TNF-alpha, and lipid peroxidation levels, as well as attenuated tissue edema and intestinal injury induced by I/R (P &lt; .05).	Thalidomide	5-16	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	57-60
20307255-2	2010	Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	74-83
20307255-2	2010	Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	86-110
20307255-2	2010	Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	colony stimulating factor 2	Homo sapiens	123-171
20307255-2	2010	Thalidomide and IMiDs inhibit the cytokines tumour necrosis factor-alpha (TNF-alpha), interleukins (IL) 1-beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	colony stimulating factor 2	Homo sapiens	173-179
20307255-5	2010	Thalidomide analogues have been used as inhibitors of alpha glucosidase and could be potential drugs for diabetes treatment.	Thalidomide	0-11	sucrase-isomaltase	Homo sapiens	54-71
20620488-9	2010	Both thalidomide and pentoxyphylline effectively reduced AST, LDH, TNF-alpha, and lipid peroxidation levels, as well as attenuated tissue edema and intestinal injury induced by I/R (P &lt; .05).	Thalidomide	5-16	tumor necrosis factor	Rattus norvegicus	67-76
20419594-5	2010	In addition, GlaxoSmithKline plc is developing 256066, an inhaled formulation of a PDE4 inhibitor that has demonstrated efficacy in trials in asthma, and apremilast from Celgene Corp has been reported to be effective for the treatment of psoriasis.	Thalidomide	170-177	heparan sulfate proteoglycan 2	Homo sapiens	29-32
20382589-8	2010	In the thalidomide-treated group, the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages, and nodular hyperplasia or a little atypical hyperplasia at the final stages, with the expression of NF-kappaB (X2=9.93, P&lt;0.001) and VEGF (X2=8.024, P&lt;0.001) lower than that in the 2-FAA group.	Thalidomide	7-18	vascular endothelial growth factor A	Rattus norvegicus	278-282
19713194-3	2010	Thalidomide has been shown to be anti-angiogenic via reduction of VEGF levels.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	66-70
20015241-2	2010	Increased concentration of hepatocyte growth factor (HGF) is associated with poor prognosis in patients treated with conventional chemotherapy or thalidomide.	Thalidomide	146-157	hepatocyte growth factor	Homo sapiens	27-51
20015241-2	2010	Increased concentration of hepatocyte growth factor (HGF) is associated with poor prognosis in patients treated with conventional chemotherapy or thalidomide.	Thalidomide	146-157	hepatocyte growth factor	Homo sapiens	53-56
19815837-5	2010	RESULTS: Thalidomide strongly inhibited gelatinase production by B-cell lines and primary myeloma cells in response to fibronectin, the most efficient gelatinase inducer identified in lymphoid cells.	Thalidomide	9-20	fibronectin 1	Homo sapiens	119-130
20514789-1	2010	Thalidomide is anti-inflammatory under some conditions, yet has been reported to up-regulate Th1 (T helper 1) immunity measured by increased IL-2 (Interleukin-2) and gamma interferon.	Thalidomide	0-11	interleukin 2	Mus musculus	141-145
20514789-1	2010	Thalidomide is anti-inflammatory under some conditions, yet has been reported to up-regulate Th1 (T helper 1) immunity measured by increased IL-2 (Interleukin-2) and gamma interferon.	Thalidomide	0-11	interleukin 2	Mus musculus	147-160
20514789-6	2010	Inhibition of inducible nitric oxide synthase (iNOS) may prove to be an important target for the anti-inflammatory and anti-cancer effects of thalidomide and related immunomodulatory drugs (IMiDs).	Thalidomide	142-153	nitric oxide synthase 2, inducible	Mus musculus	14-45
20514789-6	2010	Inhibition of inducible nitric oxide synthase (iNOS) may prove to be an important target for the anti-inflammatory and anti-cancer effects of thalidomide and related immunomodulatory drugs (IMiDs).	Thalidomide	142-153	nitric oxide synthase 2, inducible	Mus musculus	47-51
20364125-5	2010	In mice heterozygous for a null mutation in the Eng gene (encoding endoglin), an experimental model of HHT, thalidomide treatment stimulated mural cell coverage and thus rescued vessel wall defects.	Thalidomide	108-119	endoglin	Mus musculus	48-51
20364125-5	2010	In mice heterozygous for a null mutation in the Eng gene (encoding endoglin), an experimental model of HHT, thalidomide treatment stimulated mural cell coverage and thus rescued vessel wall defects.	Thalidomide	108-119	endoglin	Mus musculus	67-75
20364125-6	2010	Thalidomide treatment increased platelet-derived growth factor-B (PDGF-B) expression in endothelial cells and stimulated mural cell activation.	Thalidomide	0-11	platelet derived growth factor subunit B	Homo sapiens	32-64
20364125-6	2010	Thalidomide treatment increased platelet-derived growth factor-B (PDGF-B) expression in endothelial cells and stimulated mural cell activation.	Thalidomide	0-11	platelet derived growth factor subunit B	Homo sapiens	66-72
20223979-5	2010	Thalidomide initiates its teratogenic effects by binding to CRBN and inhibiting the associated ubiquitin ligase activity.	Thalidomide	0-11	cereblon	Homo sapiens	60-64
19815837-6	2010	Thalidomide disrupted integrin-mediated signaling pathways involved in gelatinase induction and release, such as Src and MAP-kinase ERK activation, resulting in decreased cell motility and invasiveness.	Thalidomide	0-11	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	113-116
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	29-40	fibronectin 1	Homo sapiens	65-76
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	29-40	AKT serine/threonine kinase 1	Homo sapiens	85-88
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	29-40	fibronectin 1	Homo sapiens	188-199
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	29-40	AKT serine/threonine kinase 1	Homo sapiens	281-284
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	166-177	fibronectin 1	Homo sapiens	65-76
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	166-177	AKT serine/threonine kinase 1	Homo sapiens	85-88
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	166-177	fibronectin 1	Homo sapiens	188-199
19757088-0	2010	Anti-fibrotic effect of thalidomide through inhibiting TGF-beta-induced ERK1/2 pathways in bleomycin-induced lung fibrosis in mice.	Thalidomide	24-35	transforming growth factor, beta 1	Mus musculus	55-63
19757088-0	2010	Anti-fibrotic effect of thalidomide through inhibiting TGF-beta-induced ERK1/2 pathways in bleomycin-induced lung fibrosis in mice.	Thalidomide	24-35	mitogen-activated protein kinase 3	Mus musculus	72-78
19757088-5	2010	RESULTS: Thalidomide administration significantly inhibits TGF-beta1 mRNA expression in a dose-dependant manner following administration of IL-6 and IL-6R.	Thalidomide	9-20	transforming growth factor, beta 1	Mus musculus	59-68
19815837-7	2010	Unexpectedly, treatment with thalidomide elicited an increase in fibronectin-induced Akt phosphorylation through phosphoinositide 3-kinase-independent pathways since thalidomide decreased fibronectin-induced phosphoinositide 3-kinase phosphorylation and reversed the inhibition of Akt phosphorylation achieved by the phosphoinositide 3-kinase inhibitors wortmannin and LY294002.	Thalidomide	166-177	AKT serine/threonine kinase 1	Homo sapiens	281-284
19815837-9	2010	The unexpected effects of thalidomide on Akt activation indicate the need for further studies to elucidate whether the interference with Akt downstream effects would synergize with the anti-tumor activity of thalidomide.	Thalidomide	26-37	AKT serine/threonine kinase 1	Homo sapiens	41-44
20034904-1	2009	OBJECTIVE: To investigate the expression of B7 co-stimulatory molecules in human multiple myeloma (MM) and the immunoregulatory effects of thalidomide on B7.1 co-stimulator.	Thalidomide	139-150	CD80 molecule	Homo sapiens	154-158
19757088-5	2010	RESULTS: Thalidomide administration significantly inhibits TGF-beta1 mRNA expression in a dose-dependant manner following administration of IL-6 and IL-6R.	Thalidomide	9-20	interleukin 6	Mus musculus	140-144
19757088-5	2010	RESULTS: Thalidomide administration significantly inhibits TGF-beta1 mRNA expression in a dose-dependant manner following administration of IL-6 and IL-6R.	Thalidomide	9-20	interleukin 6 receptor, alpha	Mus musculus	149-154
19757088-6	2010	In the analysis of BAL fluids, total BAL inflammatory cell counts, TGF-beta1, and IL-6 levels in thalidomide-treated mice were significantly reduced when compared with bleomycin-treated mice (p &lt; 0.01, p &lt; 0.01, and p &lt; 0.001, respectively).	Thalidomide	97-108	transforming growth factor, beta 1	Mus musculus	67-76
19757088-6	2010	In the analysis of BAL fluids, total BAL inflammatory cell counts, TGF-beta1, and IL-6 levels in thalidomide-treated mice were significantly reduced when compared with bleomycin-treated mice (p &lt; 0.01, p &lt; 0.01, and p &lt; 0.001, respectively).	Thalidomide	97-108	interleukin 6	Mus musculus	82-86
19757088-7	2010	Thalidomide inhibited total ERK1/2 and phospho-ERK1/2 expression after TGF-beta1 stimulation in the RT-PCR and western blotting.	Thalidomide	0-11	mitogen-activated protein kinase 3	Mus musculus	28-34
19757088-7	2010	Thalidomide inhibited total ERK1/2 and phospho-ERK1/2 expression after TGF-beta1 stimulation in the RT-PCR and western blotting.	Thalidomide	0-11	mitogen-activated protein kinase 3	Mus musculus	47-53
19757088-7	2010	Thalidomide inhibited total ERK1/2 and phospho-ERK1/2 expression after TGF-beta1 stimulation in the RT-PCR and western blotting.	Thalidomide	0-11	transforming growth factor, beta 1	Mus musculus	71-80
19757088-8	2010	CONCLUSION: The results of our study suggest that the anti-fibrotic effect of thalidomide on lung fibrosis may be related to suppression of the TGF-beta1-induced ERK1/2 signaling pathway.	Thalidomide	78-89	transforming growth factor, beta 1	Mus musculus	144-153
19757088-8	2010	CONCLUSION: The results of our study suggest that the anti-fibrotic effect of thalidomide on lung fibrosis may be related to suppression of the TGF-beta1-induced ERK1/2 signaling pathway.	Thalidomide	78-89	mitogen-activated protein kinase 3	Mus musculus	162-168
19926820-1	2010	The glutamic acid derivative thalidomide is a transcriptional inhibitor of TNF-alpha but is also known to affect human blood vessels, which may underlie its teratogenicity.	Thalidomide	29-40	tumor necrosis factor	Homo sapiens	75-84
19926820-7	2010	Effects of thalidomide on NF-kappaB activation, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) expression in TNF-alpha/LPS-activated HIMEC were determined by RT-PCR and Western blotting.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	129-138
19926820-7	2010	Effects of thalidomide on NF-kappaB activation, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) expression in TNF-alpha/LPS-activated HIMEC were determined by RT-PCR and Western blotting.	Thalidomide	11-22	interferon regulatory factor 6	Homo sapiens	139-142
19926820-11	2010	VEGF-induced HIMEC transmigration, growth, proliferation, tube formation, and Akt phosphorylation were significantly inhibited by thalidomide.	Thalidomide	130-141	vascular endothelial growth factor A	Homo sapiens	0-4
20522972-3	2010	BALB/c mice sensitized and challenged with ovalbumin (OVA) were treated orally with thalidomide (30, 100, or 300 mg/kg) or a vehicle.	Thalidomide	84-95	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	43-52
20522972-6	2010	Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) in BALF by OVA challenges.	Thalidomide	0-11	interleukin 5	Mus musculus	45-58
20522972-6	2010	Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) in BALF by OVA challenges.	Thalidomide	0-11	interleukin 5	Mus musculus	60-64
20522972-6	2010	Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) in BALF by OVA challenges.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	70-97
20522972-6	2010	Thalidomide inhibited the elevated levels of interleukin-5 (IL-5) and tumor necrosis factor-alpha (TNF-alpha) in BALF by OVA challenges.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	99-108
21048383-3	2010	The suppressive effect of thalidomide on the activation of the nuclear transcription factor NF-kappaB may explain these effects of thalidomide.	Thalidomide	26-37	nuclear factor kappa B subunit 1	Homo sapiens	92-101
21048383-3	2010	The suppressive effect of thalidomide on the activation of the nuclear transcription factor NF-kappaB may explain these effects of thalidomide.	Thalidomide	131-142	nuclear factor kappa B subunit 1	Homo sapiens	92-101
20306635-9	2009	Treatment with thalidomide showed a significant benefit compared to aspirin (RR 2.43; 95% CI 1.28 to 4.59).	Thalidomide	15-26	ribonucleotide reductase regulatory subunit M2	Homo sapiens	77-81
20304198-9	2010	Therapy with either thalidomide or tamoxifen effectively maintained alpha-smooth muscle actin expression in the media, similar to uninjured arteries.	Thalidomide	20-31	actin gamma 2, smooth muscle	Rattus norvegicus	68-93
20034801-0	2010	New thalidomide analogues derived through Sonogashira or Suzuki reactions and their TNF expression inhibition profiles.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	84-87
20034801-2	2010	All thalidomide analogues were tested for their ability to inhibit the expression of the proinflammatory cytokine Tumor Necrosis Factor (TNF).	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	114-135
20034801-2	2010	All thalidomide analogues were tested for their ability to inhibit the expression of the proinflammatory cytokine Tumor Necrosis Factor (TNF).	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	137-140
20034801-4	2010	Several compounds either containing either an aryl-isobutyl or aryl-isopropoxy group were the most effective in inhibiting TNF expression, and were several times more active than thalidomide itself.	Thalidomide	179-190	tumor necrosis factor	Homo sapiens	123-126
20039400-4	2010	The aim of this study was to assess the efficacy of thalidomide in patients with severe EOS, based on etiology supporting an initial role of NF-kappaB in activation of this disease.	Thalidomide	52-63	nuclear factor kappa B subunit 1	Homo sapiens	141-150
20039400-10	2010	CONCLUSION: The ability of thalidomide to improve clinical symptoms and laboratory findings in patients with EOS indicates a central role for NF-kappaB activity in this disorder.	Thalidomide	27-38	nuclear factor kappa B subunit 1	Homo sapiens	142-151
20039400-11	2010	Inhibition of IKK might be a pharmacologic action by which thalidomide down-regulates NF-kappaB signaling.	Thalidomide	59-70	nuclear factor kappa B subunit 1	Homo sapiens	86-95
20823570-11	2010	Pretreatment with quercetin or thalidomide significantly attenuated the severity of cerulein-induced acute pancreatitis as evidenced by effective reductions in the pancreatic wet weight/body weight ratio, biochemical indices, proinflammatory cytokines, myeloperoxidase activity, malondialdehyde formation, and an increase in antiinflammatory cytokine IL-10.	Thalidomide	31-42	myeloperoxidase	Mus musculus	253-268
20823570-11	2010	Pretreatment with quercetin or thalidomide significantly attenuated the severity of cerulein-induced acute pancreatitis as evidenced by effective reductions in the pancreatic wet weight/body weight ratio, biochemical indices, proinflammatory cytokines, myeloperoxidase activity, malondialdehyde formation, and an increase in antiinflammatory cytokine IL-10.	Thalidomide	31-42	interleukin 10	Mus musculus	351-356
20190484-2	2010	Thus, we treated the patient with thalidomide plus dexamethasone, which brought about a marked improvement of systolic dysfunction, POEMS syndrome-related symptoms and the serum concentrations of vascular endothelial growth factor.	Thalidomide	34-45	vascular endothelial growth factor A	Homo sapiens	196-230
20034904-2	2009	METHODS: The immunoregulatory effects of thalidomide on the expression of B7-1 in human MM cell line was examined by detecting the changes in the expression of B7 co-stimulator on the cells using flow cytometry following the drug treatment.	Thalidomide	41-52	CD80 molecule	Homo sapiens	74-78
20034904-6	2009	Thalidomide can up-regulate the expression of B7-1 molecules on myeloma cells, which is probably one of the therapeutic mechanisms of thalidomide.	Thalidomide	0-11	CD80 molecule	Homo sapiens	46-50
20034904-6	2009	Thalidomide can up-regulate the expression of B7-1 molecules on myeloma cells, which is probably one of the therapeutic mechanisms of thalidomide.	Thalidomide	134-145	CD80 molecule	Homo sapiens	46-50
19843943-0	2009	Thalidomide inhibits activation of caspase-1.	Thalidomide	0-11	caspase 1	Mus musculus	35-44
19458984-3	2009	We sought to investigate the effects of Thalidomide (Th), a potent anti-angiogenic drug on vasa vasorum (VV) neovascularization, vessel wall inflammation, and neointima formation in early experimental atherosclerosis.	Thalidomide	40-51	DEAD-box helicase 4	Sus scrofa	91-95
19458984-8	2009	Treatment with Thalidomide preserved VV spatial density [2.7 +/- 0.3 (N), 6.4 +/- 0.7 (HC), 3.5 +/- 0.8 (HC + Th); p = ns HC + Th vs. N] and inhibited the expression of VEGF, TNF-alpha and LOX-1, but not NFkappabeta activity in the coronary vessel wall.	Thalidomide	15-26	vascular endothelial growth factor A	Sus scrofa	169-173
19458984-8	2009	Treatment with Thalidomide preserved VV spatial density [2.7 +/- 0.3 (N), 6.4 +/- 0.7 (HC), 3.5 +/- 0.8 (HC + Th); p = ns HC + Th vs. N] and inhibited the expression of VEGF, TNF-alpha and LOX-1, but not NFkappabeta activity in the coronary vessel wall.	Thalidomide	15-26	tumor necrosis factor	Sus scrofa	175-184
19458984-8	2009	Treatment with Thalidomide preserved VV spatial density [2.7 +/- 0.3 (N), 6.4 +/- 0.7 (HC), 3.5 +/- 0.8 (HC + Th); p = ns HC + Th vs. N] and inhibited the expression of VEGF, TNF-alpha and LOX-1, but not NFkappabeta activity in the coronary vessel wall.	Thalidomide	15-26	oxidized low density lipoprotein receptor 1	Sus scrofa	189-194
19843943-5	2009	Thalidomide-treated cells also released less of other leaderless proteins, which require caspase-1 activity for their secretion.	Thalidomide	0-11	caspase 1	Mus musculus	89-98
19843943-8	2009	The anti-inflammatory activity of thalidomide was also mediated via caspase-1 in mice.	Thalidomide	34-45	caspase 1	Mus musculus	68-77
19843943-9	2009	These findings represent a novel mechanism by which thalidomide exerts its pharmacological activity and suggest that inhibition of the activity of IL-1 might represent a novel strategy to substitute thalidomide.	Thalidomide	52-63	interleukin 1 complex	Mus musculus	147-151
19843943-9	2009	These findings represent a novel mechanism by which thalidomide exerts its pharmacological activity and suggest that inhibition of the activity of IL-1 might represent a novel strategy to substitute thalidomide.	Thalidomide	199-210	interleukin 1 complex	Mus musculus	147-151
19639185-3	2009	Besides its well-documented anti-angiogenic effects, thalidomide therapy could result in a decrease in ABCB1 gene expression.	Thalidomide	53-64	ATP binding cassette subfamily B member 1	Homo sapiens	103-108
19814869-12	2009	Thalidomide also provided significant protection against TNBS-induced colonic damage in terms of morphological and histological score and levels of lipid peroxidation, superoxide dismutase, catalase and glutathione peroxidase in colonic tissue.	Thalidomide	0-11	catalase	Rattus norvegicus	190-198
19954656-0	2009	[Effect of TNF-alpha gene polymorphism on outcome of thalidomide-based regimens for multiple myeloma].	Thalidomide	53-64	tumor necrosis factor	Homo sapiens	11-20
19954656-1	2009	OBJECTIVE: To evaluate the effect of polymorphism at the -238 and -308 position of the TNF-alpha promotor region on the clinical outcome of thalidomide (Thal)-based regimens for the treatment of multiple myeloma (MM).	Thalidomide	140-151	tumor necrosis factor	Homo sapiens	87-96
19954656-1	2009	OBJECTIVE: To evaluate the effect of polymorphism at the -238 and -308 position of the TNF-alpha promotor region on the clinical outcome of thalidomide (Thal)-based regimens for the treatment of multiple myeloma (MM).	Thalidomide	153-157	tumor necrosis factor	Homo sapiens	87-96
19954656-8	2009	CONCLUSION: The TNF-alpha -238 polymorphic status is associated with a favorable clinical outcome in MM patients treated with thalidomide-based regimen.	Thalidomide	126-137	tumor necrosis factor	Homo sapiens	16-25
19922130-2	2009	We conducted a preliminary phase II trial of thalidomide, which reduces levels of TNF-alpha pre-transcriptionally and post-transcriptionally in vivo and has been shown to prolong disease duration and extend the lifespan of transgenic animal models of ALS.	Thalidomide	45-56	tumor necrosis factor	Homo sapiens	82-91
19922130-10	2009	In conclusion, treatment of ALS with the TNF-alpha inhibitor, thalidomide, does not appear to effectively modulate disease progression and can cause adverse effects.	Thalidomide	62-73	tumor necrosis factor	Homo sapiens	41-50
19394719-0	2009	Discovering a new analogue of thalidomide which may be used as a potent modulator of TNF-alpha production.	Thalidomide	30-41	tumor necrosis factor	Homo sapiens	85-94
19394719-1	2009	A new series of imide derivatives related to thalidomide were synthesized and evaluated as modulators of TNF-alpha production.	Thalidomide	45-56	tumor necrosis factor	Homo sapiens	105-114
19639185-8	2009	Conversely thalidomide and PGA induced down-regulation of VEGF gene expression in both drug-sensitive and -resistant myeloma cells.	Thalidomide	11-22	vascular endothelial growth factor A	Homo sapiens	58-62
19680075-7	2009	Thalidomide also caused a substantial reduction of 1) the rise in myeloperoxidase activity (mucosa); 2) the expression in the tissue of TNF-alpha, IL-1beta, transforming growth factor-beta, and vascular endothelial growth factor; 3) the increase in staining (immunohistochemistry) for nitrotyrosine and for poly(ADP ribose), as well as 4) the nuclear factor-kappaB activation caused by CG in the peritoneum.	Thalidomide	0-11	myeloperoxidase	Rattus norvegicus	66-81
21172267-1	2009	BACKGROUND: Thalidomide, one of whose activities is to inhibit Tumour Necrosis Factor (TNF)-alpha production, has been reported to be an effective treatment for refractory inflammatory bowel disease (IBD).	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	63-97
21172267-2	2009	TNF-alpha driven production of matrix metalloproteinase (MMP)-3 by gut lamina propria mononuclear cells (LPMCs) is a major pathway of tissue injury in IBD; however the effect of thalidomide and newer more potent immunomodulatory derivatives on this pathway has not been studied.	Thalidomide	178-189	tumor necrosis factor	Homo sapiens	0-9
21172267-2	2009	TNF-alpha driven production of matrix metalloproteinase (MMP)-3 by gut lamina propria mononuclear cells (LPMCs) is a major pathway of tissue injury in IBD; however the effect of thalidomide and newer more potent immunomodulatory derivatives on this pathway has not been studied.	Thalidomide	178-189	matrix metallopeptidase 3	Homo sapiens	31-63
19680075-7	2009	Thalidomide also caused a substantial reduction of 1) the rise in myeloperoxidase activity (mucosa); 2) the expression in the tissue of TNF-alpha, IL-1beta, transforming growth factor-beta, and vascular endothelial growth factor; 3) the increase in staining (immunohistochemistry) for nitrotyrosine and for poly(ADP ribose), as well as 4) the nuclear factor-kappaB activation caused by CG in the peritoneum.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	136-145
19680075-7	2009	Thalidomide also caused a substantial reduction of 1) the rise in myeloperoxidase activity (mucosa); 2) the expression in the tissue of TNF-alpha, IL-1beta, transforming growth factor-beta, and vascular endothelial growth factor; 3) the increase in staining (immunohistochemistry) for nitrotyrosine and for poly(ADP ribose), as well as 4) the nuclear factor-kappaB activation caused by CG in the peritoneum.	Thalidomide	0-11	interleukin 1 beta	Rattus norvegicus	147-155
19604271-7	2009	THD inhibited the up-regulation of HYP protein, pro-collagen III mRNA and alpha-SMA protein induced by TGF-beta1 in HFL-F cells, and additionally inhibited pro-collagen III mRNA expression on trans-differentiated MF.	Thalidomide	0-3	actin alpha 2, smooth muscle, aorta	Mus musculus	74-83
19604271-7	2009	THD inhibited the up-regulation of HYP protein, pro-collagen III mRNA and alpha-SMA protein induced by TGF-beta1 in HFL-F cells, and additionally inhibited pro-collagen III mRNA expression on trans-differentiated MF.	Thalidomide	0-3	transforming growth factor, beta 1	Mus musculus	103-112
19604271-8	2009	THD reduced HYP synthesis in the lung tissues of BLM-treated mice at week 4, and slightly reduced the numbers of alpha-SMA-positive cells.	Thalidomide	0-3	actin alpha 2, smooth muscle, aorta	Mus musculus	113-122
19698226-5	2009	The combination of THD in concentration of 80 or 100 microg/ml with Dx in concentration of 4 microg/ml decreased the expression of IL-6, TNF-alpha and survivin, increased the expression of ES, while no influence on VEGF expression was found.	Thalidomide	19-22	interleukin 6	Homo sapiens	131-135
19538513-5	2009	Further, thalidomide inhibited the MyD88 augmentation in lipopolysaccharide-stimulated cells, whereas it did not alter the expression of TIR domain-containing adaptor-inducing IFN-beta in the MyD88-independent pathway.	Thalidomide	9-20	myeloid differentiation primary response gene 88	Mus musculus	35-40
19538513-6	2009	Thalidomide significantly inhibited the NO production in response to Pam(3)Cys, CpG DNA and imiquimod as MyD88-dependent Toll-like receptor (TLR) ligands, but not polyI:C as a MyD88-independent TLR ligand.	Thalidomide	0-11	myeloid differentiation primary response gene 88	Mus musculus	105-110
19538513-6	2009	Thalidomide significantly inhibited the NO production in response to Pam(3)Cys, CpG DNA and imiquimod as MyD88-dependent Toll-like receptor (TLR) ligands, but not polyI:C as a MyD88-independent TLR ligand.	Thalidomide	0-11	myeloid differentiation primary response gene 88	Mus musculus	176-181
19538513-7	2009	Therefore, thalidomide was suggested to inhibit lipopolysaccharide-induced NO production via downregulation of the MyD88-dependent signal pathway.	Thalidomide	11-22	myeloid differentiation primary response gene 88	Mus musculus	115-120
19434479-2	2009	In this study we examined the effect of drugs interfering with TNF expression (thalidomide) and activity (infliximab) and compared it to that of a H(1)R histamine receptor antagonist (loratadine) in a model of histamine-induced rat hind-paw oedema formation.	Thalidomide	79-90	tumor necrosis factor	Rattus norvegicus	63-66
19663116-4	2009	We report a case of deep venous thrombosis (DVT) and pulmonary embolus (PE) following thalidomide use in a patient with leprosy (erythema nodosum leprosum, ENL) who was concurrently treated with prednisone, as well as a review of relevant literature.	Thalidomide	86-97	MLLT1 super elongation complex subunit	Homo sapiens	156-159
19698226-5	2009	The combination of THD in concentration of 80 or 100 microg/ml with Dx in concentration of 4 microg/ml decreased the expression of IL-6, TNF-alpha and survivin, increased the expression of ES, while no influence on VEGF expression was found.	Thalidomide	19-22	tumor necrosis factor	Homo sapiens	137-146
19698226-6	2009	It is concluded that THD combined with Dx shows the synergistic inhibitory effect on KM3 cells, they bring the effect resistant to multiple myeloma probably through down-regulating the expression of IL-6, TNF-alpha and survivin, and up-regulating the expression of ES in KM3 cell.	Thalidomide	21-24	interleukin 6	Homo sapiens	199-203
19698226-6	2009	It is concluded that THD combined with Dx shows the synergistic inhibitory effect on KM3 cells, they bring the effect resistant to multiple myeloma probably through down-regulating the expression of IL-6, TNF-alpha and survivin, and up-regulating the expression of ES in KM3 cell.	Thalidomide	21-24	tumor necrosis factor	Homo sapiens	205-214
20021944-11	2009	The caspase-3 positivity of SMMC-7721 cells treated with thalidomide was increasing along with the increase of treatment time or drug concentration, but not in the control cells.	Thalidomide	57-68	caspase 3	Homo sapiens	4-13
20021944-12	2009	The VEGF content in SMMC-7721 cells was lowering when thalidomide was used in an increasing concentration.	Thalidomide	54-65	vascular endothelial growth factor A	Homo sapiens	4-8
19822087-8	2009	Autocrinal TNF-alpha production and modulation of cadhelin expression to regulate cell adhesion might be involved in this inhibitory action of thalidomide.	Thalidomide	143-154	tumor necrosis factor	Homo sapiens	11-20
19569016-3	2009	The aim of our study was to examine the direct effect of various adiponectin concentrations applied separately or in combination with thalidomide on the growth of the murine endothelial cell line HECa 10 in 24- and 72-hour cell cultures.	Thalidomide	134-145	hdc homolog, cell cycle regulator	Mus musculus	196-200
20981323-6	2009	Treatment with thalidomide, an immunomodulatory agent, showed elevation of CCL5 by GEP but was not cytotoxic to CLL cells.	Thalidomide	15-26	C-C motif chemokine ligand 5	Homo sapiens	75-79
18976811-0	2009	Thalidomide treatment down-regulates SDF-1alpha and CXCR4 expression in multiple myeloma patients.	Thalidomide	0-11	C-X-C motif chemokine receptor 4	Homo sapiens	52-57
18976811-2	2009	Here, we show that the expression of SDF-1alpha and CXCR4 was significantly down-regulated in patients treated with thalidomide (n=10) as compared to newly diagnosed MM patients (n=31) and MM patients treated with other drugs (n=38).	Thalidomide	116-127	C-X-C motif chemokine receptor 4	Homo sapiens	52-57
18976811-3	2009	SDF-1 alpha and CXCR4 expression was also significantly decreased in a RPMI 8226 cell line treated with 10 and 20micromol/L of thalidomide.	Thalidomide	127-138	C-X-C motif chemokine receptor 4	Homo sapiens	16-21
18976811-4	2009	Our findings indicate that thalidomide therapy induces down-regulation of CXCR4 and its ligand SDF-1alpha in multiple myeloma.	Thalidomide	27-38	C-X-C motif chemokine receptor 4	Homo sapiens	74-79
19954599-0	2009	[Effects of thalidomide on Annexin II gene regulation].	Thalidomide	12-23	annexin A2	Homo sapiens	27-37
19954599-1	2009	OBJECTIVE: To investigate the effect of thalidomide on Annexin II (AnxA2) gene regulation in multiple myeloma cell line RPMI8226 and human microvascular endothelial cell line HMEC-1 cells in vitro, and explore the potential mechanism of thrombosis induced by thalidomide.	Thalidomide	40-51	annexin A2	Homo sapiens	55-65
19954599-1	2009	OBJECTIVE: To investigate the effect of thalidomide on Annexin II (AnxA2) gene regulation in multiple myeloma cell line RPMI8226 and human microvascular endothelial cell line HMEC-1 cells in vitro, and explore the potential mechanism of thrombosis induced by thalidomide.	Thalidomide	40-51	annexin A2	Homo sapiens	67-72
19954599-3	2009	Real time quantitative PCR (RQ-PCR) was used to detect the influence of thalidomide at different concentration on the expression of AnxA2 mRNA, flow cytometry (FCM) and confocal microscopy were used to detect the cell surface protein level after the samples were stimulated with different concentrations of thalidomide.	Thalidomide	72-83	annexin A2	Homo sapiens	132-137
19954599-6	2009	CONCLUSIONS: Thalidomide can inhibit the expression of AnxA2 mRNA and protein in RPMI8226 and HMEC-1 cells, which may be one of the mechanisms for the development of thrombosis induced by thalidomide in multiple myeloma patients.	Thalidomide	13-24	annexin A2	Homo sapiens	55-60
19954599-6	2009	CONCLUSIONS: Thalidomide can inhibit the expression of AnxA2 mRNA and protein in RPMI8226 and HMEC-1 cells, which may be one of the mechanisms for the development of thrombosis induced by thalidomide in multiple myeloma patients.	Thalidomide	188-199	annexin A2	Homo sapiens	55-60
19675744-2	2009	Thalidomide has been described as inhibitor of the fibroblast growth factor (FGF) and the vascular endothelial growth factor (VEGF).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	90-124
19675744-2	2009	Thalidomide has been described as inhibitor of the fibroblast growth factor (FGF) and the vascular endothelial growth factor (VEGF).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	126-130
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	178-189	phosphatase and tensin homolog	Homo sapiens	82-86
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	178-189	AKT serine/threonine kinase 1	Homo sapiens	134-137
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	178-189	mechanistic target of rapamycin kinase	Homo sapiens	138-142
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	191-202	phosphatase and tensin homolog	Homo sapiens	82-86
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	191-202	AKT serine/threonine kinase 1	Homo sapiens	134-137
19567134-15	2009	The expression level of phosphatase and tensin homolog deleted on chromosome ten (PTEN), which promoted autophagy by suppressing PI3K/Akt/mTOR signaling pathway, was elevated by thalidomide (thalidomide group: P = 0.000; combined group: P = 0.002).	Thalidomide	191-202	mechanistic target of rapamycin kinase	Homo sapiens	138-142
19567134-17	2009	Contributing to the up-regulation of PTEN by thalidomide, the expression of autophagy associated protein-MAP1LC3 and Beclin1 was enhanced, which leads to a reinforced autophagy in the combined treatment of temozolomide and thalidomide in vitro.	Thalidomide	45-56	phosphatase and tensin homolog	Homo sapiens	37-41
19567134-17	2009	Contributing to the up-regulation of PTEN by thalidomide, the expression of autophagy associated protein-MAP1LC3 and Beclin1 was enhanced, which leads to a reinforced autophagy in the combined treatment of temozolomide and thalidomide in vitro.	Thalidomide	45-56	beclin 1	Homo sapiens	117-124
19567134-17	2009	Contributing to the up-regulation of PTEN by thalidomide, the expression of autophagy associated protein-MAP1LC3 and Beclin1 was enhanced, which leads to a reinforced autophagy in the combined treatment of temozolomide and thalidomide in vitro.	Thalidomide	223-234	phosphatase and tensin homolog	Homo sapiens	37-41
19567134-17	2009	Contributing to the up-regulation of PTEN by thalidomide, the expression of autophagy associated protein-MAP1LC3 and Beclin1 was enhanced, which leads to a reinforced autophagy in the combined treatment of temozolomide and thalidomide in vitro.	Thalidomide	223-234	beclin 1	Homo sapiens	117-124
19220680-6	2009	For the thalidomide treated group, despite the fact that MVD-CD34 of larger metastases was more than that of small metastases (P &lt; 0.01), the MVD and BD were similar to those of small metastases respectively (P &gt; 0.05).	Thalidomide	8-19	CD34 antigen	Mus musculus	61-65
19413671-3	2009	Thalidomide, which inhibited TNF-alpha effectively, has been used clinically in states of chronic TNF-alpha elevation with encouraging results.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	29-38
19467946-0	2009	Chronic thalidomide administration enhances vascular responsiveness to vasopressin in portal-systemic collaterals of bile duct-ligated rats.	Thalidomide	8-19	arginine vasopressin	Rattus norvegicus	71-82
19467946-2	2009	It has been shown that chronic thalidomide treatment decreases portal pressure, attenuates hyperdynamic circulation and inhibits vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-alpha in partially portal vein-ligated rats.	Thalidomide	31-42	vascular endothelial growth factor A	Rattus norvegicus	129-163
19467946-2	2009	It has been shown that chronic thalidomide treatment decreases portal pressure, attenuates hyperdynamic circulation and inhibits vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-alpha in partially portal vein-ligated rats.	Thalidomide	31-42	vascular endothelial growth factor A	Rattus norvegicus	165-169
19467946-2	2009	It has been shown that chronic thalidomide treatment decreases portal pressure, attenuates hyperdynamic circulation and inhibits vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-alpha in partially portal vein-ligated rats.	Thalidomide	31-42	tumor necrosis factor	Rattus norvegicus	175-208
19467946-11	2009	Compared with the control group, thalidomide-treated rats had significantly lower plasma VEGF levels (p &lt; 0.001), accompanied by an insignificant reduction in plasma TNF-alpha levels (p &gt; 0.05).	Thalidomide	33-44	vascular endothelial growth factor A	Rattus norvegicus	89-93
19467946-12	2009	The expressions of VEGF and TNF-alpha mRNA in the left adrenal veins of thalidomide-treated CBDL rats were not significantly changed compared with those of the control group.	Thalidomide	72-83	vascular endothelial growth factor A	Rattus norvegicus	19-23
19467946-12	2009	The expressions of VEGF and TNF-alpha mRNA in the left adrenal veins of thalidomide-treated CBDL rats were not significantly changed compared with those of the control group.	Thalidomide	72-83	tumor necrosis factor	Rattus norvegicus	28-37
19467946-14	2009	CONCLUSION: In cirrhotic rats, chronic thalidomide treatment improves the portal-systemic collateral vascular responsiveness to AVP, which was partly related to VEGF inhibition.	Thalidomide	39-50	vascular endothelial growth factor A	Rattus norvegicus	161-165
19413671-3	2009	Thalidomide, which inhibited TNF-alpha effectively, has been used clinically in states of chronic TNF-alpha elevation with encouraging results.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	98-107
19413671-11	2009	CONCLUSIONS: Thalidomide decreased the PVP and IHR through the attenuation of anandamide-induced constrictive response, decreasing the production of TNF-alpha, IL-6 and TXA(2) in the liver and the suppression of hepatic fibrogenesis of rats with biliary cirrhosis of this study.	Thalidomide	13-24	tumor necrosis factor	Rattus norvegicus	149-158
19413671-11	2009	CONCLUSIONS: Thalidomide decreased the PVP and IHR through the attenuation of anandamide-induced constrictive response, decreasing the production of TNF-alpha, IL-6 and TXA(2) in the liver and the suppression of hepatic fibrogenesis of rats with biliary cirrhosis of this study.	Thalidomide	13-24	interleukin 6	Rattus norvegicus	160-164
19370684-2	2009	High levels of tumour necrosis factor-alpha (TNF-alpha) have been associated with the development of intestinal inflammation in Crohn"s disease.Thalidomide, has been demonstrated to have anti TNF-alpha properties in experimental and clinical studies.	Thalidomide	144-155	tumor necrosis factor	Homo sapiens	45-54
19050852-9	2009	Serum TNF-alpha level rose threefold after LPS treatment, but this rise was abolished by thalidomide.	Thalidomide	89-100	tumor necrosis factor	Rattus norvegicus	6-15
19370684-2	2009	High levels of tumour necrosis factor-alpha (TNF-alpha) have been associated with the development of intestinal inflammation in Crohn"s disease.Thalidomide, has been demonstrated to have anti TNF-alpha properties in experimental and clinical studies.	Thalidomide	144-155	tumor necrosis factor	Homo sapiens	192-201
19370685-2	2009	Thalidomide, a tumour necrosis factor-alpha (TNF-alpha) inhibitor and its analogue, lenalidomide, may have a role in the management of Crohn"s disease, but it is not clear whether it is an effective maintenance therapy.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	45-54
19271121-8	2009	Furthermore, thalidomide, a TNF-alpha antagonist, treatment abolished the LPS pretreatment-associated protective effects.	Thalidomide	13-24	tumor necrosis factor	Mus musculus	28-37
19222454-0	2009	Multifocal primary cutaneous CD30+ anaplastic large cell lymphoma responsive to thalidomide: the molecular mechanism and the clinical application.	Thalidomide	80-91	TNF receptor superfamily member 8	Homo sapiens	29-33
19423468-7	2009	Treatment with thalidomide alone significantly (p&lt;0.05) decreased interleukin-1 alpha (IL-1alpha), nitric oxide (NO) and malondialdehyde (MDA) levels in the serum without significantly (p&lt;0.05) decreasing the bacterial count in blood.	Thalidomide	15-26	interleukin 1 alpha	Mus musculus	69-88
19423468-7	2009	Treatment with thalidomide alone significantly (p&lt;0.05) decreased interleukin-1 alpha (IL-1alpha), nitric oxide (NO) and malondialdehyde (MDA) levels in the serum without significantly (p&lt;0.05) decreasing the bacterial count in blood.	Thalidomide	15-26	interleukin 1 alpha	Mus musculus	90-99
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	AKT serine/threonine kinase 1	Homo sapiens	142-145
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	cyclin D1	Homo sapiens	236-245
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	BCL2 like 1	Homo sapiens	247-253
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	BCL2 apoptosis regulator	Homo sapiens	255-260
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	TNF receptor associated factor 1	Homo sapiens	262-267
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	baculoviral IAP repeat containing 2	Homo sapiens	269-275
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	X-linked inhibitor of apoptosis	Homo sapiens	277-281
19372569-4	2009	Curcumin also potentiated the apoptotic effects of thalidomide and bortezomib by down-regulating the constitutive activation of NF-kappaB and Akt, and this correlated with the suppression of NF-kappaB-regulated gene products, including cyclin D1, Bcl-xL, Bcl-2, TRAF1, cIAP-1, XIAP, survivin, and vascular endothelial growth factor.	Thalidomide	51-62	vascular endothelial growth factor A	Homo sapiens	297-331
19285019-2	2009	We evaluated the effects of thalidomide-related inhibition of TNF-alpha upon the hepatic microcirculation of cirrhosis in rats.	Thalidomide	28-39	tumor necrosis factor	Rattus norvegicus	62-71
19576118-9	2009	Real-time quantitative PCR and Western blot discovered that thalidomide inhibited the expression of VEGF/HIF-1alpha of HUVEC (P &lt; 0.05).	Thalidomide	60-71	vascular endothelial growth factor A	Homo sapiens	100-104
19576118-9	2009	Real-time quantitative PCR and Western blot discovered that thalidomide inhibited the expression of VEGF/HIF-1alpha of HUVEC (P &lt; 0.05).	Thalidomide	60-71	hypoxia inducible factor 1 subunit alpha	Homo sapiens	105-115
19576118-11	2009	CONCLUSIONS: Thalidomide can suppress the expression of HIF-1alpha and VEGF in HUVEC in vitro and then inhibit angiodysplasia, which may play a significant role in stopping the rebleeding in patients with recurrent gastrointestinal bleeding.	Thalidomide	13-24	hypoxia inducible factor 1 subunit alpha	Homo sapiens	56-66
19576118-11	2009	CONCLUSIONS: Thalidomide can suppress the expression of HIF-1alpha and VEGF in HUVEC in vitro and then inhibit angiodysplasia, which may play a significant role in stopping the rebleeding in patients with recurrent gastrointestinal bleeding.	Thalidomide	13-24	vascular endothelial growth factor A	Homo sapiens	71-75
19070887-7	2009	The findings suggest that a thalidomide-based regimen may overcome the poor prognosis associated with a cyclin D1-negative or fibroblast growth factor receptor 3-positive phenotype.	Thalidomide	28-39	cyclin D1	Homo sapiens	104-113
19070887-7	2009	The findings suggest that a thalidomide-based regimen may overcome the poor prognosis associated with a cyclin D1-negative or fibroblast growth factor receptor 3-positive phenotype.	Thalidomide	28-39	fibroblast growth factor receptor 3	Homo sapiens	126-161
19098937-0	2009	In vitro anticancer property of a novel thalidomide analogue through inhibition of NF-kappaB activation in HL-60 cells.	Thalidomide	40-51	nuclear factor kappa B subunit 1	Homo sapiens	83-92
18937212-2	2009	Several inhibitors of NF-kappaB, like caffeic acid, captopril, curcumin, pyrrolidine dithiocarbamate, resveratrol, silymarin and thalidomide, have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the liver.	Thalidomide	129-140	nuclear factor kappa B subunit 1	Homo sapiens	22-31
19167733-2	2009	MATERIALS AND METHODS: A total of 159 patients were enrolled in a double-blind randomized trial to determine if thalidomide can improve the efficacy of a gonadotropin-releasing hormone agonist in hormone responsive patients with an increasing prostate specific antigen after primary definitive therapy for prostate cancer.	Thalidomide	112-123	gonadotropin releasing hormone 1	Homo sapiens	154-184
19167733-2	2009	MATERIALS AND METHODS: A total of 159 patients were enrolled in a double-blind randomized trial to determine if thalidomide can improve the efficacy of a gonadotropin-releasing hormone agonist in hormone responsive patients with an increasing prostate specific antigen after primary definitive therapy for prostate cancer.	Thalidomide	112-123	kallikrein related peptidase 3	Homo sapiens	243-268
19167733-7	2009	RESULTS: During oral phase A the median time to prostate specific antigen progression was 15 months for the thalidomide group compared to 9.6 months on placebo (p = 0.21).	Thalidomide	108-119	kallikrein related peptidase 3	Homo sapiens	48-73
19167733-8	2009	The median time to prostate specific antigen progression during oral phase B for the thalidomide group was 17.1 vs 6.6 months on placebo (p = 0.0002).	Thalidomide	85-96	kallikrein related peptidase 3	Homo sapiens	19-44
19201823-6	2009	Thalidomide significantly inhibited the TNF-alpha production in response to palmitoyl-Cys(RS)-2,3-di(palmitoyloxy) propyl)-Ala-Gly-OH (Pam(3)Cys) as a MyD88-dependent TLR2 ligand.	Thalidomide	0-11	toll-like receptor 2	Mus musculus	167-171
19201823-7	2009	Therefore, it is suggested that thalidomide might impair LPS signalling via down-regulation of MyD88 protein and mRNA and inhibit LPS-induced TNF-alpha production.	Thalidomide	32-43	myeloid differentiation primary response gene 88	Mus musculus	95-100
19201823-7	2009	Therefore, it is suggested that thalidomide might impair LPS signalling via down-regulation of MyD88 protein and mRNA and inhibit LPS-induced TNF-alpha production.	Thalidomide	32-43	tumor necrosis factor	Mus musculus	142-151
19201823-8	2009	The putative mechanism of thalidomide-induced MyD88 down-regulation is discussed.	Thalidomide	26-37	myeloid differentiation primary response gene 88	Mus musculus	46-51
19236757-0	2009	[Antiangiogenic activity of thalidomide in vitro mediated by cytochrome CYP2C19].	Thalidomide	28-39	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	72-79
19236757-7	2009	When omeprazole, a specific inhibitor of cytochrome CYP2C19, was added into the co-incubation mixture, the effects of thalidomide on cell proliferation ability, apoptosis, migration and tube formation decreased.	Thalidomide	118-129	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	52-59
19236757-8	2009	It is concluded that effect of human hepatic cell microsome is required for thalidomide"s antiangiogenic activity in vitro and cytochrome CYP2C19 may be involved in the antiangiogenic effect of thalidomide.	Thalidomide	194-205	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	138-145
19201823-0	2009	Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor-alpha production via down-regulation of MyD88 expression.	Thalidomide	0-11	myeloid differentiation primary response gene 88	Mus musculus	110-115
19201823-1	2009	The effect of thalidomide on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-alpha production was studied by using RAW 264.7 murine macrophage-like cells.	Thalidomide	14-25	tumor necrosis factor	Mus musculus	62-95
19201823-2	2009	Thalidomide significantly inhibited LPS-induced TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	48-57
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, beta	Mus musculus	101-121
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, beta	Mus musculus	123-126
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	conserved helix-loop-helix ubiquitous kinase	Mus musculus	133-155
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	inhibitor of kappaB kinase beta	Mus musculus	160-168
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	mitogen-activated protein kinase 14	Mus musculus	237-240
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	mitogen-activated protein kinase 8	Mus musculus	284-287
19201823-3	2009	Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	179-190	conserved helix-loop-helix ubiquitous kinase	Mus musculus	133-155
19201823-4	2009	The expression of myeloid differentiation factor 88 (MyD88) protein and mRNA was markedly reduced in thalidomide-treated RAW 264.7 cells but there was no significant alteration in the expression of interleukin-1 receptor-associated kinase (IRAK) 1 and TNF receptor-associated factor (TRAF) 6 in the cells.	Thalidomide	101-112	myeloid differentiation primary response gene 88	Mus musculus	18-51
19201823-4	2009	The expression of myeloid differentiation factor 88 (MyD88) protein and mRNA was markedly reduced in thalidomide-treated RAW 264.7 cells but there was no significant alteration in the expression of interleukin-1 receptor-associated kinase (IRAK) 1 and TNF receptor-associated factor (TRAF) 6 in the cells.	Thalidomide	101-112	myeloid differentiation primary response gene 88	Mus musculus	53-58
19201823-4	2009	The expression of myeloid differentiation factor 88 (MyD88) protein and mRNA was markedly reduced in thalidomide-treated RAW 264.7 cells but there was no significant alteration in the expression of interleukin-1 receptor-associated kinase (IRAK) 1 and TNF receptor-associated factor (TRAF) 6 in the cells.	Thalidomide	101-112	TNF receptor-associated factor 6	Mus musculus	252-291
19201823-6	2009	Thalidomide significantly inhibited the TNF-alpha production in response to palmitoyl-Cys(RS)-2,3-di(palmitoyloxy) propyl)-Ala-Gly-OH (Pam(3)Cys) as a MyD88-dependent TLR2 ligand.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	40-49
19201823-6	2009	Thalidomide significantly inhibited the TNF-alpha production in response to palmitoyl-Cys(RS)-2,3-di(palmitoyloxy) propyl)-Ala-Gly-OH (Pam(3)Cys) as a MyD88-dependent TLR2 ligand.	Thalidomide	0-11	myeloid differentiation primary response gene 88	Mus musculus	151-156
18687985-6	2009	Studies suggest that DKK1 activation in osteoblasts is the underlying cause of glucocorticoid- and estrogen deficiency-mediated osteoporosis, and at least partially underlies the teratogenic effects of thalidomide on limb development.	Thalidomide	202-213	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	21-25
19098937-10	2009	CONCLUSION: A novel sugar-substituted thalidomide derivative, STA-35, is potent toward HL-60 cells in vitro and induces apoptosis by the suppression of NF-kappaB activation.	Thalidomide	38-49	nuclear factor kappa B subunit 1	Homo sapiens	152-161
19067746-3	2009	In this study, the effect of different treatment regimens for MM on serum DKK-1 was evaluated and correlated with the response to treatment in 101 myeloma patients receiving bortezomib, thalidomide, lenalidomide, adriamycin and dexamethasone (AD) or high-dose chemotherapy (HDCT) followed by autologous stem cell transplantation (ASCT).	Thalidomide	186-197	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	74-79
19754423-5	2009	Typical CYP1A2 substrates generally contain planar ring that can fit the narrow and planar active site of the enzyme, such as propranolol, clozapine, guanabenz, flutamide, imatinib, thalidomide, carbamazepine, lidocaine, theophylline, tacrine, tizanidine, zolpidem, riluzole, zileuton, and leflunomide.	Thalidomide	182-193	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	8-14
18948377-0	2009	Drug interactions of thalidomide with midazolam and cyclosporine A: heterotropic cooperativity of human cytochrome P450 3A5.	Thalidomide	21-32	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	104-123
18948377-8	2009	Enhanced midazolam hydroxylation by thalidomide was also seen in liver microsomal samples harboring the CYP3A5*1 allele.	Thalidomide	36-47	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	104-110
19689289-10	2009	Moreover, we examine recent reports providing important insights into the understanding of efficacy of thalidomide and its analogs, as TNF-alpha activity inhibitories, especially in therapies of several inflammatory diseases within the nervous system.	Thalidomide	103-114	tumor necrosis factor	Homo sapiens	135-144
19067746-7	2009	Thalidomide led to a non-significant decrease in DKK-1 (1705 pg/mL vs. 1269 pg/mL, P = 0.081).	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	49-54
18691254-0	2008	Survival and outcome of blastoid variant myeloma following treatment with the novel thalidomide containing regime DT-PACE.	Thalidomide	84-95	furin, paired basic amino acid cleaving enzyme	Homo sapiens	117-121
18957334-7	2009	In addition, the systemic pretreatment with the preferential inhibitor of TNFalpha synthesis thalidomide (25 and 50 mg/kg, p.o) promoted a marked reduction of the first and second phases of formalin-evoked nociception.	Thalidomide	93-104	tumor necrosis factor	Rattus norvegicus	74-82
18621563-5	2009	The immunomodulatory effects of thalidomide are at least partially mediated through its ability to down-regulate the pathogenic over-production of tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	147-174
18621563-5	2009	The immunomodulatory effects of thalidomide are at least partially mediated through its ability to down-regulate the pathogenic over-production of tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	176-185
18621563-8	2009	Thalidomide has been shown to down-regulate the production of TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	62-71
18367123-1	2009	OBJECTIVE: To assess the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) in combination with thalidomide on prostate-specific antigen (PSA) reduction in hormone-naive prostate carcinoma (HNPC) patients with rising PSA levels after definitive local treatment.	Thalidomide	115-126	kallikrein related peptidase 3	Homo sapiens	130-161
18367123-1	2009	OBJECTIVE: To assess the efficacy of granulocyte macrophage colony-stimulating factor (GM-CSF) in combination with thalidomide on prostate-specific antigen (PSA) reduction in hormone-naive prostate carcinoma (HNPC) patients with rising PSA levels after definitive local treatment.	Thalidomide	115-126	kallikrein related peptidase 3	Homo sapiens	157-160
19152168-0	2009	Thalidomide inhibits leukemia cell invasion and migration by upregulation of early growth response gene 1.	Thalidomide	0-11	early growth response 1	Homo sapiens	77-105
19152168-2	2009	In this study, 10 microM thalidomide treatment markedly increased the expression of the early growth response gene 1 (Egr-1) at both mRNA and protein levels in HL-60 leukemic cells.	Thalidomide	25-36	early growth response 1	Homo sapiens	88-116
19152168-2	2009	In this study, 10 microM thalidomide treatment markedly increased the expression of the early growth response gene 1 (Egr-1) at both mRNA and protein levels in HL-60 leukemic cells.	Thalidomide	25-36	early growth response 1	Homo sapiens	118-123
19152168-5	2009	Our data indicated thalidomide could suppress leukemia cell invasion and migration by upregulation of Egr-1, suggesting a novel mechanism of thalidomide in the treatment of leukemia.	Thalidomide	19-30	early growth response 1	Homo sapiens	102-107
19152168-5	2009	Our data indicated thalidomide could suppress leukemia cell invasion and migration by upregulation of Egr-1, suggesting a novel mechanism of thalidomide in the treatment of leukemia.	Thalidomide	141-152	early growth response 1	Homo sapiens	102-107
19152168-6	2009	Further investigations are needed to explore the detailed mechanism of Egr-1 induction by thalidomide and the downstream pathways involved in the regulation of leukemia cell invasion.	Thalidomide	90-101	early growth response 1	Homo sapiens	71-76
18799726-5	2008	Among lenalidomide + dexamethasone-treated patients, ORR was higher in thalidomide-naive versus thalidomide-exposed patients (P = .04), with longer median TTP (P = .04) and PFS (P = .02).	Thalidomide	71-82	ZFP36 ring finger protein	Homo sapiens	155-158
18799726-11	2008	Although prior thalidomide may have contributed to inferior TTP and PFS compared with thalidomide-naive patients, these parameters remained superior compared with placebo + dexamethasone; similar benefits compared with placebo + dexamethasone were not evident for thalidomide-exposed patients in terms of overall survival.	Thalidomide	15-26	ZFP36 ring finger protein	Homo sapiens	60-63
18436450-6	2008	A promising approach is the pharmacological inhibition of tumor angiogenesis with anti-vascular endothelial growth factor (VEGF) agents, such as bevacizumab, cyclooxygenase-2 inhibitors (celecoxib), thalidomide and others.	Thalidomide	199-210	vascular endothelial growth factor A	Homo sapiens	82-121
18436450-6	2008	A promising approach is the pharmacological inhibition of tumor angiogenesis with anti-vascular endothelial growth factor (VEGF) agents, such as bevacizumab, cyclooxygenase-2 inhibitors (celecoxib), thalidomide and others.	Thalidomide	199-210	vascular endothelial growth factor A	Homo sapiens	123-127
19052974-8	2008	The number of blood mDC1 in patients taking thalidomide was also significantly higher than at relapse.	Thalidomide	44-55	mediator of DNA damage checkpoint 1	Mus musculus	20-24
18983651-9	2008	CONCLUSION: Thalidomide inhibits vasculogenic mimicry channel and mosaic vessels formation in melanoma through the regulation of vasculogenic factors, and it can induce necrosis of melanoma cells, which may be related with the NF-kappaB signaling pathway.	Thalidomide	12-23	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	227-236
19099634-0	2008	[Efficacy of different thalidomide regimens for patients with multiple myeloma and its relationship with TNF-alpha level].	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	105-114
19099634-1	2008	The study was aimed to investigate the clinical efficacy and adverse reactions of different thalidomide regimens in the treatment of multiple myeloma (MM), and to explore the relationship between efficacy of thalidomide and serum level of TNF-alpha in MM patients.	Thalidomide	208-219	tumor necrosis factor	Homo sapiens	239-248
19099634-6	2008	At the same time, serum levels of TNF-alpha in 30 cases of MM treated with thalidomide (15 cases effective and 15 cases ineffective) before and after treatment were detected by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) and were compared with the clinical efficacy.	Thalidomide	75-86	tumor necrosis factor	Homo sapiens	34-43
19099634-10	2008	At the same time, it was found that the serum levels of TNF-alpha in ineffective group treated with thalidomide were 44.7+/-5.7 pg/ml and 46.3+/-4.0 pg/ml before and after thalidomide treatment, and there was no significant difference (p&gt;0.05).	Thalidomide	100-111	tumor necrosis factor	Homo sapiens	56-65
19099634-10	2008	At the same time, it was found that the serum levels of TNF-alpha in ineffective group treated with thalidomide were 44.7+/-5.7 pg/ml and 46.3+/-4.0 pg/ml before and after thalidomide treatment, and there was no significant difference (p&gt;0.05).	Thalidomide	172-183	tumor necrosis factor	Homo sapiens	56-65
19099634-14	2008	Serum level of TNF-alpha is an indicator for finding effects of thalidomide, and plays a role in the pathogenesis of MM.	Thalidomide	64-75	tumor necrosis factor	Homo sapiens	15-24
18662673-2	2008	Thalidomide inhibited EGF-induced cell growth in mouse and human monocytic leukemia cells, RAW 264.7, U937 and THP-1.	Thalidomide	0-11	GLI family zinc finger 2	Homo sapiens	111-116
18469028-0	2008	Thalidomide reduces serum VEGF levels and improves peripheral neuropathy in POEMS syndrome.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	26-30
18662673-3	2008	Thalidomide inhibited EGF-induced phosphorylation of extracellular signal regulated kinase (ERK) 1/2, but not p38 and stress-activated protein kinase (SAPK)/JNK.	Thalidomide	0-11	mitogen-activated protein kinase 1	Homo sapiens	53-100
18662673-4	2008	The phosphorylation of MEK1/2 and Raf at Ser 338 as the upstream molecules of ERK 1/2 was also prevented by thalidomide.	Thalidomide	108-119	mitogen-activated protein kinase kinase 1	Homo sapiens	23-29
18662673-4	2008	The phosphorylation of MEK1/2 and Raf at Ser 338 as the upstream molecules of ERK 1/2 was also prevented by thalidomide.	Thalidomide	108-119	zinc fingers and homeoboxes 2	Homo sapiens	34-37
18662673-4	2008	The phosphorylation of MEK1/2 and Raf at Ser 338 as the upstream molecules of ERK 1/2 was also prevented by thalidomide.	Thalidomide	108-119	mitogen-activated protein kinase 3	Homo sapiens	78-85
18662673-6	2008	Thalidomide inhibited the Ras activation induced by lipopolysaccharide (LPS) and vascular endothelial growth factor (VEGF) as well as EGF.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	81-115
18662673-6	2008	Thalidomide inhibited the Ras activation induced by lipopolysaccharide (LPS) and vascular endothelial growth factor (VEGF) as well as EGF.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	117-121
18197140-2	2008	We tested the neuroprotective effects of thalidomide, an immunomodulatory agent that inhibits TNF-alpha production, which have not been investigated so far.	Thalidomide	41-52	tumor necrosis factor	Mus musculus	94-103
18854284-0	2008	Serum C-reactive protein at diagnosis and response to therapy is the most powerful factor predicting outcome of multiple myeloma treated with thalidomide/ anthracycline-based therapy.	Thalidomide	142-153	C-reactive protein	Homo sapiens	6-24
18854284-9	2008	CONCLUSION: Serum C-reactive protein before therapy and response after therapy are the only factors useful in identifying patients benefiting from anthracycline/thalidomide-based therapy.	Thalidomide	161-172	C-reactive protein	Homo sapiens	18-36
18701263-15	2008	TNFalpha levels in both plasma and brain were reduced following thalidomide treatment (p&lt;0.002) in arthritis group.	Thalidomide	64-75	tumor necrosis factor	Rattus norvegicus	0-8
18701263-19	2008	Thalidomide was also effective in reducing TNFalpha levels thus contributing to its antiepileptic activity.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	43-51
19176055-0	2008	[Effect of cytochrome CYP2C19 on the anti-myeloma activity of thalidomide in vitro].	Thalidomide	62-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-29
18389516-8	2008	Our structural development studies on thalidomide are reviewed focusing on recent development of tubulin polymerization inhibitors, alpha-glucosidase inhibitors, and nuclear liver X receptors antagonists.	Thalidomide	38-49	sucrase-isomaltase	Homo sapiens	132-149
18787470-13	2008	The serum concentrations of vascular endothelial growth factor and endostatin increased significantly (P=0.039 and P=0.024, respectively) after 3 months of thalidomide treatment.	Thalidomide	156-167	vascular endothelial growth factor A	Homo sapiens	28-62
18787470-13	2008	The serum concentrations of vascular endothelial growth factor and endostatin increased significantly (P=0.039 and P=0.024, respectively) after 3 months of thalidomide treatment.	Thalidomide	156-167	collagen type XVIII alpha 1 chain	Homo sapiens	67-77
18723357-2	2008	We designed and prepared a new C(60) fullerene hybrid bearing thalidomide as a potential double-action anti-inflammatory agent, capable of simultaneous inhibition of LPS-induced NO and TNF-alpha production.	Thalidomide	62-73	tumor necrosis factor	Homo sapiens	185-194
18662682-4	2008	The animals, which received thalidomide alone orally or in combination with augmentin, 30 min prior to bacterial instillation into the lungs via intranasal route, showed significant (P&lt;0.05) decrease in neutrophil influx into the lungs and there was significant (P&lt;0.05) decrease in the production of malondialdehyde, nitric oxide and myeloperoxidase activity.	Thalidomide	28-39	myeloperoxidase	Mus musculus	341-356
18670095-0	2008	Effect of thalidomide on endotoxin-induced decreases in activity and expression of hepatic cytochrome P450 3A2.	Thalidomide	10-21	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	91-110
18720539-8	2008	Expression of TM was significantly lower in the endothelial cells (EC) of the radiation group than in the control and thalidomide groups (P&lt;0.001).	Thalidomide	118-129	thrombomodulin	Rattus norvegicus	14-16
18720539-10	2008	The intensity of VEGF expression in capillaries was greater in the radiation group than in the control group and was also attenuated by thalidomide (P=0.003).	Thalidomide	136-147	vascular endothelial growth factor A	Rattus norvegicus	17-21
18670095-1	2008	Thalidomide has been reported to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) that are involved in the down-regulation of hepatic cytochrome P450 (CYP) induced by endotoxin.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	59-86
18670095-1	2008	Thalidomide has been reported to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) that are involved in the down-regulation of hepatic cytochrome P450 (CYP) induced by endotoxin.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	88-97
18670095-1	2008	Thalidomide has been reported to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) that are involved in the down-regulation of hepatic cytochrome P450 (CYP) induced by endotoxin.	Thalidomide	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	173-188
18670095-1	2008	Thalidomide has been reported to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) that are involved in the down-regulation of hepatic cytochrome P450 (CYP) induced by endotoxin.	Thalidomide	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	190-193
18670095-2	2008	In the present study, we investigated the effects of thalidomide on endotoxin-induced decreases in the activity and expression of hepatic CYP3A2 in rats.	Thalidomide	53-64	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	138-144
18670095-7	2008	Western blot analysis revealed that thalidomide had no effect on the protein levels of hepatic CYP3A2, whereas it enhanced the down-regulation of hepatic CYP3A2 by endotoxin.	Thalidomide	36-47	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	154-160
18670095-9	2008	The present findings suggest that thalidomide enhances endotoxin-induced decreases in the activity and expression of hepatic CYP3A2.	Thalidomide	34-45	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	125-131
18525301-3	2008	This study assessed whether GM-CSF would improve the response rate of MRCC patients to the thalidomide plus IL-2 regimen.	Thalidomide	91-102	colony stimulating factor 2	Homo sapiens	28-34
18687660-0	2008	The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma.	Thalidomide	100-111	fibroblast growth factor 2	Homo sapiens	50-80
18687660-4	2008	Using U-87 MG cell lines, we found that thalidomide, especially when encapsulated in a liposome, down-regulated the transcription and translation of the FGF-2 gene by interacting with G-rich regions present in the promoter and the internal ribosome entry site of its transcript at concentrations much lower than therapeutic serum concentrations.	Thalidomide	40-51	fibroblast growth factor 2	Homo sapiens	153-158
18687660-5	2008	Thalidomide treatment also dramatically suppressed the anchorage-independent growth of U-87 MG and other glioma cells by over a thousand fold without affecting its anchorage-dependent growth, which may be accomplished by knocking down endogenous bFGF expression in these cells.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	246-250
18687660-7	2008	Our data suggest that by targeting the G-rich regions of bFGF, thalidomide (at 0.1 microg/mL) can reduce cellular bFGF levels and affect tumor anchorage-independent growth, the hallmark of tumorigenicity.	Thalidomide	63-74	fibroblast growth factor 2	Homo sapiens	57-61
18687660-7	2008	Our data suggest that by targeting the G-rich regions of bFGF, thalidomide (at 0.1 microg/mL) can reduce cellular bFGF levels and affect tumor anchorage-independent growth, the hallmark of tumorigenicity.	Thalidomide	63-74	fibroblast growth factor 2	Homo sapiens	114-118
18381653-6	2008	Furthermore thalidomide, which prevents TNFalpha production, was without effect on hypoxic suppression of EAAT-1 but prevented hypoxic suppression of EAAT-2.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	40-48
18381653-6	2008	Furthermore thalidomide, which prevents TNFalpha production, was without effect on hypoxic suppression of EAAT-1 but prevented hypoxic suppression of EAAT-2.	Thalidomide	12-23	solute carrier family 1 member 2	Homo sapiens	150-156
18671617-9	2008	Thalidomide may be an ideal therapy for life-threatening hemangiomas because it inhibits new blood vessel formation by antagonizing both the bFGF and VEGF pathways and has a more acceptable toxicity profile than other agents.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	141-145
18671617-9	2008	Thalidomide may be an ideal therapy for life-threatening hemangiomas because it inhibits new blood vessel formation by antagonizing both the bFGF and VEGF pathways and has a more acceptable toxicity profile than other agents.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	150-154
18598295-10	2008	Treatment with thalidomide restored malondialdehyde as well as reduction of myeloperoxidase and tumour necrosis factor-alpha towards normal levels.	Thalidomide	15-26	myeloperoxidase	Rattus norvegicus	76-91
18536579-5	2008	Moreover, several drugs that are effective against multiple myeloma, including bortezomib, thalidomide, lenalidomide and arsenic trioxide, have been found to block activation of NF-kappaB.	Thalidomide	91-102	nuclear factor kappa B subunit 1	Homo sapiens	178-187
18549624-8	2008	The population of CD3(+) T, CD4(+) T, CD8(+) T, NK and CD4(+)CD25(+) Treg significantly increased in patients with positive response to thalidomide, but the population of CD8(+) T remained unchanged.	Thalidomide	136-147	CD4 molecule	Homo sapiens	55-58
18343940-7	2008	Thalidomide (200 mg/Kg) was administered daily intraperitoneally to control and ROP mice in two protocols: (1) from P12 to P16, and (2) from P11 to P15 .	Thalidomide	0-11	polymerase (DNA-directed), delta 4	Mus musculus	116-119
18343940-7	2008	Thalidomide (200 mg/Kg) was administered daily intraperitoneally to control and ROP mice in two protocols: (1) from P12 to P16, and (2) from P11 to P15 .	Thalidomide	0-11	cyclin dependent kinase inhibitor 2A	Mus musculus	123-126
18343940-7	2008	Thalidomide (200 mg/Kg) was administered daily intraperitoneally to control and ROP mice in two protocols: (1) from P12 to P16, and (2) from P11 to P15 .	Thalidomide	0-11	S100 calcium binding protein A10 (calpactin)	Mus musculus	141-144
18343940-7	2008	Thalidomide (200 mg/Kg) was administered daily intraperitoneally to control and ROP mice in two protocols: (1) from P12 to P16, and (2) from P11 to P15 .	Thalidomide	0-11	cyclin dependent kinase inhibitor 2B	Mus musculus	148-151
18549624-0	2008	[Effects of thalidomide on CD4(+)CD25(+) T regulatory cells in patients with multiple myeloma].	Thalidomide	12-23	CD4 molecule	Homo sapiens	27-30
18549624-1	2008	The study was purposed to explore the changes of CD4(+)CD25(+) T regulatory cells in patients with multiple myeloma before and (MM) after treatment with thalidomide so as to provide evidences for effective immunotherapy.	Thalidomide	153-164	CD4 molecule	Homo sapiens	49-52
18549624-9	2008	It is concluded that the significant increase of CD4(+)CD25(+) regulatory T cells in peripheral blood of patients with MM is concerned with the MM pathogenesis; thalidomide may exert its anti-MM effects by down-regulating CD4(+)CD25(+) Treg.	Thalidomide	161-172	CD4 molecule	Homo sapiens	49-52
18549624-6	2008	The population of CD4(+)CD25(+ high) Treg cells in patients with response to thalidomide was significantly decreased (p &lt; 0.01), but the population of these cells in patients without response not changed significantly (p &gt; 0.05), as compared with patients before treatment.	Thalidomide	77-88	CD4 molecule	Homo sapiens	18-21
18549624-8	2008	The population of CD3(+) T, CD4(+) T, CD8(+) T, NK and CD4(+)CD25(+) Treg significantly increased in patients with positive response to thalidomide, but the population of CD8(+) T remained unchanged.	Thalidomide	136-147	CD4 molecule	Homo sapiens	28-31
18549624-8	2008	The population of CD3(+) T, CD4(+) T, CD8(+) T, NK and CD4(+)CD25(+) Treg significantly increased in patients with positive response to thalidomide, but the population of CD8(+) T remained unchanged.	Thalidomide	136-147	CD8a molecule	Homo sapiens	38-41
18549624-9	2008	It is concluded that the significant increase of CD4(+)CD25(+) regulatory T cells in peripheral blood of patients with MM is concerned with the MM pathogenesis; thalidomide may exert its anti-MM effects by down-regulating CD4(+)CD25(+) Treg.	Thalidomide	161-172	CD4 molecule	Homo sapiens	222-225
18325608-0	2008	Restraining tumor necrosis factor-alpha by thalidomide prevents the amyloid beta-induced impairment of recognition memory in mice.	Thalidomide	43-54	tumor necrosis factor	Mus musculus	12-39
19040069-1	2008	OBJECTIVE: To evaluate the effects of four agents including cyclophosphamide, thalidomide, total glucosides of peony (TGP) and simvastatin on cell-proliferation and endothelin-1 secretion of human endothelial cells (ECs).	Thalidomide	78-89	endothelin 1	Homo sapiens	165-177
18325608-8	2008	Daily treatment with thalidomide (20 mg/kg), a preferential degrader of TNF-alpha mRNA, or i.c.v.-injection of an anti-TNF-alpha antibody (10 etag/mouse) prevented the nitration of proteins in the hippocampus and the impairment of recognition memory induced by Abeta(25-35) or Abeta(1-40) in mice.	Thalidomide	21-32	tumor necrosis factor	Mus musculus	72-81
18325608-8	2008	Daily treatment with thalidomide (20 mg/kg), a preferential degrader of TNF-alpha mRNA, or i.c.v.-injection of an anti-TNF-alpha antibody (10 etag/mouse) prevented the nitration of proteins in the hippocampus and the impairment of recognition memory induced by Abeta(25-35) or Abeta(1-40) in mice.	Thalidomide	21-32	amyloid beta (A4) precursor protein	Mus musculus	261-266
18953944-1	2008	OBJECTIVE: To investigate the release and intracellular localization of high mobility group box chromosomal protein 1 (HMGB1) in the peripheral blood monocytes of rheumatoid arthritis (RA) patients and the inhibitive effect of thalidomide.	Thalidomide	227-238	structure specific recognition protein 1	Homo sapiens	72-95
18953944-10	2008	Thalidomide (40 microg/ml) could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFalpha (P &lt; 0.05).	Thalidomide	0-11	high mobility group box 1	Homo sapiens	56-61
18953944-10	2008	Thalidomide (40 microg/ml) could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFalpha (P &lt; 0.05).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	112-120
18418038-5	2008	We extend this model by presenting new data demonstrating an involvement of the transcription factors Tbx5 and Sall4 in thalidomide-induced molecular pathology.	Thalidomide	120-131	T-box transcription factor 5	Homo sapiens	102-106
18418038-5	2008	We extend this model by presenting new data demonstrating an involvement of the transcription factors Tbx5 and Sall4 in thalidomide-induced molecular pathology.	Thalidomide	120-131	spalt like transcription factor 4	Homo sapiens	111-116
18953944-12	2008	Treatment with TNFalpha (100 ng/ml) for 24 hours resulted in a cytoplasmic translocation of HMGB1, which was inhibited significantly by thalidomide.	Thalidomide	136-147	tumor necrosis factor	Homo sapiens	15-23
18953944-1	2008	OBJECTIVE: To investigate the release and intracellular localization of high mobility group box chromosomal protein 1 (HMGB1) in the peripheral blood monocytes of rheumatoid arthritis (RA) patients and the inhibitive effect of thalidomide.	Thalidomide	227-238	high mobility group box 1	Homo sapiens	119-124
18953944-12	2008	Treatment with TNFalpha (100 ng/ml) for 24 hours resulted in a cytoplasmic translocation of HMGB1, which was inhibited significantly by thalidomide.	Thalidomide	136-147	high mobility group box 1	Homo sapiens	92-97
17786465-1	2008	BACKGROUND: To evaluate the effects of thalidomide treatment on the temporal course of TNF-alpha, VEGF production and the histopathological changes in ischemia/reperfusion (I/R) injured guinea pigs retina.	Thalidomide	39-50	tumor necrosis factor	Cavia porcellus	87-96
18953944-13	2008	CONCLUSION: TNFalpha induces the release and cytoplasmic translocation of HMGB1 in the peripheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.	Thalidomide	133-144	high mobility group box 1	Homo sapiens	74-79
18953944-13	2008	CONCLUSION: TNFalpha induces the release and cytoplasmic translocation of HMGB1 in the peripheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.	Thalidomide	133-144	high mobility group box 1	Homo sapiens	187-192
18034203-7	2008	These results suggest that thalidomide tends to decrease TNF-alpha receptor levels, CD8/CD11b+ T cells and natural killer cells in early treatment and increases CD4+CD45RO+ memory T and gammadelta+ T cells later in BD.	Thalidomide	27-38	CD8a molecule	Homo sapiens	84-87
18034203-7	2008	These results suggest that thalidomide tends to decrease TNF-alpha receptor levels, CD8/CD11b+ T cells and natural killer cells in early treatment and increases CD4+CD45RO+ memory T and gammadelta+ T cells later in BD.	Thalidomide	27-38	integrin subunit alpha M	Homo sapiens	88-93
18034203-7	2008	These results suggest that thalidomide tends to decrease TNF-alpha receptor levels, CD8/CD11b+ T cells and natural killer cells in early treatment and increases CD4+CD45RO+ memory T and gammadelta+ T cells later in BD.	Thalidomide	27-38	CD4 molecule	Homo sapiens	161-164
18343126-2	2008	On this basis, we have already developed novel LXR antagonists based upon alpha-glucosidase inhibitors derived from thalidomide.	Thalidomide	116-127	sucrase-isomaltase	Homo sapiens	74-91
18070197-1	2008	OBJECTIVE: To investigate how thalidomide confers its survival benefit in prostate cancer, by assessing its effect on circulating endothelial cells (CECs) and progenitors (CEPs) in a combined therapy of thalidomide and chemotherapy drugs in a human prostate cancer xenograft model, as in clinical trials patients treated with both thalidomide and docetaxel had a &gt;50% decrease in prostate-specific antigen (PSA) levels and longer median overall survival than those treated with docetaxel monotherapy.	Thalidomide	30-41	kallikrein related peptidase 3	Homo sapiens	383-414
17473922-4	2008	Thalidomide is an anti-inflammatory agent that potentiates the anti-tumour activity of DMXAA but decreases induction of TNF in plasma.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	120-123
17473922-17	2008	Co-administration of thalidomide increases the effective dose of DMXAA by reducing clearance but also, by inhibiting production of circulating TNF, reduces the host toxicity of DMXAA.	Thalidomide	21-32	tumor necrosis factor	Mus musculus	143-146
17786465-1	2008	BACKGROUND: To evaluate the effects of thalidomide treatment on the temporal course of TNF-alpha, VEGF production and the histopathological changes in ischemia/reperfusion (I/R) injured guinea pigs retina.	Thalidomide	39-50	Vegfa	Cavia porcellus	98-102
17786465-8	2008	The thalidomide/ischemia group retinal VEGF level was significantly lower versus the ischemia group.	Thalidomide	4-15	Vegfa	Cavia porcellus	39-43
17786465-10	2008	Also, the retinal TNF-alpha level was significantly lower in the thalidomide/ischemia group versus the ischemia group.	Thalidomide	65-76	tumor necrosis factor	Cavia porcellus	18-27
17786465-13	2008	CONCLUSION: Thalidomide treatment decreases PMNL infiltration, retinal edema, VEGF, and TNF-alpha synthesis following I/R injury to the guinea pig retina.	Thalidomide	12-23	Vegfa	Cavia porcellus	78-82
17786465-13	2008	CONCLUSION: Thalidomide treatment decreases PMNL infiltration, retinal edema, VEGF, and TNF-alpha synthesis following I/R injury to the guinea pig retina.	Thalidomide	12-23	tumor necrosis factor	Cavia porcellus	88-97
18291259-13	2008	The expression of mRNA for Fas, caspase-3, and Bax of cholangiocarcinoma in the thalidomide-treated rats was greater than for saline-treated rats.	Thalidomide	80-91	caspase 3	Rattus norvegicus	32-41
18291259-13	2008	The expression of mRNA for Fas, caspase-3, and Bax of cholangiocarcinoma in the thalidomide-treated rats was greater than for saline-treated rats.	Thalidomide	80-91	BCL2 associated X, apoptosis regulator	Rattus norvegicus	47-50
18291259-15	2008	The expression of TNFalpha and TGFbeta1 of soleus muscles for thalidomide-treated rats was less than for saline-treated rats.	Thalidomide	62-73	tumor necrosis factor	Rattus norvegicus	18-26
18291259-15	2008	The expression of TNFalpha and TGFbeta1 of soleus muscles for thalidomide-treated rats was less than for saline-treated rats.	Thalidomide	62-73	transforming growth factor, beta 1	Rattus norvegicus	31-39
18291259-16	2008	CONCLUSIONS: Using our rat cholangiocarcinoma model, we demonstrated that thalidomide inhibited tumor growth and was associated with a decrease in expression of reduced eIF4E and VEGF expression; in addition, thalidomide preserved fast-twitch skeletal muscle fibers and was associated with decreased expression of TNFalpha and TGFbeta1.	Thalidomide	74-85	eukaryotic translation initiation factor 4E	Rattus norvegicus	169-174
18291259-16	2008	CONCLUSIONS: Using our rat cholangiocarcinoma model, we demonstrated that thalidomide inhibited tumor growth and was associated with a decrease in expression of reduced eIF4E and VEGF expression; in addition, thalidomide preserved fast-twitch skeletal muscle fibers and was associated with decreased expression of TNFalpha and TGFbeta1.	Thalidomide	74-85	vascular endothelial growth factor A	Rattus norvegicus	179-183
18291259-16	2008	CONCLUSIONS: Using our rat cholangiocarcinoma model, we demonstrated that thalidomide inhibited tumor growth and was associated with a decrease in expression of reduced eIF4E and VEGF expression; in addition, thalidomide preserved fast-twitch skeletal muscle fibers and was associated with decreased expression of TNFalpha and TGFbeta1.	Thalidomide	74-85	tumor necrosis factor	Rattus norvegicus	314-322
18291259-16	2008	CONCLUSIONS: Using our rat cholangiocarcinoma model, we demonstrated that thalidomide inhibited tumor growth and was associated with a decrease in expression of reduced eIF4E and VEGF expression; in addition, thalidomide preserved fast-twitch skeletal muscle fibers and was associated with decreased expression of TNFalpha and TGFbeta1.	Thalidomide	74-85	transforming growth factor, beta 1	Rattus norvegicus	327-335
17964176-0	2008	Thalidomide inhibition of perturbed vasculature and glial-derived tumor necrosis factor-alpha in an animal model of inflamed Alzheimer"s disease brain.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	66-93
17618052-0	2008	Thalidomide decreases the plasma levels of IL-1 and TNF following burn injury: is it a new drug for modulation of systemic inflammatory response.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	52-55
17618052-3	2008	Thalidomide has been shown to decrease the secretion of TNF from phagocytic cells, therefore suppression of TNF and IL-1 production from activated phagocytic cells might be a successful treatment modality for prevention of systemic inflammatory response following severe burn.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	56-59
17618052-3	2008	Thalidomide has been shown to decrease the secretion of TNF from phagocytic cells, therefore suppression of TNF and IL-1 production from activated phagocytic cells might be a successful treatment modality for prevention of systemic inflammatory response following severe burn.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	108-111
17618052-4	2008	To address this issue, we aimed to show whether thalidomide treatment decreased or suppressed plasma levels of TNF and IL-1 following burn in rats.	Thalidomide	48-59	tumor necrosis factor	Rattus norvegicus	111-114
17618052-7	2008	Thalidomide treatment decreased TNF and IL-1 significantly in both experimental groups at both the points (P&lt;0.05).	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	32-35
17618052-8	2008	Although in this study we just showed inhibitory effect of thalidomide on plasma the level of TNF and IL-1, we speculate that thalidomide may have modulatory effect on the systemic inflammatory response after burn by decreasing plasma levels of TNF and IL-1.	Thalidomide	59-70	tumor necrosis factor	Rattus norvegicus	94-97
17618052-8	2008	Although in this study we just showed inhibitory effect of thalidomide on plasma the level of TNF and IL-1, we speculate that thalidomide may have modulatory effect on the systemic inflammatory response after burn by decreasing plasma levels of TNF and IL-1.	Thalidomide	126-137	tumor necrosis factor	Rattus norvegicus	245-248
17964176-4	2008	Thalidomide inhibition of the glial-derived proinflammatory/angiogenic factor TNF-alpha (tumor necrosis factor-alpha) in Abeta(1-42)-injected brain and also in vitro from peptide-activated human microglia could underly the changes in vascular processes.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	89-116
17964176-6	2008	Our findings suggest altered cerebral vasculature as an integral component of inflammatory responses with thalidomide an effective inhibitor of gliosis, vascular changes and TNF-alpha leading to neuroprotection in an animal model of inflamed AD brain.	Thalidomide	106-117	tumor necrosis factor	Homo sapiens	174-183
17964176-2	2008	We report the anti-angiogenic and anti-inflammatory compound, thalidomide, to significantly inhibit peptide-induced vascular changes including endothelial cell proliferation (marker rat endothelial cell antigen-1, RECA-1), angiogenic activity (marker laminin) and leakiness of blood-brain barrier (BBB, marker albumin).	Thalidomide	62-73	albumin	Rattus norvegicus	310-317
17964176-4	2008	Thalidomide inhibition of the glial-derived proinflammatory/angiogenic factor TNF-alpha (tumor necrosis factor-alpha) in Abeta(1-42)-injected brain and also in vitro from peptide-activated human microglia could underly the changes in vascular processes.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	78-87
18178729-0	2008	Thalidomide induces limb anomalies by PTEN stabilization, Akt suppression, and stimulation of caspase-dependent cell death.	Thalidomide	0-11	phosphatase and tensin homolog	Homo sapiens	38-42
18668392-0	2008	Thalidomide suppressed IL-1beta while enhancing TNF-alpha and IL-10, when cells in whole blood were stimulated with lipopolysaccharide.	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	23-31
18668392-0	2008	Thalidomide suppressed IL-1beta while enhancing TNF-alpha and IL-10, when cells in whole blood were stimulated with lipopolysaccharide.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	48-57
18668392-0	2008	Thalidomide suppressed IL-1beta while enhancing TNF-alpha and IL-10, when cells in whole blood were stimulated with lipopolysaccharide.	Thalidomide	0-11	interleukin 10	Homo sapiens	62-67
18668392-3	2008	Thalidomide"s ability to inhibit tumor necrosis factor alpha (TNF-alpha) in vitro has been proposed as a partial explanation of its effective treatment of ENL.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	33-60
18668392-3	2008	Thalidomide"s ability to inhibit tumor necrosis factor alpha (TNF-alpha) in vitro has been proposed as a partial explanation of its effective treatment of ENL.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	62-71
18668392-4	2008	In in vitro assays, thalidomide can enhance or suppress TNF-alpha.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	56-65
18668392-7	2008	Thalidomide suppressed interleukin 1 beta (IL-1beta) (p = 0.007), and it enhanced TNF-alpha (p = 0.007) and interleukin 10 (IL-10) (p = 0.031).	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	23-41
18668392-7	2008	Thalidomide suppressed interleukin 1 beta (IL-1beta) (p = 0.007), and it enhanced TNF-alpha (p = 0.007) and interleukin 10 (IL-10) (p = 0.031).	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	43-51
18668392-7	2008	Thalidomide suppressed interleukin 1 beta (IL-1beta) (p = 0.007), and it enhanced TNF-alpha (p = 0.007) and interleukin 10 (IL-10) (p = 0.031).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	82-91
18668392-7	2008	Thalidomide suppressed interleukin 1 beta (IL-1beta) (p = 0.007), and it enhanced TNF-alpha (p = 0.007) and interleukin 10 (IL-10) (p = 0.031).	Thalidomide	0-11	interleukin 10	Homo sapiens	108-122
18668392-7	2008	Thalidomide suppressed interleukin 1 beta (IL-1beta) (p = 0.007), and it enhanced TNF-alpha (p = 0.007) and interleukin 10 (IL-10) (p = 0.031).	Thalidomide	0-11	interleukin 10	Homo sapiens	124-129
17638016-8	2008	Treatment 1 h before IFS injection with etoricoxib, indomethacin, thalidomide, and pentoxifylline reduced COX-2 expression and some macroscopic and microscopic parameters in IFS-induced HC.	Thalidomide	66-77	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	106-111
18178729-0	2008	Thalidomide induces limb anomalies by PTEN stabilization, Akt suppression, and stimulation of caspase-dependent cell death.	Thalidomide	0-11	AKT serine/threonine kinase 1	Homo sapiens	58-61
18178729-3	2008	Here we demonstrate in primary human embryonic cells and in the chicken embryo that thalidomide-induced signaling through bone morphogenetic proteins (Bmps) protects active PTEN from proteasomal degradation, resulting in suppression of Akt signaling.	Thalidomide	84-95	phosphatase and tensin homolog	Gallus gallus	173-177
18178729-3	2008	Here we demonstrate in primary human embryonic cells and in the chicken embryo that thalidomide-induced signaling through bone morphogenetic proteins (Bmps) protects active PTEN from proteasomal degradation, resulting in suppression of Akt signaling.	Thalidomide	84-95	AKT serine/threonine kinase 1	Homo sapiens	236-239
18178729-5	2008	Most importantly, thalidomide-induced limb deformities and microphthalmia in chicken embryos could be rescued by a pharmacological PTEN inhibitor as well as by insulin, a stimulant of Akt signaling.	Thalidomide	18-29	phosphatase and tensin homolog	Gallus gallus	131-135
18178729-5	2008	Most importantly, thalidomide-induced limb deformities and microphthalmia in chicken embryos could be rescued by a pharmacological PTEN inhibitor as well as by insulin, a stimulant of Akt signaling.	Thalidomide	18-29	insulin	Gallus gallus	160-167
18178729-5	2008	Most importantly, thalidomide-induced limb deformities and microphthalmia in chicken embryos could be rescued by a pharmacological PTEN inhibitor as well as by insulin, a stimulant of Akt signaling.	Thalidomide	18-29	AKT serine/threonine kinase 1	Homo sapiens	184-187
18178729-6	2008	We therefore conclude that perturbation of PTEN/Akt signaling and stimulation of caspase activity is central to the teratogenic effects of thalidomide.	Thalidomide	139-150	phosphatase and tensin homolog	Homo sapiens	43-47
18178729-6	2008	We therefore conclude that perturbation of PTEN/Akt signaling and stimulation of caspase activity is central to the teratogenic effects of thalidomide.	Thalidomide	139-150	AKT serine/threonine kinase 1	Homo sapiens	48-51
18246603-3	2008	Recently, it has been shown that TNF-[alpha] may be a novel target for the treatment of acute pancreatitis; but the role of thalidomide, an immunomodulatory agent that inhibits TNF-(alpha) and angiogenesis, has not been investigated so far.	Thalidomide	124-135	tumor necrosis factor	Mus musculus	177-188
17851074-0	2007	Synthesis and TNF expression inhibitory properties of new thalidomide analogues derived via Heck cross coupling.	Thalidomide	58-69	tumor necrosis factor	Homo sapiens	14-17
17710103-8	2007	CONCLUSION: Thalidomide is an immunomodulatory agent that acts to inhibit production of tumor-necrosis factor-alpha (TNF-alpha), an important mediator in CNS inflammation, by enhancing TNF-alpha mRNA degradation.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	88-115
17710103-8	2007	CONCLUSION: Thalidomide is an immunomodulatory agent that acts to inhibit production of tumor-necrosis factor-alpha (TNF-alpha), an important mediator in CNS inflammation, by enhancing TNF-alpha mRNA degradation.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	117-126
17710103-8	2007	CONCLUSION: Thalidomide is an immunomodulatory agent that acts to inhibit production of tumor-necrosis factor-alpha (TNF-alpha), an important mediator in CNS inflammation, by enhancing TNF-alpha mRNA degradation.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	185-194
17916085-0	2007	Downregulation of neuropilin-1 in patients with acute myeloid leukemia treated with thalidomide.	Thalidomide	84-95	neuropilin 1	Homo sapiens	18-30
17916085-5	2007	Under thalidomide treatment, a marked difference in the course of NRP-1 expression between responders and non-responders was observed, however, without a statistical significance (P = 0.071) being reached.	Thalidomide	6-17	neuropilin 1	Homo sapiens	66-71
17916085-6	2007	Additionally, a significant correlation of the NRP-1 expression level to microvessel density could be detected under treatment with thalidomide (P = 0.018).	Thalidomide	132-143	neuropilin 1	Homo sapiens	47-52
17916085-8	2007	Additionally, our results suggest that thalidomide-induced antileukemic properties might at least in part be mediated by NRP-1 downregulation.	Thalidomide	39-50	neuropilin 1	Homo sapiens	121-126
17557286-8	2007	Furthermore, we could show that antiangiogenic effects of thalidomide are related to tumor-cell derived factors including vascular endothelial growth factor, basic fibroblast growth factor, hepatocyte growth factor and Il-8 some known and with, granulocyte colony stimulating growth factor and granulocyte macrophage colony stimulating growth factor, some new target molecules of thalidomide.	Thalidomide	58-69	fibroblast growth factor 2	Mus musculus	158-188
17534579-6	2007	Cisplatin combined with thalidomide caused a significant decrease in vascular endothelial growth factor (VEGF) levels by 73% in intracranial tumors (P &lt; 0.05) and by 50% in subcutaneous tumors (P &lt; 0.05) and caused the level of active hepatic growth factor (a-HGF) to double in both the subcutaneous and intracranial tumors (P &lt; 0.05), suggesting this treatment altered the vasculature in these tumors.	Thalidomide	24-35	vascular endothelial growth factor A	Rattus norvegicus	69-103
17534579-6	2007	Cisplatin combined with thalidomide caused a significant decrease in vascular endothelial growth factor (VEGF) levels by 73% in intracranial tumors (P &lt; 0.05) and by 50% in subcutaneous tumors (P &lt; 0.05) and caused the level of active hepatic growth factor (a-HGF) to double in both the subcutaneous and intracranial tumors (P &lt; 0.05), suggesting this treatment altered the vasculature in these tumors.	Thalidomide	24-35	vascular endothelial growth factor A	Rattus norvegicus	105-109
18050580-5	2007	Thalidomide"s mechanism of action in RAUs still is not understood completely, but it appears to be mediated by inhibition of the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	155-182
18050580-5	2007	Thalidomide"s mechanism of action in RAUs still is not understood completely, but it appears to be mediated by inhibition of the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	184-193
17964516-0	2007	Thalidomide suppressed interleukin-6 but not tumor necrosis factor-alpha in volunteers with experimental endotoxemia.	Thalidomide	0-11	interleukin 6	Homo sapiens	23-36
17964516-1	2007	An early rationale for using thalidomide to treat erythema nodosum leprosum had been based on some reports that it suppresses tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	29-40	tumor necrosis factor	Homo sapiens	126-153
17964516-1	2007	An early rationale for using thalidomide to treat erythema nodosum leprosum had been based on some reports that it suppresses tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	29-40	tumor necrosis factor	Homo sapiens	155-164
17964516-2	2007	However, in vivo and in vitro studies have yielded variable results, having shown that thalidomide can either enhance or suppress TNF-alpha.	Thalidomide	87-98	tumor necrosis factor	Homo sapiens	130-139
17964516-11	2007	Using the area under the dose response curve (AUC(0 to 24) h), thalidomide reduced the AUC for IL-6 by 56%, for IL-8 by 30%, and TNF-alpha by 32%.	Thalidomide	63-74	interleukin 6	Homo sapiens	95-99
17964516-11	2007	Using the area under the dose response curve (AUC(0 to 24) h), thalidomide reduced the AUC for IL-6 by 56%, for IL-8 by 30%, and TNF-alpha by 32%.	Thalidomide	63-74	C-X-C motif chemokine ligand 8	Homo sapiens	112-116
17964516-11	2007	Using the area under the dose response curve (AUC(0 to 24) h), thalidomide reduced the AUC for IL-6 by 56%, for IL-8 by 30%, and TNF-alpha by 32%.	Thalidomide	63-74	tumor necrosis factor	Homo sapiens	129-138
17964516-12	2007	In this model, thalidomide did not suppress TNF-alpha or IL-8, but it did suppress IL-6 at 4-h postinfusion with lipopolysaccharide (P=0.004), at 6 h (P=0.014), at 12 h (P=0.001), and at 16 h (P=0.012).	Thalidomide	15-26	interleukin 6	Homo sapiens	83-87
17620452-0	2007	Thalidomide induces gamma-globin gene expression through increased reactive oxygen species-mediated p38 MAPK signaling and histone H4 acetylation in adult erythropoiesis.	Thalidomide	0-11	mitogen-activated protein kinase 14	Homo sapiens	100-103
17620452-1	2007	Although thalidomide has been shown to improve anemia in some patients with myelodysplastic syndromes and stimulates erythropoietin in patients with multiple myeloma, thalidomide"s specific effects on gamma-globin gene expression during erythroid differentiation have not been studied.	Thalidomide	9-20	erythropoietin	Homo sapiens	117-131
17557286-8	2007	Furthermore, we could show that antiangiogenic effects of thalidomide are related to tumor-cell derived factors including vascular endothelial growth factor, basic fibroblast growth factor, hepatocyte growth factor and Il-8 some known and with, granulocyte colony stimulating growth factor and granulocyte macrophage colony stimulating growth factor, some new target molecules of thalidomide.	Thalidomide	58-69	chemokine (C-X-C motif) ligand 15	Mus musculus	219-223
17635852-7	2007	Furthermore, thalidomide increased renal expression of endothelial NO synthase and decreased tumor necrosis factor-alpha and renal inflammation but did not decrease oxidative stress.	Thalidomide	13-24	tumor necrosis factor	Sus scrofa	93-120
17620452-1	2007	Although thalidomide has been shown to improve anemia in some patients with myelodysplastic syndromes and stimulates erythropoietin in patients with multiple myeloma, thalidomide"s specific effects on gamma-globin gene expression during erythroid differentiation have not been studied.	Thalidomide	167-178	erythropoietin	Homo sapiens	117-131
17620452-5	2007	Western blot analysis demonstrated that thalidomide activated the p38 mitogen-activated protein kinase (MAPK) signaling pathway in a time- and dose-dependent manner and increased histone H4 acetylation.	Thalidomide	40-51	mitogen-activated protein kinase 14	Homo sapiens	66-102
17620452-6	2007	Pretreatment of cells with the antioxidant enzyme catalase and the intracellular hydroxyl scavenger dimethylthiourea (DMTU) abrogated the thalidomide-induced p38 MAPK activation and histone H4 acetylation.	Thalidomide	138-149	mitogen-activated protein kinase 14	Homo sapiens	158-161
17620452-8	2007	These data indicate that thalidomide induces increased expression of the gamma-globin gene via ROS-dependent activation of the p38 MAPK signaling pathway and histone H4 acetylation.	Thalidomide	25-36	mitogen-activated protein kinase 14	Homo sapiens	127-130
17514648-3	2007	The purpose was to test if thalidomide can inhibit 13-cis RA-induced HOXB7 expression and whether thalidomide may enhance the antiproliferative effect of 13-cis RA in U343MG glioblastoma cells.	Thalidomide	27-38	homeobox B7	Homo sapiens	69-74
18399167-0	2007	[Effect of CYP2C19 gene polymorphism on efficacy of thalidomide-based regimens for the treatment of multiple myeloma].	Thalidomide	52-63	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	11-18
18399167-8	2007	CONCLUSION: CYP2C19 genotype has no difference between MM patients and healthy person, but exhibits an effect on the treatment efficacy of thalidomide for MM.	Thalidomide	139-150	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
17514648-4	2007	Quantitative real-time PCR showed significant inhibition of 13-cis RA-induced HOXB7 expression by thalidomide with IC(50) approximately 0.1-0.2 microg/ml when given simultaneously with 13-cis RA but not when administered 18 h later (p &lt; 0.0001).	Thalidomide	98-109	homeobox B7	Homo sapiens	78-83
17514648-7	2007	It is concluded that thalidomide inhibits the RA-induced HOXB7 expression in glioblastoma cells and that 13-cis RA/thalidomide combinations can in principle enhance cytotoxicity.	Thalidomide	21-32	homeobox B7	Homo sapiens	57-62
17724360-2	2007	SUMMARY: Lenalidomide is an analogue of thalidomide and has been shown to be more potent than thalidomide in the stimulation of T-cell, interleukin-2, and interferon-gamma production.	Thalidomide	94-105	interleukin 2	Homo sapiens	136-149
17724360-2	2007	SUMMARY: Lenalidomide is an analogue of thalidomide and has been shown to be more potent than thalidomide in the stimulation of T-cell, interleukin-2, and interferon-gamma production.	Thalidomide	94-105	interferon gamma	Homo sapiens	155-171
17666363-0	2007	Polymorphisms of CYP2C19 gene are associated with the efficacy of thalidomide based regimens in multiple myeloma.	Thalidomide	66-77	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	17-24
17908040-10	2007	However, thalidomide, a small molecule drug, can inhibit TNF-alpha protein synthesis and, unlike larger molecules, is readily capable of crossing the blood-brain barrier.	Thalidomide	9-20	tumor necrosis factor	Homo sapiens	57-66
17908040-11	2007	Thus thalidomide and its analogs are excellent candidate agents for use in determining the potential value of anti-TNF-alpha therapies in a variety of diseases underpinned by inflammation within the nervous system.	Thalidomide	5-16	tumor necrosis factor	Homo sapiens	115-124
17908040-13	2007	Additionally, we consider the utilization of thalidomide-derived agents as anti-TNF-alpha therapeutics in the setting of neuroinflammation.	Thalidomide	45-56	tumor necrosis factor	Homo sapiens	80-89
17666363-5	2007	For the first time, our primary data suggested that the polymorphisms of CYP2C19 gene are associated with the efficacy of thalidomide based regimens in MM.	Thalidomide	122-133	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-80
17597196-13	2007	Treatment with thalidomide was associated with a significant decrease in plasma bFGF (p=0.008) and serum sEPCR (p=0.006), but not in plasma VEGF.	Thalidomide	15-26	fibroblast growth factor 2	Homo sapiens	80-84
17547733-0	2007	Deep vein thrombosis occurring on treatment of patients receiving thalidomide with erythropoietin.	Thalidomide	66-77	erythropoietin	Homo sapiens	83-97
17581613-4	2007	Among those mobilized with granulocyte-colony stimulating factor (G-CSF) alone, there was a significant decrease in total CD34(+) cells collected (P&lt;0.001), average daily collection (P&lt;0.001), day 1 collection (P&lt;0.001) and increased number of aphereses (P=0.004) in patients treated with lenalidomide compared to those receiving dexamethasone, thalidomide-dexamethasone or VAD.	Thalidomide	354-365	colony stimulating factor 3	Homo sapiens	27-64
17581613-4	2007	Among those mobilized with granulocyte-colony stimulating factor (G-CSF) alone, there was a significant decrease in total CD34(+) cells collected (P&lt;0.001), average daily collection (P&lt;0.001), day 1 collection (P&lt;0.001) and increased number of aphereses (P=0.004) in patients treated with lenalidomide compared to those receiving dexamethasone, thalidomide-dexamethasone or VAD.	Thalidomide	354-365	colony stimulating factor 3	Homo sapiens	66-71
17498949-1	2007	Alpha-glucosidase inhibitors with a chlorinated phthalimide or a thiophthalimide skeleton, derived from thalidomide, were found to possess liver X receptor (LXR) antagonistic activity.	Thalidomide	104-115	sucrase-isomaltase	Homo sapiens	0-17
17437439-13	2007	The combination of estramustine, docetaxel and thalidomide is an advantageous treatment in pre-clinical models of prostate cancer and is a safe, tolerable and active regimen in patients with AIPC.	Thalidomide	47-58	PDZ domain containing 2	Homo sapiens	191-195
17255354-5	2007	Despite its role as a tumor suppressor and mediator of apoptosis in other cell types including osteoblasts, our data suggest that DKK1, a stress-responsive gene in MM, does not mediate apoptotic signaling, is not activated by TP53, and its forced overexpression could not inhibit cell growth or sensitize MM cells to apoptosis following treatment with thalidomide or lenalidomide.	Thalidomide	352-363	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	130-134
17579094-5	2007	Thalidomide (Thal) has been used in the treatment of multiple myeloma through the inhibitory effect on IL-6-dependent cell growth and angiogenesis.	Thalidomide	0-11	interleukin 6	Mus musculus	103-107
17579094-5	2007	Thalidomide (Thal) has been used in the treatment of multiple myeloma through the inhibitory effect on IL-6-dependent cell growth and angiogenesis.	Thalidomide	0-4	interleukin 6	Mus musculus	103-107
17352720-4	2007	Thalidomide, a tumor necrosis factor-alpha antagonist, has been suggested as an alternative treatment option for recalcitrant prurigo nodularis.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	15-42
17940990-13	2007	Due to the progression of the disease, a thalidomide was used in therapy (it is anti-VEGF agent).	Thalidomide	41-52	vascular endothelial growth factor A	Homo sapiens	85-89
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	130-134
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	glycogen synthase kinase 3 beta	Homo sapiens	140-148
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	catenin beta 1	Homo sapiens	152-164
17283219-6	2007	Thalidomide-induced cell death was dramatically reduced in HEFs and in embryonic limb buds by the use of inhibitors against Bmps, Dkk1, and Gsk3beta, a beta-catenin antagonist acting downstream of Dkk1 in the Wnt pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	197-201
17283219-7	2007	Most interestingly, blocking of Dkk1 or Gsk3beta dramatically counteracts thalidomide-induced limb truncations and microphthalmia.	Thalidomide	74-85	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	32-36
17283219-7	2007	Most interestingly, blocking of Dkk1 or Gsk3beta dramatically counteracts thalidomide-induced limb truncations and microphthalmia.	Thalidomide	74-85	glycogen synthase kinase 3 beta	Homo sapiens	40-48
17283219-8	2007	From this, we conclude that perturbing of Bmp/Dkk1/Wnt signaling is central to the teratogenic effects of thalidomide.	Thalidomide	106-117	bone morphogenetic protein 1	Homo sapiens	42-45
17283219-8	2007	From this, we conclude that perturbing of Bmp/Dkk1/Wnt signaling is central to the teratogenic effects of thalidomide.	Thalidomide	106-117	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	46-50
17409565-0	2007	Hydrolyzed metabolites of thalidomide: synthesis and TNF-alpha production-inhibitory activity.	Thalidomide	26-37	tumor necrosis factor	Homo sapiens	53-62
17409565-1	2007	Putative hydrolyzed metabolites of thalidomide were prepared and characterized, and their inhibitory activity on tumor necrosis factor (TNF)-alpha production in the human monocytic leukemia cell line THP-1 was evaluated.	Thalidomide	35-46	tumor necrosis factor	Homo sapiens	113-146
17409565-1	2007	Putative hydrolyzed metabolites of thalidomide were prepared and characterized, and their inhibitory activity on tumor necrosis factor (TNF)-alpha production in the human monocytic leukemia cell line THP-1 was evaluated.	Thalidomide	35-46	GLI family zinc finger 2	Homo sapiens	200-205
17283219-0	2007	Thalidomide induces limb deformities by perturbing the Bmp/Dkk1/Wnt signaling pathway.	Thalidomide	0-11	bone morphogenetic protein 1	Homo sapiens	55-58
17283219-0	2007	Thalidomide induces limb deformities by perturbing the Bmp/Dkk1/Wnt signaling pathway.	Thalidomide	0-11	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	59-63
17465495-0	2007	Therapeutic and prophylactic thalidomide in TNBS-induced colitis: synergistic effects on TNF-alpha, IL-12 and VEGF production.	Thalidomide	29-40	tumor necrosis factor	Homo sapiens	89-98
17465495-0	2007	Therapeutic and prophylactic thalidomide in TNBS-induced colitis: synergistic effects on TNF-alpha, IL-12 and VEGF production.	Thalidomide	29-40	vascular endothelial growth factor A	Homo sapiens	110-114
17465495-2	2007	Thalidomide has been reported to downregulate the expression of tumor necrosis factor alpha (TNF-alpha), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohnos disease (CD).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	64-91
17465495-2	2007	Thalidomide has been reported to downregulate the expression of tumor necrosis factor alpha (TNF-alpha), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohnos disease (CD).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	93-102
17465495-2	2007	Thalidomide has been reported to downregulate the expression of tumor necrosis factor alpha (TNF-alpha), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohnos disease (CD).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	116-150
17465495-2	2007	Thalidomide has been reported to downregulate the expression of tumor necrosis factor alpha (TNF-alpha), IL-12, and vascular endothelial growth factor (VEGF), hallmarks of intestinal inflammation in Crohnos disease (CD).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	152-156
17465495-10	2007	RESULTS: Significant reduction in the inflammatory score and in the percentage of VEGF+ cells was observed in the group treated with thalidomide compared with animals not treated with thalidomide.	Thalidomide	133-144	vascular endothelial growth factor A	Homo sapiens	82-86
17465495-11	2007	Both TNF-alpha and IL-12 levels were significantly reduced among TNBS induced colitis animals treated with thalidomide compared with animals that did not receive thalidomide.	Thalidomide	107-118	tumor necrosis factor	Homo sapiens	5-14
17465495-12	2007	TNF-alpha levels were also significantly reduced among the animals receiving thalidomide prophylaxis compared with untreated animals with TNBS-induced colitis.	Thalidomide	77-88	tumor necrosis factor	Homo sapiens	0-9
17465495-14	2007	CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-alpha, IL-12, and VEGF.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	113-122
17465495-14	2007	CONCLUSION: Thalidomide significantly attenuates TNBS-induced colitis by inhibiting the intestinal production of TNF-alpha, IL-12, and VEGF.	Thalidomide	12-23	vascular endothelial growth factor A	Homo sapiens	135-139
17367589-5	2007	Thalidomide was found to be effective in animal models by inhibiting TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	69-78
17208222-5	2007	These data suggest that one of the molecular mechanisms of thalidomide may be destabilization of COX-2 mRNA through inhibition of cytoplasmic shuttling of HuR and p38 MAPK.	Thalidomide	59-70	mitogen-activated protein kinase 14	Homo sapiens	163-166
17383526-0	2007	Effects of geldanamycin and thalidomide on the Th1/Th2 cytokine balance in mice subjected to operative trauma.	Thalidomide	28-39	negative elongation factor complex member C/D, Th1l	Mus musculus	47-50
17383526-0	2007	Effects of geldanamycin and thalidomide on the Th1/Th2 cytokine balance in mice subjected to operative trauma.	Thalidomide	28-39	heart and neural crest derivatives expressed 2	Mus musculus	51-54
17383526-13	2007	Geldanamycin and thalidomide improved the Th1/Th2 imbalance independently after major operative injury.	Thalidomide	17-28	negative elongation factor complex member C/D, Th1l	Mus musculus	42-45
17383526-13	2007	Geldanamycin and thalidomide improved the Th1/Th2 imbalance independently after major operative injury.	Thalidomide	17-28	heart and neural crest derivatives expressed 2	Mus musculus	46-49
17208222-0	2007	Thalidomide destabilizes cyclooxygenase-2 mRNA by inhibiting p38 mitogen-activated protein kinase and cytoplasmic shuttling of HuR.	Thalidomide	0-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	25-41
17258708-8	2007	Intraperitoneal injection of thalidomide, an inhibitor of TNF-alpha synthesis, prevented p38 activation in DRG and spinal cord.	Thalidomide	29-40	tumor necrosis factor	Homo sapiens	58-67
17208222-0	2007	Thalidomide destabilizes cyclooxygenase-2 mRNA by inhibiting p38 mitogen-activated protein kinase and cytoplasmic shuttling of HuR.	Thalidomide	0-11	mitogen-activated protein kinase 14	Homo sapiens	61-97
17208222-0	2007	Thalidomide destabilizes cyclooxygenase-2 mRNA by inhibiting p38 mitogen-activated protein kinase and cytoplasmic shuttling of HuR.	Thalidomide	0-11	ELAV like RNA binding protein 1	Homo sapiens	127-130
17208222-1	2007	We investigated the effect of thalidomide on transcriptional and post-transcriptional cyclooxygenase-2 (COX-2) expression, including a pathway leading to COX-2 mRNA destabilization.	Thalidomide	30-41	prostaglandin-endoperoxide synthase 2	Homo sapiens	86-102
17208222-1	2007	We investigated the effect of thalidomide on transcriptional and post-transcriptional cyclooxygenase-2 (COX-2) expression, including a pathway leading to COX-2 mRNA destabilization.	Thalidomide	30-41	prostaglandin-endoperoxide synthase 2	Homo sapiens	104-109
17208222-2	2007	We found that thalidomide inhibited the interleukin-1beta (IL-1beta)-mediated induction of COX-2 protein and mRNA in Caco-2 cells.	Thalidomide	14-25	interleukin 1 beta	Homo sapiens	40-57
17208222-2	2007	We found that thalidomide inhibited the interleukin-1beta (IL-1beta)-mediated induction of COX-2 protein and mRNA in Caco-2 cells.	Thalidomide	14-25	interleukin 1 beta	Homo sapiens	59-67
17208222-2	2007	We found that thalidomide inhibited the interleukin-1beta (IL-1beta)-mediated induction of COX-2 protein and mRNA in Caco-2 cells.	Thalidomide	14-25	prostaglandin-endoperoxide synthase 2	Homo sapiens	91-96
17208222-5	2007	These data suggest that one of the molecular mechanisms of thalidomide may be destabilization of COX-2 mRNA through inhibition of cytoplasmic shuttling of HuR and p38 MAPK.	Thalidomide	59-70	prostaglandin-endoperoxide synthase 2	Homo sapiens	97-102
17208222-5	2007	These data suggest that one of the molecular mechanisms of thalidomide may be destabilization of COX-2 mRNA through inhibition of cytoplasmic shuttling of HuR and p38 MAPK.	Thalidomide	59-70	ELAV like RNA binding protein 1	Homo sapiens	155-158
17327701-12	2007	The MTD was 100 mg thalidomide.	Thalidomide	19-30	metallothionein 1E	Homo sapiens	4-7
17562330-6	2007	The TNF antagonist thalidomide suppressed ADCC whereas pentoxifylline proved to be ineffective.	Thalidomide	19-30	tumor necrosis factor	Homo sapiens	4-7
17258708-8	2007	Intraperitoneal injection of thalidomide, an inhibitor of TNF-alpha synthesis, prevented p38 activation in DRG and spinal cord.	Thalidomide	29-40	mitogen-activated protein kinase 14	Homo sapiens	89-92
17295769-3	2007	The aim of the study was to evaluate the effectiveness of thalidomide, an immunomodulator that exerts an inhibitory action on TNF-alpha by enhancing mRNA degradation, in reducing post-ERCP pancreatitis in a rat model.	Thalidomide	58-69	tumor necrosis factor	Rattus norvegicus	126-135
17223105-3	2007	Moreover, the actions of thalidomide were assessed on the cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression in retinal tissue.	Thalidomide	25-36	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	58-80
17223105-3	2007	Moreover, the actions of thalidomide were assessed on the cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression in retinal tissue.	Thalidomide	25-36	nitric oxide synthase 2	Rattus norvegicus	85-116
17223105-3	2007	Moreover, the actions of thalidomide were assessed on the cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression in retinal tissue.	Thalidomide	25-36	nitric oxide synthase 2	Rattus norvegicus	118-122
17223105-7	2007	The oral pre-treatment with thalidomide decreased, in a dose-dependent manner, the number of inflammatory cells, the protein concentration, and the levels of IL-1beta and TNF-alpha in the AqH.	Thalidomide	28-39	interleukin 1 beta	Rattus norvegicus	158-166
17223105-7	2007	The oral pre-treatment with thalidomide decreased, in a dose-dependent manner, the number of inflammatory cells, the protein concentration, and the levels of IL-1beta and TNF-alpha in the AqH.	Thalidomide	28-39	tumor necrosis factor	Rattus norvegicus	171-180
17295769-7	2007	The prophylactic use of thalidomide significantly reduced serum amylase, pancreatic edema and the histologic grade of pancreatitis accompanied by a decrease in mRNA expression of TNF-alpha in the pancreatic tissue.	Thalidomide	24-35	tumor necrosis factor	Rattus norvegicus	179-188
17295769-9	2007	The mechanism of the protective effects of thalidomide seems to be the reduction of expression of TNF-alpha mRNA in pancreatic tissue.	Thalidomide	43-54	tumor necrosis factor	Rattus norvegicus	98-107
17268092-0	2007	Thalidomide analogs from diamines: Synthesis and evaluation as inhibitors of TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	77-86
17223105-9	2007	Furthermore, oral (50 mg/kg) and local (5%) thalidomide treatment also reduced expression of the pro-inflammatory proteins COX-2 and iNOS in the posterior segment of the eye.	Thalidomide	44-55	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	123-128
17223105-9	2007	Furthermore, oral (50 mg/kg) and local (5%) thalidomide treatment also reduced expression of the pro-inflammatory proteins COX-2 and iNOS in the posterior segment of the eye.	Thalidomide	44-55	nitric oxide synthase 2	Rattus norvegicus	133-137
17223105-10	2007	Thalidomide exhibited marked preventive and curative ocular effects in EIU in rats, a property that might be associated with its ability to inhibit the production of inflammatory cytokines and the expression of COX-2 and iNOS.	Thalidomide	0-11	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	211-216
17223105-10	2007	Thalidomide exhibited marked preventive and curative ocular effects in EIU in rats, a property that might be associated with its ability to inhibit the production of inflammatory cytokines and the expression of COX-2 and iNOS.	Thalidomide	0-11	nitric oxide synthase 2	Rattus norvegicus	221-225
16568139-2	2007	OBJECTIVES: To evaluate the effects of thalidomide on spinal cord ischemia/reperfusion injury via reduced TNF-alpha production.	Thalidomide	39-50	tumor necrosis factor	Oryctolagus cuniculus	106-115
16815546-2	2007	Thalidomide has been shown to inhibit production of TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	52-61
17503883-6	2007	Although thalidomide has been regarded as an anti-TNF drug, it was found to increase plasma levels of TNFalpha in a placebo-controlled study in patients with HF, suggesting that other mechanisms may contribute to its beneficial effects.	Thalidomide	9-20	tumor necrosis factor	Homo sapiens	50-53
17208262-0	2007	Differential surface expression of CD18 and CD44 by neutrophils in bone marrow and spleen contributed to the neutrophilia in thalidomide-treated female B6C3F1 mice.	Thalidomide	125-136	integrin beta 2	Mus musculus	35-39
17208262-0	2007	Differential surface expression of CD18 and CD44 by neutrophils in bone marrow and spleen contributed to the neutrophilia in thalidomide-treated female B6C3F1 mice.	Thalidomide	125-136	CD44 antigen	Mus musculus	44-48
17208262-7	2007	Flow cytometric analysis of the surface expression of adhesion molecules suggested that Thd treatment for either 14 or 28 days decreased the surface expression of either CD18 or CD44 by bone marrow neutrophils.	Thalidomide	88-91	integrin beta 2	Mus musculus	170-174
17208262-7	2007	Flow cytometric analysis of the surface expression of adhesion molecules suggested that Thd treatment for either 14 or 28 days decreased the surface expression of either CD18 or CD44 by bone marrow neutrophils.	Thalidomide	88-91	CD44 antigen	Mus musculus	178-182
17208262-8	2007	On the other hand, the surface expression of both CD18 and CD44 by splenic neutrophils was increased following Thd treatment for 28 days but not for 14 days.	Thalidomide	111-114	integrin beta 2	Mus musculus	50-54
17208262-8	2007	On the other hand, the surface expression of both CD18 and CD44 by splenic neutrophils was increased following Thd treatment for 28 days but not for 14 days.	Thalidomide	111-114	CD44 antigen	Mus musculus	59-63
17208262-10	2007	It was possible that decreased surface expressions of CD18 and CD44 facilitated neutrophils" release from the bone marrow; increased surface expressions of CD44 and CD18 by splenic neutrophils after 28 days of Thd treatment increased their ability to remain in the periphery.	Thalidomide	210-213	integrin beta 2	Mus musculus	54-58
17208262-10	2007	It was possible that decreased surface expressions of CD18 and CD44 facilitated neutrophils" release from the bone marrow; increased surface expressions of CD44 and CD18 by splenic neutrophils after 28 days of Thd treatment increased their ability to remain in the periphery.	Thalidomide	210-213	CD44 antigen	Mus musculus	63-67
17208262-10	2007	It was possible that decreased surface expressions of CD18 and CD44 facilitated neutrophils" release from the bone marrow; increased surface expressions of CD44 and CD18 by splenic neutrophils after 28 days of Thd treatment increased their ability to remain in the periphery.	Thalidomide	210-213	CD44 antigen	Mus musculus	156-160
17208262-10	2007	It was possible that decreased surface expressions of CD18 and CD44 facilitated neutrophils" release from the bone marrow; increased surface expressions of CD44 and CD18 by splenic neutrophils after 28 days of Thd treatment increased their ability to remain in the periphery.	Thalidomide	210-213	integrin beta 2	Mus musculus	165-169
17208262-11	2007	Taken together, Thd treatment increased neutrophils in female B6C3F1 mice, at least partially, through differentially modulating the surface expression of CD18 and CD44 by the neutrophils in the bone marrow and spleen.	Thalidomide	16-19	integrin beta 2	Mus musculus	155-159
17208262-11	2007	Taken together, Thd treatment increased neutrophils in female B6C3F1 mice, at least partially, through differentially modulating the surface expression of CD18 and CD44 by the neutrophils in the bone marrow and spleen.	Thalidomide	16-19	CD44 antigen	Mus musculus	164-168
17174718-2	2007	This study was designed to investigate the effects of thalidomide on expressions of NF-kappaB, IkappaB and intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule (VCAM-1) in established rat liver cirrhosis.	Thalidomide	54-65	intercellular adhesion molecule 1	Rattus norvegicus	107-140
17174718-2	2007	This study was designed to investigate the effects of thalidomide on expressions of NF-kappaB, IkappaB and intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule (VCAM-1) in established rat liver cirrhosis.	Thalidomide	54-65	intercellular adhesion molecule 1	Rattus norvegicus	142-148
17503883-6	2007	Although thalidomide has been regarded as an anti-TNF drug, it was found to increase plasma levels of TNFalpha in a placebo-controlled study in patients with HF, suggesting that other mechanisms may contribute to its beneficial effects.	Thalidomide	9-20	tumor necrosis factor	Homo sapiens	102-110
18257406-4	2007	The newest trend in the treatment of this multi-organ granulomatose disease of unknown origin is the use of TNF inhibitors--pentoxifyllin, infliximab, adalimumab, leflunomid, thalidomid.	Thalidomide	175-185	tumor necrosis factor	Homo sapiens	108-111
17106197-2	2007	Thalidomide has recently shown to improve LVEF in chronic heart failure patients, accompanied by a marked decrease in plasma levels of tumor necrosis factor alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	135-162
17106197-2	2007	Thalidomide has recently shown to improve LVEF in chronic heart failure patients, accompanied by a marked decrease in plasma levels of tumor necrosis factor alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	164-173
17106197-7	2007	TNF-alpha levels were initially of 5.88 +/- 0.9 and 6.49 +/- 1.82 vs. 6.32 +/- 1.6 and 7.94 +/- 3.8 pg/ml during follow-up, for thalidomide and control groups, respectively.	Thalidomide	128-139	tumor necrosis factor	Homo sapiens	0-9
17106197-9	2007	CONCLUSION: In conclusion, although there is a large amount of information supporting a direct relationship between TNF-alpha and worsening of symptoms and prognosis in patients with HF and recently, the beneficial effect on thalidomide treatment has been suggested, these preliminary observations should be confirmed in a larger prospective study, specially trying to clarify the action mechanisms.	Thalidomide	225-236	tumor necrosis factor	Homo sapiens	116-125
17852116-3	2007	Our group were the first to demonstrate activity of thalidomide in RCC, believed to be in part related to the modulation of tumor necrosis factor (TNF-a), a cytokine secreted by RCC with a number of tumor promoting properties.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	124-145
17852116-3	2007	Our group were the first to demonstrate activity of thalidomide in RCC, believed to be in part related to the modulation of tumor necrosis factor (TNF-a), a cytokine secreted by RCC with a number of tumor promoting properties.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	147-152
17139107-0	2006	Mono- and dihydroxylated metabolites of thalidomide: synthesis and TNF-alpha production-inhibitory activity.	Thalidomide	40-51	tumor necrosis factor	Homo sapiens	67-76
17369076-4	2007	Furthermore, vascular endothelial growth factor (VEGF) and beta fibroblast growth factor (bFGF) secretion and cellular response are suppressed by thalidomide, thus antagonizing neoangiogenesis and altering the bone marrow stromal microenvironment in hematologic malignancies.	Thalidomide	146-157	vascular endothelial growth factor A	Homo sapiens	13-47
17369076-4	2007	Furthermore, vascular endothelial growth factor (VEGF) and beta fibroblast growth factor (bFGF) secretion and cellular response are suppressed by thalidomide, thus antagonizing neoangiogenesis and altering the bone marrow stromal microenvironment in hematologic malignancies.	Thalidomide	146-157	vascular endothelial growth factor A	Homo sapiens	49-53
17369076-4	2007	Furthermore, vascular endothelial growth factor (VEGF) and beta fibroblast growth factor (bFGF) secretion and cellular response are suppressed by thalidomide, thus antagonizing neoangiogenesis and altering the bone marrow stromal microenvironment in hematologic malignancies.	Thalidomide	146-157	fibroblast growth factor 2	Homo sapiens	90-94
17369076-5	2007	The thalidomide analogs, lenalidomide (CC-5013; Revlimid) and CC-4047 (Actimid), have enhanced potency as inhibitors of TNF-alpha and other inflammatory cytokines, as well as greater capacity to promote T-cell activation and suppress angiogenesis.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	120-129
16333818-3	2007	Thalidomide inhibits TNF-alpha production by affecting the gene promoter as well as other anti-cytokine effects.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	21-30
17164777-0	2007	Therapeutic angiogenesis inhibits or rescues chemotherapy-induced peripheral neuropathy: taxol- and thalidomide-induced injury of vasa nervorum is ameliorated by VEGF.	Thalidomide	100-111	vascular endothelial growth factor A	Homo sapiens	162-166
17139107-1	2006	Mono- and dihydroxylated metabolites of thalidomide were efficiently prepared and characterized, and their inhibitory activity on tumor necrosis factor (TNF)-alpha production in the human monocytic leukemia cell line THP-1 was evaluated.	Thalidomide	40-51	tumor necrosis factor	Homo sapiens	130-163
17139107-1	2006	Mono- and dihydroxylated metabolites of thalidomide were efficiently prepared and characterized, and their inhibitory activity on tumor necrosis factor (TNF)-alpha production in the human monocytic leukemia cell line THP-1 was evaluated.	Thalidomide	40-51	GLI family zinc finger 2	Homo sapiens	217-222
17139107-2	2006	5,N-Dihydroxythalidomide was a much more potent TNF-alpha production inhibitor than thalidomide.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	48-57
16549389-7	2006	(iii) Thalidomide appeared to have immunostimulatory effects on the myocardium as evident by increased MIP-1alpha gene expression (p&lt;0.05).	Thalidomide	6-17	C-C motif chemokine ligand 3	Rattus norvegicus	103-113
17145842-0	2006	A novel anticancer effect of thalidomide: inhibition of intercellular adhesion molecule-1-mediated cell invasion and metastasis through suppression of nuclear factor-kappaB.	Thalidomide	29-40	intercellular adhesion molecule 1	Homo sapiens	56-89
17145842-12	2006	Thalidomide also suppressed tumor necrosis factor-alpha-induced ICAM-1 expression through inhibition of nuclear factor-kappaB binding to the ICAM-1 promoter.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	28-55
17145842-12	2006	Thalidomide also suppressed tumor necrosis factor-alpha-induced ICAM-1 expression through inhibition of nuclear factor-kappaB binding to the ICAM-1 promoter.	Thalidomide	0-11	intercellular adhesion molecule 1	Homo sapiens	64-70
17145842-12	2006	Thalidomide also suppressed tumor necrosis factor-alpha-induced ICAM-1 expression through inhibition of nuclear factor-kappaB binding to the ICAM-1 promoter.	Thalidomide	0-11	intercellular adhesion molecule 1	Homo sapiens	141-147
16549389-8	2006	(iv) Treating HF rats with thalidomide reduced myocardial collagen content, as assessed by markedly decreased levels of hydroxyproline ( approximately 40% reduction; p&lt;0.05), accompanied by lower TGF-beta(1) gene expression (p&lt;0.05).	Thalidomide	27-38	transforming growth factor, beta 1	Rattus norvegicus	199-210
17099831-15	2006	CONCLUSIONS: We conclude that outpatient administration of thalidomide/IL-2 is feasible in patients with heavily pretreated and progressive RCC who desire further active treatment.	Thalidomide	59-70	interleukin 2	Homo sapiens	71-75
17204188-3	2006	The results showed that thalidomide enhanced the proliferations of the CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, increased the secretion of IL-6 significantly, and decreased the secretion of IFN-gamma, and the secretions of IL-2 and IL-10 were not affected.	Thalidomide	24-35	interleukin 6	Homo sapiens	164-168
17204188-3	2006	The results showed that thalidomide enhanced the proliferations of the CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, increased the secretion of IL-6 significantly, and decreased the secretion of IFN-gamma, and the secretions of IL-2 and IL-10 were not affected.	Thalidomide	24-35	interferon gamma	Homo sapiens	215-224
17204188-3	2006	The results showed that thalidomide enhanced the proliferations of the CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, increased the secretion of IL-6 significantly, and decreased the secretion of IFN-gamma, and the secretions of IL-2 and IL-10 were not affected.	Thalidomide	24-35	interleukin 2	Homo sapiens	248-252
17204188-3	2006	The results showed that thalidomide enhanced the proliferations of the CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, increased the secretion of IL-6 significantly, and decreased the secretion of IFN-gamma, and the secretions of IL-2 and IL-10 were not affected.	Thalidomide	24-35	interleukin 10	Homo sapiens	257-262
17204188-5	2006	It is concluded that thalidomide preferentially enhances the proliferations of CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, and enhances the cytotoxic activity of PBMNC by increasing the secretion of IL-6 significantly, in short, thalidomide can exert anti-myeloma effects by increasing cellular immune function.	Thalidomide	21-32	interleukin 6	Homo sapiens	221-225
17204188-5	2006	It is concluded that thalidomide preferentially enhances the proliferations of CD8+ T, NK cells in PHA-stimulated PBMNC from healthy volunteers, and enhances the cytotoxic activity of PBMNC by increasing the secretion of IL-6 significantly, in short, thalidomide can exert anti-myeloma effects by increasing cellular immune function.	Thalidomide	251-262	interleukin 6	Homo sapiens	221-225
17162660-6	2006	In thalidomide-treated mice, TNF-alpha RNA levels were reduced in the SCN.	Thalidomide	3-14	tumor necrosis factor	Mus musculus	29-38
17195429-2	2006	Thalidomide (Thalomid, Celgene Corp., Summit, NJ), an angiogenesis inhibitor and immunomodulator that reduces tumor necrosis factor-alpha, is used for the treatment of multiple myeloma.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	110-137
17195429-2	2006	Thalidomide (Thalomid, Celgene Corp., Summit, NJ), an angiogenesis inhibitor and immunomodulator that reduces tumor necrosis factor-alpha, is used for the treatment of multiple myeloma.	Thalidomide	13-21	tumor necrosis factor	Homo sapiens	110-137
16965441-0	2006	Increased mortality in toxic epidermal necrolysis with thalidomide: corroborating or exonerating the pathogenetic role of TNF-alpha?	Thalidomide	55-66	tumor necrosis factor	Homo sapiens	122-131
16843662-1	2006	In the present study, we describe a new 3D-QSAR analysis of 42 previously reported thalidomide analogues, with the ability to modulate the pro-inflammatory cytokine TNFalpha, by using comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA).	Thalidomide	83-94	tumor necrosis factor	Homo sapiens	165-173
16815871-0	2006	A mechanistic study on reduced toxicity of irinotecan by coadministered thalidomide, a tumor necrosis factor-alpha inhibitor.	Thalidomide	72-83	tumor necrosis factor	Rattus norvegicus	87-114
16837501-0	2006	Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease.	Thalidomide	0-11	interleukin 18	Homo sapiens	20-25
16837501-0	2006	Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	27-31
16837501-0	2006	Thalidomide reduces IL-18, IL-8 and TNF-alpha release from alveolar macrophages in interstitial lung disease.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	36-45
16837501-2	2006	The efficacy of thalidomide treatment in sarcoidosis with lupus pernio is thought to be due to inhibition of tumour necrosis factor (TNF)-alpha.	Thalidomide	16-27	tumor necrosis factor	Homo sapiens	109-143
16837501-5	2006	In sarcoidosis and HP patients, thalidomide induced a dose-dependent, partial suppression of lipopolysacchride (LPS)-stimulated TNF-alpha, IL-12p40 and IL-18 release.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	128-137
16837501-5	2006	In sarcoidosis and HP patients, thalidomide induced a dose-dependent, partial suppression of lipopolysacchride (LPS)-stimulated TNF-alpha, IL-12p40 and IL-18 release.	Thalidomide	32-43	interleukin 18	Homo sapiens	152-157
16837501-6	2006	At the highest thalidomide concentration (0.1 mM), LPS-stimulated IL-8 production was also suppressed.	Thalidomide	15-26	C-X-C motif chemokine ligand 8	Homo sapiens	66-70
16837501-7	2006	In IPF patients, although spontaneous production of TNF-alpha, IL-12p40, IL-18 and IL-8 was lower than in sarcoidosis and HP patients, with LPS stimulation the cytokines were significantly elevated and also partially inhibited by thalidomide.	Thalidomide	230-241	tumor necrosis factor	Homo sapiens	52-61
16837501-7	2006	In IPF patients, although spontaneous production of TNF-alpha, IL-12p40, IL-18 and IL-8 was lower than in sarcoidosis and HP patients, with LPS stimulation the cytokines were significantly elevated and also partially inhibited by thalidomide.	Thalidomide	230-241	C-X-C motif chemokine ligand 8	Homo sapiens	83-87
16837501-8	2006	In conclusion, thalidomide has the potential to improve the therapeutic regimens for sarcoidosis, hypersensitivity pneumonitis and idiopathic pulmonary fibrosis by reducing tumour necrosis factor-alpha, interleukin-12p40, interleukin-18 and interleukin-8 production.	Thalidomide	15-26	interleukin 12B	Homo sapiens	203-220
16837501-8	2006	In conclusion, thalidomide has the potential to improve the therapeutic regimens for sarcoidosis, hypersensitivity pneumonitis and idiopathic pulmonary fibrosis by reducing tumour necrosis factor-alpha, interleukin-12p40, interleukin-18 and interleukin-8 production.	Thalidomide	15-26	interleukin 18	Homo sapiens	222-236
16837501-8	2006	In conclusion, thalidomide has the potential to improve the therapeutic regimens for sarcoidosis, hypersensitivity pneumonitis and idiopathic pulmonary fibrosis by reducing tumour necrosis factor-alpha, interleukin-12p40, interleukin-18 and interleukin-8 production.	Thalidomide	15-26	C-X-C motif chemokine ligand 8	Homo sapiens	241-254
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Thalidomide	0-11	PGP	Canis lupus familiaris	65-68
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Thalidomide	0-11	ATP binding cassette subfamily B member 1	Canis lupus familiaris	69-73
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Thalidomide	0-11	ATP binding cassette subfamily C member 1	Canis lupus familiaris	76-121
16815871-14	2006	Thalidomide and PGA also significantly inhibited P-glycoprotein (PgP/MDR1), multidrug resistance-associated protein (MRP1)- and MRP2-mediated CPT-11 and SN-38 transport in MDCKII cells.	Thalidomide	0-11	ATP binding cassette subfamily C member 2	Canis lupus familiaris	128-132
16846617-3	2006	The purpose of this study was to examine the effects of thalidomide on secretion of prolactin (PRL) and vascular endothelial growth factor (VEGF), cell proliferation, apoptosis and angiogenesis within the anterior pituitary gland in long-term diethylstilboestrol (DES)-treated male F344 rats in vivo and in vitro.	Thalidomide	56-67	prolactin	Rattus norvegicus	84-93
16846617-5	2006	On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion.	Thalidomide	60-71	prolactin	Rattus norvegicus	155-158
16846617-5	2006	On the other hand, simultaneous treatment of F344 rats with thalidomide for the last 15 days of the experiment attenuated the stimulatory effect of DES on PRL and VEGF secretion.	Thalidomide	60-71	vascular endothelial growth factor A	Rattus norvegicus	163-167
16846617-8	2006	In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro.	Thalidomide	13-24	prolactin	Rattus norvegicus	76-85
16846617-8	2006	In addition, thalidomide (10(-4) to 10(-6) M) inhibited cell proliferation, prolactin and VEGF secretion from rat pituitary prolactinoma cells cultured in vitro.	Thalidomide	13-24	vascular endothelial growth factor A	Rattus norvegicus	90-94
16923192-14	2006	CONCLUSION: Results suggest that exposure to valproate, thalidomide or alcohol during the first trimester of pregnancy may change the ultrastructure of the placenta by altering the migration of trophoblast cells and this effect may be mediated by drug- or alcohol-induced changes in the expression levels of beta1 and alpha5 integrin subunits.	Thalidomide	56-67	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	308-324
17031469-1	2006	INTRODUCTION: Thalidomide is a derivative of glutamic acid with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that was found to inhibit the production of tumor necrosis factor alpha in vitro, stimulate reactive oxygen species production, and inhibit vascular endothelial growth factor receptor in acute leukemias.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	188-215
16995741-3	2006	Thalidomide was chosen as the skeleton on which to base the new lead series, as it moderately inhibits MMP-3, is antiangiogenic, and lends itself easily to structural modifications.	Thalidomide	0-11	matrix metallopeptidase 3	Homo sapiens	103-108
16877307-0	2006	Preparation and in vitro analysis of microcapsule thalidomide formulation for targeted suppression of TNF-alpha.	Thalidomide	50-61	tumor necrosis factor	Mus musculus	102-111
16877307-2	2006	Thalidomide has been shown to decrease this inflammation by the suppression of TNF-alpha secretion.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	79-88
16675114-8	2006	Intraperitoneal injection of thalidomide, an inhibitor of TNF-alpha synthesis, started at 2h before surgery, blocked mechanical allodynia and thermal hyperalgesia.	Thalidomide	29-40	tumor necrosis factor	Rattus norvegicus	58-67
16765039-12	2006	It is concluded that thalidomide shows single-agent activity in patients with heavily pre-treated GCT, AFP elevations and slowly progressive disease.	Thalidomide	21-32	alpha fetoprotein	Homo sapiens	103-106
17013434-2	2006	Thalidomide exerts its effects by decreasing circulating CD4 positive T-cells and stimulating CD8 positive T-cells, by increasing the number of Natural Killer cells and T-helper 2 cells.	Thalidomide	0-11	CD4 molecule	Homo sapiens	57-60
16616857-0	2006	Thalidomide alters c-MYB and PIM-1 signaling in K-562 cells.	Thalidomide	0-11	MYB proto-oncogene, transcription factor	Homo sapiens	19-24
16616857-0	2006	Thalidomide alters c-MYB and PIM-1 signaling in K-562 cells.	Thalidomide	0-11	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	29-34
16616857-3	2006	We hypothesize that thalidomide acts by interfering with the c-Myb signaling pathway.	Thalidomide	20-31	MYB proto-oncogene, transcription factor	Homo sapiens	61-66
16616857-6	2006	Cells exposed to thalidomide (40 microg/ml) had significantly decreased c-Myb activity.	Thalidomide	17-28	MYB proto-oncogene, transcription factor	Homo sapiens	72-77
16616857-7	2006	Pre-incubation of cells with the anti-oxidative enzyme catalase (1600 units/ml), prevented thalidomide-induced decreased c-Myb activity, suggesting a role for ROS in the c-Myb signaling pathway.	Thalidomide	91-102	MYB proto-oncogene, transcription factor	Homo sapiens	121-126
16616857-7	2006	Pre-incubation of cells with the anti-oxidative enzyme catalase (1600 units/ml), prevented thalidomide-induced decreased c-Myb activity, suggesting a role for ROS in the c-Myb signaling pathway.	Thalidomide	91-102	MYB proto-oncogene, transcription factor	Homo sapiens	170-175
16616857-9	2006	Western blot analysis on thalidomide exposed cells showed a decrease in both Pim-1 protein expression and phosphorylated c-Myb protein expression, suggesting that the decrease in Pim-1 and the amount of phosphorylated c-Myb protein may be responsible for the observed decreases in c-Myb activity.	Thalidomide	25-36	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	77-82
16616857-9	2006	Western blot analysis on thalidomide exposed cells showed a decrease in both Pim-1 protein expression and phosphorylated c-Myb protein expression, suggesting that the decrease in Pim-1 and the amount of phosphorylated c-Myb protein may be responsible for the observed decreases in c-Myb activity.	Thalidomide	25-36	MYB proto-oncogene, transcription factor	Homo sapiens	121-126
16616857-9	2006	Western blot analysis on thalidomide exposed cells showed a decrease in both Pim-1 protein expression and phosphorylated c-Myb protein expression, suggesting that the decrease in Pim-1 and the amount of phosphorylated c-Myb protein may be responsible for the observed decreases in c-Myb activity.	Thalidomide	25-36	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	179-184
16616857-9	2006	Western blot analysis on thalidomide exposed cells showed a decrease in both Pim-1 protein expression and phosphorylated c-Myb protein expression, suggesting that the decrease in Pim-1 and the amount of phosphorylated c-Myb protein may be responsible for the observed decreases in c-Myb activity.	Thalidomide	25-36	MYB proto-oncogene, transcription factor	Homo sapiens	218-223
16616857-9	2006	Western blot analysis on thalidomide exposed cells showed a decrease in both Pim-1 protein expression and phosphorylated c-Myb protein expression, suggesting that the decrease in Pim-1 and the amount of phosphorylated c-Myb protein may be responsible for the observed decreases in c-Myb activity.	Thalidomide	25-36	MYB proto-oncogene, transcription factor	Homo sapiens	218-223
16616857-10	2006	Together these results demonstrate that thalidomide affects c-Myb signaling, in part, through increased ROS production.	Thalidomide	40-51	MYB proto-oncogene, transcription factor	Homo sapiens	60-65
16702985-9	2006	A noteworthy decrease in inflammatory and nociceptive responses caused by carrageenan was also observed when mice were previously treated with the preferential inhibitor of TNF-alpha synthesis, thalidomide.	Thalidomide	194-205	tumor necrosis factor	Mus musculus	173-182
16714224-0	2006	The neutropenia induced by the thalidomide analogue CC-4047 in patients with multiple myeloma is associated with an increased percentage of neutrophils bearing CD64.	Thalidomide	31-42	Fc gamma receptor Ia	Homo sapiens	160-164
17013434-2	2006	Thalidomide exerts its effects by decreasing circulating CD4 positive T-cells and stimulating CD8 positive T-cells, by increasing the number of Natural Killer cells and T-helper 2 cells.	Thalidomide	0-11	CD8a molecule	Homo sapiens	94-97
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	tumor necrosis factor	Homo sapiens	51-59
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	interleukin 5	Homo sapiens	61-65
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	interleukin 6	Homo sapiens	67-71
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	C-X-C motif chemokine ligand 8	Homo sapiens	73-77
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	interleukin 2	Homo sapiens	124-128
17013434-5	2006	It has been demonstrated that thalidomide inhibits TNFalpha, IL-5, IL-6, IL-8, IL-12 production and increases production of IL-2, IL-10 and INFgamma.	Thalidomide	30-41	interleukin 10	Homo sapiens	130-135
17013434-6	2006	Moreover thalidomide plays an important role in inhibition of VEGF and FGF-2 mediated angiogenesis.	Thalidomide	9-20	vascular endothelial growth factor A	Homo sapiens	62-66
17013434-6	2006	Moreover thalidomide plays an important role in inhibition of VEGF and FGF-2 mediated angiogenesis.	Thalidomide	9-20	fibroblast growth factor 2	Homo sapiens	71-76
16775497-6	2006	Serum levels of vascular endothelial growth factor (VEGF) correlate with disease activity in human IBD and fall with the use of steroids, thalidomide, or infliximab.	Thalidomide	138-149	vascular endothelial growth factor A	Homo sapiens	16-50
16740776-0	2006	Importance of the stress kinase p38alpha in mediating the direct cytotoxic effects of the thalidomide analogue, CPS49, in cancer cells and endothelial cells.	Thalidomide	90-101	mitogen-activated protein kinase 14	Homo sapiens	32-40
16775497-6	2006	Serum levels of vascular endothelial growth factor (VEGF) correlate with disease activity in human IBD and fall with the use of steroids, thalidomide, or infliximab.	Thalidomide	138-149	vascular endothelial growth factor A	Homo sapiens	52-56
16136308-6	2006	In this study, we investigated thalidomide"s potential to cause drug-drug interactions on the level of P-gp.	Thalidomide	31-42	ATP binding cassette subfamily B member 1	Homo sapiens	103-107
16840205-1	2006	Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	152-161
16840205-1	2006	Thalidomide is a drug with anti-angiogenic, anti-inflammatory, immunomodulatory and anti-cancer properties that were found to inhibit the production of TNF-alpha in vitro, stimulate reactive oxygen species production, and inhibit VEGFR in acute leukemias.	Thalidomide	0-11	kinase insert domain receptor	Homo sapiens	230-235
16136308-8	2006	A human leukaemia cell line over-expressing MDR1 (CCRF-CEM/MDR1) was used to measure uptake of rhodamine 123, a P-gp substrate, in the presence of thalidomide.	Thalidomide	147-158	ATP binding cassette subfamily B member 1	Homo sapiens	44-48
16136308-8	2006	A human leukaemia cell line over-expressing MDR1 (CCRF-CEM/MDR1) was used to measure uptake of rhodamine 123, a P-gp substrate, in the presence of thalidomide.	Thalidomide	147-158	ATP binding cassette subfamily B member 1	Homo sapiens	50-63
16136308-16	2006	Therefore, P-gp-related drug-drug interactions with thalidomide are not likely.	Thalidomide	52-63	ATP binding cassette subfamily B member 1	Homo sapiens	11-15
16724931-2	2006	Recent clinical studies indicate that thalidomide, a known tumor necrosis factor-alpha inhibitor, ameliorated the toxicities induced by CPT-11.	Thalidomide	38-49	tumor necrosis factor	Rattus norvegicus	59-86
16680017-4	2006	When compared with DNBS-treated mice, thalidomide-treated (200 mg/kg orally starting 30 min after the administration of DNBS) mice subjected to DNBS-induced colitis experienced a significantly reduced rate of the extent and severity of the histological signs of colon injury associated with a significant reduction of plasma and colon tumor necrosis factor alpha levels.	Thalidomide	38-49	tumor necrosis factor	Mus musculus	335-362
16597438-3	2006	Furthermore, thalidomide pretreatment significantly reduced the concentration of tumor necrosis factor-alpha (TNF-alpha, -68.4%) in the exudate of zymosan-injected joints, but not those of interleukin-1beta, interleukin-6, CINC-1 or interleukin-10.	Thalidomide	13-24	tumor necrosis factor	Rattus norvegicus	81-108
16597438-3	2006	Furthermore, thalidomide pretreatment significantly reduced the concentration of tumor necrosis factor-alpha (TNF-alpha, -68.4%) in the exudate of zymosan-injected joints, but not those of interleukin-1beta, interleukin-6, CINC-1 or interleukin-10.	Thalidomide	13-24	tumor necrosis factor	Rattus norvegicus	110-119
16597438-3	2006	Furthermore, thalidomide pretreatment significantly reduced the concentration of tumor necrosis factor-alpha (TNF-alpha, -68.4%) in the exudate of zymosan-injected joints, but not those of interleukin-1beta, interleukin-6, CINC-1 or interleukin-10.	Thalidomide	13-24	interleukin 6	Rattus norvegicus	208-221
16597438-3	2006	Furthermore, thalidomide pretreatment significantly reduced the concentration of tumor necrosis factor-alpha (TNF-alpha, -68.4%) in the exudate of zymosan-injected joints, but not those of interleukin-1beta, interleukin-6, CINC-1 or interleukin-10.	Thalidomide	13-24	C-X-C motif chemokine ligand 1	Rattus norvegicus	223-229
16597438-3	2006	Furthermore, thalidomide pretreatment significantly reduced the concentration of tumor necrosis factor-alpha (TNF-alpha, -68.4%) in the exudate of zymosan-injected joints, but not those of interleukin-1beta, interleukin-6, CINC-1 or interleukin-10.	Thalidomide	13-24	interleukin 10	Rattus norvegicus	233-247
16086096-9	2006	CONCLUSION: This study demonstrates antitumor activity of combination IFN-alpha/capecitabine/thalidomide in MRCC.	Thalidomide	93-104	interferon alpha 1	Homo sapiens	70-79
16597438-4	2006	The expression of TNF-alpha, determined by immunohistochemical staining, in synovial tissues obtained from articular joints injected with zymosan was also inhibited by thalidomide pretreatment.	Thalidomide	168-179	tumor necrosis factor	Rattus norvegicus	18-27
16597438-6	2006	In conclusion, the anti-nociceptive activity of thalidomide in zymosan-induced articular incapacitation is associated with the inhibition of TNF-alpha by resident synovial cells.	Thalidomide	48-59	tumor necrosis factor	Rattus norvegicus	141-150
16604421-3	2006	Thalidomide, alpha-N-phthalidoglutarimide, (C(13)H(10)N(2))(4), has been shown to have immunomodulatory and anti-inflammatory properties, possibly mediated through its anti-TNF-alpha effect.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	173-182
16604421-8	2006	Thalidomide (100-800 nM) concentration-dependently inhibited NFkappaB transcriptional activity induced by TNF-alpha, including IKKalpha expression and IkappaBalpha phosphorylation in HSC-T6 cells.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	106-115
16604421-8	2006	Thalidomide (100-800 nM) concentration-dependently inhibited NFkappaB transcriptional activity induced by TNF-alpha, including IKKalpha expression and IkappaBalpha phosphorylation in HSC-T6 cells.	Thalidomide	0-11	component of inhibitor of nuclear factor kappa B kinase complex	Rattus norvegicus	127-135
16604421-8	2006	Thalidomide (100-800 nM) concentration-dependently inhibited NFkappaB transcriptional activity induced by TNF-alpha, including IKKalpha expression and IkappaBalpha phosphorylation in HSC-T6 cells.	Thalidomide	0-11	NFKB inhibitor alpha	Rattus norvegicus	151-163
16604421-9	2006	In addition, thalidomide also suppressed TGF-beta1-induced alpha-SMA expression and collagen deposition in HSC-T6 cells.	Thalidomide	13-24	transforming growth factor, beta 1	Rattus norvegicus	41-50
16604421-9	2006	In addition, thalidomide also suppressed TGF-beta1-induced alpha-SMA expression and collagen deposition in HSC-T6 cells.	Thalidomide	13-24	actin gamma 2, smooth muscle	Rattus norvegicus	59-68
16604421-12	2006	Immunohistochemical double staining results showed that alpha-SMA- and NFkappaB-positive cells were decreased in the livers from DMN rats receiving either thalidomide or silymarin treatment.	Thalidomide	155-166	actin gamma 2, smooth muscle	Rattus norvegicus	56-65
16604421-13	2006	In addition, real-time PCR analysis indicated that hepatic mRNA expressions of TGF-beta1, alpha-SMA, collagen 1alpha2, TNF-alpha and iNOS genes were attenuated by thalidomide treatment.	Thalidomide	163-174	transforming growth factor, beta 1	Rattus norvegicus	79-88
16604421-13	2006	In addition, real-time PCR analysis indicated that hepatic mRNA expressions of TGF-beta1, alpha-SMA, collagen 1alpha2, TNF-alpha and iNOS genes were attenuated by thalidomide treatment.	Thalidomide	163-174	actin gamma 2, smooth muscle	Rattus norvegicus	90-99
16604421-13	2006	In addition, real-time PCR analysis indicated that hepatic mRNA expressions of TGF-beta1, alpha-SMA, collagen 1alpha2, TNF-alpha and iNOS genes were attenuated by thalidomide treatment.	Thalidomide	163-174	tumor necrosis factor	Rattus norvegicus	119-128
16604421-14	2006	In conclusion, our results showed that thalidomide inhibited activation of HSC-T6 cells by TNF-alpha and ameliorated liver fibrosis in DMN-intoxicated rats.	Thalidomide	39-50	tumor necrosis factor	Rattus norvegicus	91-100
16680017-7	2006	In particular, we have observed that thalidomide treatment resulted in a significant reduction of the following: (1) the degree of colon injury, (2) the alteration of zonula occludens 1 and occludin localization (immunohistochemistry), and (3) intestinal permeability caused by DNBS in the colon.	Thalidomide	37-48	occludin	Mus musculus	190-198
16900926-3	2006	We therefore assessed the effect of adjunctive thalidomide, a tumor necrosis factor alpha-modulating drug, in intractable intracranial tuberculosis that did not respond to standard medical and surgical therapy.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	62-89
16310808-0	2006	Effect of thalidomide affecting VEGF secretion, cell migration, adhesion and capillary tube formation of human endothelial EA.hy 926 cells.	Thalidomide	10-21	vascular endothelial growth factor A	Homo sapiens	32-36
16310808-6	2006	Thalidomide at the concentrations of 0.01 microM and 10 microM inhibited VEGF secretion into supernatants, decreased the number of formed capillary tubes and increased cell adhesion to collagen.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	73-77
16310808-9	2006	We conclude that anti-angiogenic action of thalidomide is due to direct inhibitory action on VEGF secretion and capillary microvessel formation as well as immunomodulatory influence on EA.hy 926 cells migration and adhesion.	Thalidomide	43-54	vascular endothelial growth factor A	Homo sapiens	93-97
16475152-1	2006	BACKGROUND: The purpose of the study was to determine, in a Phase I/II study, the efficacy and safety profile of thalidomide with interleukin-2 (IL-2) in patients with metastatic renal cell carcinoma (MRCC).	Thalidomide	113-124	interleukin 2	Homo sapiens	145-149
16523333-14	2006	In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone.	Thalidomide	109-120	BCL2 apoptosis regulator	Homo sapiens	22-27
16523333-14	2006	In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone.	Thalidomide	109-120	BCL2 associated X, apoptosis regulator	Homo sapiens	28-31
16523333-14	2006	In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone.	Thalidomide	186-197	BCL2 apoptosis regulator	Homo sapiens	22-27
16523333-14	2006	In most patients, the BCL-2/BAX ratio was lower in cell cultures supplemented with mixture of lovastatin and thalidomide in comparison with cell cultures supplemented with lovastatin or thalidomide alone.	Thalidomide	186-197	BCL2 associated X, apoptosis regulator	Homo sapiens	28-31
16386767-5	2006	A similar inhibition of the mechanical hypernociception was observed when treating mice with the TNFalpha synthesis inhibitor thalidomide (50 mg/kg, s.c.), either at the time of the surgery or 4 days after.	Thalidomide	126-137	tumor necrosis factor	Mus musculus	97-105
16219350-1	2006	We investigated the therapeutic activity of recombinant erythropoietin (r-EPO) in association with thalidomide in 30 patients with myelodysplastic syndromes (MDS), previously treated with r-EPO (n.15, group A) or thalidomide (n.15, group B) as single agents, respectively, without any significant benefit on their anemia.	Thalidomide	99-110	erythropoietin	Homo sapiens	56-70
16729912-1	2006	PURPOSE: The antiangiogenic and immunomodulatory effects of thalidomide induce responses in patients with androgen-independent prostate cancer (AIPC).	Thalidomide	60-71	PDZ domain containing 2	Homo sapiens	144-148
16729912-19	2006	CONCLUSION: The combined dosing of paclitaxel (100 mg/m(2) weekly), doxorubicin (20 mg/m(2) weekly), and thalidomide (300 mg daily) is tolerated by men with AIPC and merits continued phase II study.	Thalidomide	105-116	PDZ domain containing 2	Homo sapiens	157-161
16514283-6	2006	Cytokine study showed that the effect of thalidomide was not dependent on IL-12; however, it up-regulated IFN-gamma and down-regulated IL-10 production.	Thalidomide	41-52	interferon gamma	Mus musculus	106-115
16531263-0	2006	Stimulation of erythropoiesis by thalidomide in multiple myeloma patients: its influence on FasL, TRAIL and their receptors on erythroblasts.	Thalidomide	33-44	Fas ligand	Homo sapiens	92-96
16531263-0	2006	Stimulation of erythropoiesis by thalidomide in multiple myeloma patients: its influence on FasL, TRAIL and their receptors on erythroblasts.	Thalidomide	33-44	TNF superfamily member 10	Homo sapiens	98-103
16531263-3	2006	The expression of FasL, Fas, TNF-related apoptosis-inducing ligand (TRAIL) and TRAIL-R1 on erythroblasts decreased significantly during thalidomide treatment.	Thalidomide	136-147	Fas ligand	Homo sapiens	18-22
16531263-3	2006	The expression of FasL, Fas, TNF-related apoptosis-inducing ligand (TRAIL) and TRAIL-R1 on erythroblasts decreased significantly during thalidomide treatment.	Thalidomide	136-147	TNF superfamily member 10	Homo sapiens	29-66
16531263-3	2006	The expression of FasL, Fas, TNF-related apoptosis-inducing ligand (TRAIL) and TRAIL-R1 on erythroblasts decreased significantly during thalidomide treatment.	Thalidomide	136-147	TNF superfamily member 10	Homo sapiens	68-73
16531263-3	2006	The expression of FasL, Fas, TNF-related apoptosis-inducing ligand (TRAIL) and TRAIL-R1 on erythroblasts decreased significantly during thalidomide treatment.	Thalidomide	136-147	TNF receptor superfamily member 10a	Homo sapiens	79-87
16531263-4	2006	Additional in vitro studies revealed that the apoptosis of erythroblasts and the expression of FasL, TRAIL, TRAIL-R1 and TRAIL-R2 was lower in cultures with thalidomide than in control cultures.	Thalidomide	157-168	Fas ligand	Homo sapiens	95-99
16531263-4	2006	Additional in vitro studies revealed that the apoptosis of erythroblasts and the expression of FasL, TRAIL, TRAIL-R1 and TRAIL-R2 was lower in cultures with thalidomide than in control cultures.	Thalidomide	157-168	TNF superfamily member 10	Homo sapiens	101-106
16531263-4	2006	Additional in vitro studies revealed that the apoptosis of erythroblasts and the expression of FasL, TRAIL, TRAIL-R1 and TRAIL-R2 was lower in cultures with thalidomide than in control cultures.	Thalidomide	157-168	TNF receptor superfamily member 10a	Homo sapiens	108-116
16531263-4	2006	Additional in vitro studies revealed that the apoptosis of erythroblasts and the expression of FasL, TRAIL, TRAIL-R1 and TRAIL-R2 was lower in cultures with thalidomide than in control cultures.	Thalidomide	157-168	TNF receptor superfamily member 10b	Homo sapiens	121-129
16510725-5	2006	We tested the neuroprotective effect of thalidomide and its analog lenalidomide, pharmacological agents that inhibit the expression of TNF-alpha and other cytokines by destabilizing their mRNA.	Thalidomide	40-51	tumor necrosis factor	Mus musculus	135-144
16514283-6	2006	Cytokine study showed that the effect of thalidomide was not dependent on IL-12; however, it up-regulated IFN-gamma and down-regulated IL-10 production.	Thalidomide	41-52	interleukin 10	Mus musculus	135-140
16490847-2	2006	Accordingly, TNF-alpha inhibitors, such as thalidomide, infliximab (Remicade), adalimumab (Humira), and etanercept (Enbrel), have been used with success in the treatment of autoimmune disorders, including psoriasis, rheumatoid arthritis, inflammatory bowel diseases, and lymphoproliferative disorders.	Thalidomide	43-54	tumor necrosis factor	Homo sapiens	13-22
16421420-5	2006	RESULTS: Treatment with temozolomide and thalidomide was associated with an objective biochemical (chromogranin A) response rate of 40%, and a radiologic response rate of 25% (45% among pancreatic endocrine tumors, 33% among pheochromocytomas, and 7% among carcinoid tumors).	Thalidomide	41-52	chromogranin A	Homo sapiens	99-113
16484869-4	2006	Thalidomide has been shown to have antiangiogenic and immunomodulatory effects, including the inhibition of vascular endothelial growth factor, basic fibroblast growth factor and tumor necrosis factor alpha.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	108-142
16454849-1	2006	Immunomodulation of thalidomide is represented by the antiinflammatory effect through inhibition of tumor necrosis factor alpha and costimulatory effect on human CD8+ T cells.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	100-127
16454849-4	2006	Tumor necrosis factor-alpha in vitro production in mononuclear cells decreased with thalidomide in all the subjects (p = 0.028).	Thalidomide	84-95	tumor necrosis factor	Homo sapiens	0-27
16454849-9	2006	In conclusion, thalidomide was able to reduce liver enzymes in six out of eight patients with chronic hepatitis C and to reduce tumor necrosis factor alpha production, representing a promising new approach for the treatment of HCV infection.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	128-155
16327979-8	2006	We further demonstrated that the expression of angiogenic factors, such as vascular endothelial cell growth factor (VEGF) and basic fibroblastic growth factor (bFGF), were inhibited by THD.	Thalidomide	185-188	vascular endothelial growth factor A	Rattus norvegicus	116-120
16344495-7	2006	B cell numbers and expression of the adhesion molecule L-sel also declined with thalidomide.	Thalidomide	80-91	selectin L	Homo sapiens	55-60
16997792-0	2006	Effect of thalidomide on the expression of TNF-alpha m-RNA and synthesis of TNF-alpha in cells from leprosy patients with reversal reaction.	Thalidomide	10-21	tumor necrosis factor	Homo sapiens	43-52
16997792-0	2006	Effect of thalidomide on the expression of TNF-alpha m-RNA and synthesis of TNF-alpha in cells from leprosy patients with reversal reaction.	Thalidomide	10-21	tumor necrosis factor	Homo sapiens	76-85
16997792-5	2006	We assessed thalidomide"s effect on TNF-alpha in RR.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	36-45
16997792-7	2006	Thalidomide suppressed TNF-alpha, but when some RR patients" cells were stimulated with AFB, it enhanced TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	23-32
16327979-8	2006	We further demonstrated that the expression of angiogenic factors, such as vascular endothelial cell growth factor (VEGF) and basic fibroblastic growth factor (bFGF), were inhibited by THD.	Thalidomide	185-188	fibroblast growth factor 2	Rattus norvegicus	126-158
16327979-8	2006	We further demonstrated that the expression of angiogenic factors, such as vascular endothelial cell growth factor (VEGF) and basic fibroblastic growth factor (bFGF), were inhibited by THD.	Thalidomide	185-188	fibroblast growth factor 2	Rattus norvegicus	160-164
16943688-1	2006	BACKGROUND/AIMS: Thalidomide inhibited tumor necrosis factor-alpha (TNF-alpha) effectively in many trials.	Thalidomide	17-28	tumor necrosis factor	Rattus norvegicus	39-66
17047296-3	2006	Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide.	Thalidomide	221-232	intercellular adhesion molecule 1	Rattus norvegicus	97-103
17047296-3	2006	Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide.	Thalidomide	221-232	vascular cell adhesion molecule 1	Rattus norvegicus	105-111
17047296-3	2006	Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide.	Thalidomide	221-232	selectin E	Rattus norvegicus	113-123
17047296-3	2006	Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-alpha mRNA and protein were decreased significantly in rats treated with a high dose of thalidomide.	Thalidomide	221-232	tumor necrosis factor	Rattus norvegicus	129-138
17047296-5	2006	These results indicate that thalidomide exerts its effect on the downregulation of adhesion molecules via TNF-alpha signaling pathway to inhibit liver fibrosis.	Thalidomide	28-39	tumor necrosis factor	Rattus norvegicus	106-115
16943688-0	2006	Thalidomide in rat liver cirrhosis: blockade of tumor necrosis factor-alpha via inhibition of degradation of an inhibitor of nuclear factor-kappaB.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	48-75
16943688-1	2006	BACKGROUND/AIMS: Thalidomide inhibited tumor necrosis factor-alpha (TNF-alpha) effectively in many trials.	Thalidomide	17-28	tumor necrosis factor	Rattus norvegicus	68-77
16943688-7	2006	CONCLUSION: Thalidomide downregulates NF-kappaB-induced TNF-alpha and activates hepatic stellate cells (HSC) via inhibition of IkappaB degradation to prevent liver cirrhosis.	Thalidomide	12-23	tumor necrosis factor	Rattus norvegicus	56-65
16299286-4	2005	Intraperitoneal injection of a TNF inhibitor, thalidomide (TH), reduced the number of exfoliated chambers, while indomethacin had no effect.	Thalidomide	46-57	tumor necrosis factor	Mus musculus	31-34
16324117-4	2005	The suppression of LTP by Abeta was absent in mutant mice null for TNF receptor type 1 (TNF-R1) and was prevented by the inhibitors of TNFalpha, infliximab and TNF peptide antagonist, and by the inhibitor of TNFalpha production, thalidomide.	Thalidomide	229-240	tumor necrosis factor	Mus musculus	208-216
16299286-4	2005	Intraperitoneal injection of a TNF inhibitor, thalidomide (TH), reduced the number of exfoliated chambers, while indomethacin had no effect.	Thalidomide	59-61	tumor necrosis factor	Mus musculus	31-34
16301340-5	2005	(3) Thalidomide also induced a decrease in total neutrophil count and an increase in plasma levels of tumor necrosis factor-alpha, suggesting both proinflammatory and antiinflammatory effects.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	102-129
16051743-2	2005	Thalidomide is a first-generation immuno-modulating agent that down-regulates TNF-alpha and VEGF.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	78-87
16051743-2	2005	Thalidomide is a first-generation immuno-modulating agent that down-regulates TNF-alpha and VEGF.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	92-96
16249352-0	2005	Thalidomide in advanced hepatocellular carcinoma with optional low-dose interferon-alpha2a upon progression.	Thalidomide	0-11	interferon alpha 2	Homo sapiens	72-90
16039549-8	2005	A similar inhibition of B(1) receptor-mediated paw edema was observed when mice were treated with thalidomide (30 mg/kg, s.c.) [corrected] a drug known for reducing TNFalpha synthesis, 5 min prior to LPS administration.	Thalidomide	98-109	tumor necrosis factor	Mus musculus	165-173
16288038-3	2005	We examined whether thalidomide is able to suppress the expression of uPAR mRNA and protein in human ovarian cancer cell line HRA and human chondrosarcoma cell line HCS-2/8.	Thalidomide	20-31	plasminogen activator, urokinase receptor	Homo sapiens	70-74
16288038-7	2005	We conclude that thalidomide down-regulates constitutive and TGF-beta1-stimulated uPAR mRNA and protein expression possibly through suppression of NF-kappaB activation.	Thalidomide	17-28	transforming growth factor beta 1	Homo sapiens	61-70
16288038-7	2005	We conclude that thalidomide down-regulates constitutive and TGF-beta1-stimulated uPAR mRNA and protein expression possibly through suppression of NF-kappaB activation.	Thalidomide	17-28	plasminogen activator, urokinase receptor	Homo sapiens	82-86
16288038-7	2005	We conclude that thalidomide down-regulates constitutive and TGF-beta1-stimulated uPAR mRNA and protein expression possibly through suppression of NF-kappaB activation.	Thalidomide	17-28	nuclear factor kappa B subunit 1	Homo sapiens	147-156
16079895-0	2005	The combination of intermediate doses of thalidomide with dexamethasone is an effective treatment for patients with refractory/relapsed multiple myeloma and normalizes abnormal bone remodeling, through the reduction of sRANKL/osteoprotegerin ratio.	Thalidomide	41-52	TNF receptor superfamily member 11b	Homo sapiens	226-241
16079895-6	2005	Thal/Dex administration resulted in a significant reduction of sRANKL/OPG ratio, and bone resorption.	Thalidomide	0-4	TNF receptor superfamily member 11b	Homo sapiens	70-73
16079895-13	2005	These results suggest that the combination of intermediate dose of Thal/Dex is effective in patients with refractory/relapsed myeloma and improves abnormal bone remodeling through the reduction of sRANKL/OPG ratio.	Thalidomide	67-71	TNF receptor superfamily member 11b	Homo sapiens	204-207
16241859-3	2005	In the present study, we investigated the effects of one of the IMiDs, CC-4047 (Actimid, Celgene, Warren, NJ), on synthesis of IL-2 protein and mRNA and on the activity and expression of transcription factors.	Thalidomide	89-96	interleukin 2	Homo sapiens	127-131
16086360-4	2005	SALL4 mutations may also cause acro-renal-ocular syndrome (AROS), which differs from DRRS by the presence of structural eye anomalies, and phenotypes similar to thalidomide embryopathy and Holt-Oram syndrome (HOS).	Thalidomide	161-172	spalt like transcription factor 4	Homo sapiens	0-5
16344099-5	2005	First established as agents with antiangiogenic properties, thalidomide and IMiDs inhibit the production of interleukin (IL)-6, which is a growth factor for the proliferation of myeloma cells.	Thalidomide	60-71	interleukin 6	Homo sapiens	108-126
16091059-0	2005	alpha-fetoprotein response predicts survival benefits of thalidomide in advanced hepatocellular carcinoma.	Thalidomide	57-68	alpha fetoprotein	Homo sapiens	0-17
18360564-0	2005	Therapeutic effects of thalidomide in myeloma are associated with the expression of fibroblast growth factor receptor 3.	Thalidomide	23-34	fibroblast growth factor receptor 3	Homo sapiens	84-119
18360564-5	2005	FGFR3 transfected U266 clones revealed increased FGFR3 expression, but resulted in decreased DNA synthesis and increased apoptosis under Thal treatment.	Thalidomide	137-141	fibroblast growth factor receptor 3	Homo sapiens	0-5
16091059-2	2005	AIMS: To evaluate the clinical implications of tumour marker (alpha-fetoprotein) response in advanced hepatocellular carcinoma patients with thalidomide treatment.	Thalidomide	141-152	alpha fetoprotein	Homo sapiens	62-79
16091059-10	2005	CONCLUSION: alpha-fetoprotein response can more accurately reflect the biological response of advanced hepatocellular carcinoma to thalidomide therapy than radiographic response.	Thalidomide	131-142	alpha fetoprotein	Homo sapiens	12-29
16061867-1	2005	Preclinical data indicates that cyclooxygenase-2 (COX-2) inhibition impairs plasma cell growth and potentially synergizes with thalidomide.	Thalidomide	127-138	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-48
16061867-1	2005	Preclinical data indicates that cyclooxygenase-2 (COX-2) inhibition impairs plasma cell growth and potentially synergizes with thalidomide.	Thalidomide	127-138	prostaglandin-endoperoxide synthase 2	Homo sapiens	50-55
16061867-12	2005	Future studies should use newer COX-2 inhibitors with thalidomide, or their respective derivatives.	Thalidomide	54-65	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-37
15789431-6	2005	Furthermore, the effect of LPS was blocked by thalidomide, an inhibitor of TNF-alpha synthesis.	Thalidomide	46-57	tumor necrosis factor	Rattus norvegicus	75-84
15982930-7	2005	Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.	Thalidomide	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	20-25
16098027-5	2005	We also measured clearly reduced levels of tumor necrosis factor-alpha in the thalidomide-treated group.	Thalidomide	78-89	tumor necrosis factor	Homo sapiens	43-70
15920492-0	2005	Long-term thalidomide therapy resulted in lack of mdr1 gene expression in a patient with primary resistant multiple myeloma.	Thalidomide	10-21	ATP binding cassette subfamily B member 1	Homo sapiens	50-54
15982930-0	2005	Thalidomide inhibits growth of tumors through COX-2 degradation independent of antiangiogenesis.	Thalidomide	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	46-51
15982930-7	2005	Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.	Thalidomide	0-11	BCL2 apoptosis regulator	Homo sapiens	66-71
15982930-7	2005	Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	81-89
15982930-7	2005	Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	91-95
15982930-7	2005	Thalidomide reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.	Thalidomide	0-11	cytochrome c, somatic	Homo sapiens	118-130
15982930-9	2005	In our mouse xenograft model of OVCAR-3 and HCT-8, we found that thalidomide could decrease intratumoral microvessel density in both tumors; it exerted antitumor effects only on OVCAR-3 expressing COX-2 but did not on HCT-8 not expressing COX-2.	Thalidomide	65-76	cytochrome c oxidase II, mitochondrial	Mus musculus	197-202
15982930-9	2005	In our mouse xenograft model of OVCAR-3 and HCT-8, we found that thalidomide could decrease intratumoral microvessel density in both tumors; it exerted antitumor effects only on OVCAR-3 expressing COX-2 but did not on HCT-8 not expressing COX-2.	Thalidomide	65-76	cytochrome c oxidase II, mitochondrial	Mus musculus	239-244
15982930-10	2005	Effect of thalidomide on COX-1 and COX-2 in vivo was consistent with that of in vitro.	Thalidomide	10-21	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	25-30
15982930-10	2005	Effect of thalidomide on COX-1 and COX-2 in vivo was consistent with that of in vitro.	Thalidomide	10-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	35-40
15982930-11	2005	These results demonstrated that thalidomide might inhibit growth of tumors through COX-2 degradation independent of antiangiogenesis.	Thalidomide	32-43	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	83-88
15986355-8	2005	Interestingly, thalidomide and NF-kappaB small interfering RNA down-regulated cFLIP and Bcl-x(L) expression levels and sensitized BD activated T cells to CD95-induced apoptosis.	Thalidomide	15-26	BCL2 like 1	Homo sapiens	88-96
15741222-0	2005	Thalidomide-induced antiangiogenic action is mediated by ceramide through depletion of VEGF receptors, and is antagonized by sphingosine-1-phosphate.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	87-91
15741222-3	2005	Thalidomide induces the defect of major blood vessels, which is demonstrated by their morphologic loss and confirmed by the depletion of vascular endothelial growth factor (VEGF) receptors such as neuropilin-1 and Flk-1.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	137-171
15741222-3	2005	Thalidomide induces the defect of major blood vessels, which is demonstrated by their morphologic loss and confirmed by the depletion of vascular endothelial growth factor (VEGF) receptors such as neuropilin-1 and Flk-1.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	173-177
15741222-3	2005	Thalidomide induces the defect of major blood vessels, which is demonstrated by their morphologic loss and confirmed by the depletion of vascular endothelial growth factor (VEGF) receptors such as neuropilin-1 and Flk-1.	Thalidomide	0-11	neuropilin 1	Homo sapiens	197-209
15741222-3	2005	Thalidomide induces the defect of major blood vessels, which is demonstrated by their morphologic loss and confirmed by the depletion of vascular endothelial growth factor (VEGF) receptors such as neuropilin-1 and Flk-1.	Thalidomide	0-11	kinase insert domain receptor	Homo sapiens	214-219
15741222-4	2005	Transient increase of ceramide content through activation of neutral sphingomyelinase (nSMase) precedes thalidomide-induced vascular defect in the embryos.	Thalidomide	104-115	sphingomyelin phosphodiesterase 2	Homo sapiens	61-85
15741222-4	2005	Transient increase of ceramide content through activation of neutral sphingomyelinase (nSMase) precedes thalidomide-induced vascular defect in the embryos.	Thalidomide	104-115	sphingomyelin phosphodiesterase 2	Homo sapiens	87-93
15741222-6	2005	The blockade of ceramide generation by antisense morpholino oligonucleotides for nSMase prevents thalidomide-induced ceramide generation and vascular defect.	Thalidomide	97-108	sphingomyelin phosphodiesterase 2	Homo sapiens	81-87
15741222-7	2005	In contrast to ceramide, sphingosine-1-phosphate (S1P) inhibits nSMase-dependent ceramide generation and restores thalidomide-induced embryonic vascular defect with an increase of expression of VEGF receptors.	Thalidomide	114-125	vascular endothelial growth factor A	Homo sapiens	194-198
15741222-8	2005	In human umbilical vein endothelial cells (HUVECs), thalidomide-induced inhibition of cell growth, generation of ceramide through nSMase, and depletion of VEGF receptors are restored to the control levels by pretreatment with S1P.	Thalidomide	52-63	sphingomyelin phosphodiesterase 2	Homo sapiens	130-136
15741222-8	2005	In human umbilical vein endothelial cells (HUVECs), thalidomide-induced inhibition of cell growth, generation of ceramide through nSMase, and depletion of VEGF receptors are restored to the control levels by pretreatment with S1P.	Thalidomide	52-63	vascular endothelial growth factor A	Homo sapiens	155-159
16297005-4	2005	Opiate receptor antagonists, antidepressants, antiepileptics, and thalidomide are currently available therapeutic options that have benefited many patients with variegated sources of itch.	Thalidomide	66-77	itchy E3 ubiquitin protein ligase	Homo sapiens	183-187
15986355-8	2005	Interestingly, thalidomide and NF-kappaB small interfering RNA down-regulated cFLIP and Bcl-x(L) expression levels and sensitized BD activated T cells to CD95-induced apoptosis.	Thalidomide	15-26	Fas cell surface death receptor	Homo sapiens	154-158
16019550-1	2005	Thalidomide is thought to have anti-angiogenic and immunomodulatory properties, including suppression of tumor necrosis factor-alpha, effects on interleukins and interferons, down-regulation of some cell adhesion molecules, and changes in the proportion of lymphocyte subsets.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	105-132
16019550-11	2005	Although the CD4/CD8 ratio declined from 1.6 to 1.0 during 3 months of thalidomide treatment, this had no statistical significance (P = 0.1).	Thalidomide	71-82	CD4 molecule	Homo sapiens	13-16
16019550-11	2005	Although the CD4/CD8 ratio declined from 1.6 to 1.0 during 3 months of thalidomide treatment, this had no statistical significance (P = 0.1).	Thalidomide	71-82	CD8a molecule	Homo sapiens	17-20
15817259-3	2005	It is recognised that thalidomide decreases TNF production and may modulate several functions of the immune system.	Thalidomide	22-33	tumor necrosis factor	Mus musculus	44-47
16078585-6	2005	RESULTS: With respect to TNBS model, in the control, prednisone-treatment and thalidomide-treatment groups, the macroscopic and microscopic scores were 6.33 +/- 1.03, 1.67 +/- 0.82, 2.00 +/- 0.89 and 7.33 +/- 1.03, 2.67s +/- 0.82, 3.17 +/- 0.75 respectively; the expression levels of NF-kappaB P65 and TNF-alpha mRNA in the three groups were 62.45 +/- 12.38, 23.62 +/- 8.54, 34.18 +/- 9.65 and 12.42 +/- 4.63, 9.86 +/- 3.29, 4.35 +/- 1.74 respectively; the levels of TNF-alpha, IL-4, IFN-gamma were 540.32 +/- 80.76, 94.58 +/- 14.45, 486.18 +/- 68.47; 396.53 +/- 92.42, 78.45 +/- 12.69, 347.56 +/- 82.94; and 385.68 +/- 88.57, 123.68 +/- 38.15, 378.27 +/- 90.65 respectively.	Thalidomide	78-89	tumor necrosis factor	Rattus norvegicus	302-311
16078585-6	2005	RESULTS: With respect to TNBS model, in the control, prednisone-treatment and thalidomide-treatment groups, the macroscopic and microscopic scores were 6.33 +/- 1.03, 1.67 +/- 0.82, 2.00 +/- 0.89 and 7.33 +/- 1.03, 2.67s +/- 0.82, 3.17 +/- 0.75 respectively; the expression levels of NF-kappaB P65 and TNF-alpha mRNA in the three groups were 62.45 +/- 12.38, 23.62 +/- 8.54, 34.18 +/- 9.65 and 12.42 +/- 4.63, 9.86 +/- 3.29, 4.35 +/- 1.74 respectively; the levels of TNF-alpha, IL-4, IFN-gamma were 540.32 +/- 80.76, 94.58 +/- 14.45, 486.18 +/- 68.47; 396.53 +/- 92.42, 78.45 +/- 12.69, 347.56 +/- 82.94; and 385.68 +/- 88.57, 123.68 +/- 38.15, 378.27 +/- 90.65 respectively.	Thalidomide	78-89	tumor necrosis factor	Rattus norvegicus	467-476
16078585-6	2005	RESULTS: With respect to TNBS model, in the control, prednisone-treatment and thalidomide-treatment groups, the macroscopic and microscopic scores were 6.33 +/- 1.03, 1.67 +/- 0.82, 2.00 +/- 0.89 and 7.33 +/- 1.03, 2.67s +/- 0.82, 3.17 +/- 0.75 respectively; the expression levels of NF-kappaB P65 and TNF-alpha mRNA in the three groups were 62.45 +/- 12.38, 23.62 +/- 8.54, 34.18 +/- 9.65 and 12.42 +/- 4.63, 9.86 +/- 3.29, 4.35 +/- 1.74 respectively; the levels of TNF-alpha, IL-4, IFN-gamma were 540.32 +/- 80.76, 94.58 +/- 14.45, 486.18 +/- 68.47; 396.53 +/- 92.42, 78.45 +/- 12.69, 347.56 +/- 82.94; and 385.68 +/- 88.57, 123.68 +/- 38.15, 378.27 +/- 90.65 respectively.	Thalidomide	78-89	interleukin 4	Rattus norvegicus	478-482
16078585-6	2005	RESULTS: With respect to TNBS model, in the control, prednisone-treatment and thalidomide-treatment groups, the macroscopic and microscopic scores were 6.33 +/- 1.03, 1.67 +/- 0.82, 2.00 +/- 0.89 and 7.33 +/- 1.03, 2.67s +/- 0.82, 3.17 +/- 0.75 respectively; the expression levels of NF-kappaB P65 and TNF-alpha mRNA in the three groups were 62.45 +/- 12.38, 23.62 +/- 8.54, 34.18 +/- 9.65 and 12.42 +/- 4.63, 9.86 +/- 3.29, 4.35 +/- 1.74 respectively; the levels of TNF-alpha, IL-4, IFN-gamma were 540.32 +/- 80.76, 94.58 +/- 14.45, 486.18 +/- 68.47; 396.53 +/- 92.42, 78.45 +/- 12.69, 347.56 +/- 82.94; and 385.68 +/- 88.57, 123.68 +/- 38.15, 378.27 +/- 90.65 respectively.	Thalidomide	78-89	interferon gamma	Rattus norvegicus	484-493
16078585-7	2005	The results indicated that thalidomide treatment significantly reduced colonic inflammation, suppressed NF-kappaB activation,enhanced TNF-alpha mRNA degradation, inhibited the synthesis of the TNF-alpha, IEN-gamma and increased the production of IL-4.	Thalidomide	27-38	tumor necrosis factor	Rattus norvegicus	134-143
16078585-7	2005	The results indicated that thalidomide treatment significantly reduced colonic inflammation, suppressed NF-kappaB activation,enhanced TNF-alpha mRNA degradation, inhibited the synthesis of the TNF-alpha, IEN-gamma and increased the production of IL-4.	Thalidomide	27-38	tumor necrosis factor	Rattus norvegicus	193-202
16078585-7	2005	The results indicated that thalidomide treatment significantly reduced colonic inflammation, suppressed NF-kappaB activation,enhanced TNF-alpha mRNA degradation, inhibited the synthesis of the TNF-alpha, IEN-gamma and increased the production of IL-4.	Thalidomide	27-38	interleukin 4	Rattus norvegicus	246-250
15797874-7	2005	Several inhibitors of the NF-kappaB signaling pathway, including dexamethasone, thalidomide, and a proteasome inhibitor, bortezomib, showed inhibitory effects on LPS-induced GADD45beta expression as indicated by a decrease of the luciferase activity.	Thalidomide	80-91	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	26-35
15797874-7	2005	Several inhibitors of the NF-kappaB signaling pathway, including dexamethasone, thalidomide, and a proteasome inhibitor, bortezomib, showed inhibitory effects on LPS-induced GADD45beta expression as indicated by a decrease of the luciferase activity.	Thalidomide	80-91	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	174-184
15897810-12	2005	Thalidomide also caused a substantial reduction of the rise in myeloperoxidase activity (mucosa), in the increase in the tissue levels of TNF-alpha, IL-1beta, and VEGF, in the increase in staining (immunohistochemistry) for nitrotyrosine and for poly (ADP ribose), as well as in the upregulation of intercellular adhesion molecule-1 caused by DNBS in the colon.	Thalidomide	0-11	myeloperoxidase	Mus musculus	63-78
15897810-12	2005	Thalidomide also caused a substantial reduction of the rise in myeloperoxidase activity (mucosa), in the increase in the tissue levels of TNF-alpha, IL-1beta, and VEGF, in the increase in staining (immunohistochemistry) for nitrotyrosine and for poly (ADP ribose), as well as in the upregulation of intercellular adhesion molecule-1 caused by DNBS in the colon.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	138-147
15897810-12	2005	Thalidomide also caused a substantial reduction of the rise in myeloperoxidase activity (mucosa), in the increase in the tissue levels of TNF-alpha, IL-1beta, and VEGF, in the increase in staining (immunohistochemistry) for nitrotyrosine and for poly (ADP ribose), as well as in the upregulation of intercellular adhesion molecule-1 caused by DNBS in the colon.	Thalidomide	0-11	interleukin 1 beta	Mus musculus	149-157
15897810-12	2005	Thalidomide also caused a substantial reduction of the rise in myeloperoxidase activity (mucosa), in the increase in the tissue levels of TNF-alpha, IL-1beta, and VEGF, in the increase in staining (immunohistochemistry) for nitrotyrosine and for poly (ADP ribose), as well as in the upregulation of intercellular adhesion molecule-1 caused by DNBS in the colon.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	163-167
15897810-12	2005	Thalidomide also caused a substantial reduction of the rise in myeloperoxidase activity (mucosa), in the increase in the tissue levels of TNF-alpha, IL-1beta, and VEGF, in the increase in staining (immunohistochemistry) for nitrotyrosine and for poly (ADP ribose), as well as in the upregulation of intercellular adhesion molecule-1 caused by DNBS in the colon.	Thalidomide	0-11	intercellular adhesion molecule 1	Mus musculus	299-332
15915823-9	2005	Agents that inhibit NF-kappaB activation, such as resveratrol, thalidomide, ibuprofen, eicosapentaenoic acid, and beta-hydroxy-beta-methylbutyrate, are effective in the preservation of skeletal muscle mass in cachexia.	Thalidomide	63-74	nuclear factor kappa B subunit 1	Homo sapiens	20-29
15687330-0	2005	Thalidomide inhibits tumor necrosis factor-alpha-induced interleukin-8 expression in endometriotic stromal cells, possibly through suppression of nuclear factor-kappaB activation.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	57-70
16146335-4	2005	Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	colony stimulating factor 2	Homo sapiens	171-177
15618473-7	2005	In vitro exposure of ECs to thalidomide or its derivative CC-5013 inhibited gene expression of the receptors for transforming growth factor-beta and thrombin.	Thalidomide	28-39	transforming growth factor beta 1	Homo sapiens	113-144
15618473-7	2005	In vitro exposure of ECs to thalidomide or its derivative CC-5013 inhibited gene expression of the receptors for transforming growth factor-beta and thrombin.	Thalidomide	28-39	coagulation factor II, thrombin	Homo sapiens	149-157
16536004-5	2005	Corticosteroids are still the first-line treatment, but alternative therapy with anti-TNF agents, like pentoxifylline, thalidomide and anti-TNF monoclonal antibodies become more interesting, especially in refractory sarcoidosis.	Thalidomide	119-130	tumor necrosis factor	Homo sapiens	86-89
15858091-3	2005	Evaluation of response to thalidomide treatment was based on findings at computed tomography (CT) and change in serum alpha-fetoprotein level.	Thalidomide	26-37	alpha fetoprotein	Homo sapiens	118-135
16146335-4	2005	Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	44-71
16146335-4	2005	Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	73-82
16146335-4	2005	Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	85-108
16146335-7	2005	Thalidomide stimulates the Th-1 response increasing IFN-gamma levels while CC-4047 increased IL-2 as well.	Thalidomide	0-11	interferon gamma	Homo sapiens	52-61
15683845-0	2005	LASSBio-468: a new achiral thalidomide analogue which modulates TNF-alpha and NO production and inhibits endotoxic shock and arthritis in an animal model.	Thalidomide	27-38	tumor necrosis factor	Rattus norvegicus	64-73
16146335-4	2005	Thalidomide and IMiDs inhibit the cytokines tumor necrosis factor-alpha (TNF-alpha), interleukins (IL) 1beta, 6, 12, and granulocyte macrophage-colony stimulating factor (GM-CSF).	Thalidomide	0-11	colony stimulating factor 2	Homo sapiens	121-169
15683845-2	2005	This compound was planned as an N-substituted phthalimide derivate, structurally designed as a hybrid of thalidomide and aryl sulfonamides, which were previously described as tumor necrosis factor-alpha (TNF-alpha) and PDE4 inhibitors.	Thalidomide	105-116	tumor necrosis factor	Rattus norvegicus	175-202
15683845-2	2005	This compound was planned as an N-substituted phthalimide derivate, structurally designed as a hybrid of thalidomide and aryl sulfonamides, which were previously described as tumor necrosis factor-alpha (TNF-alpha) and PDE4 inhibitors.	Thalidomide	105-116	tumor necrosis factor	Rattus norvegicus	204-213
15840315-8	2005	(2) Expression of VEGF mRNA level in Thd group (55 +/- 9) and Thd + CTX group (26 +/- 7) was significantly lower than that in control group (79 +/- 7, P &lt; 0.01).	Thalidomide	37-40	vascular endothelial growth factor A	Mus musculus	18-22
15840315-8	2005	(2) Expression of VEGF mRNA level in Thd group (55 +/- 9) and Thd + CTX group (26 +/- 7) was significantly lower than that in control group (79 +/- 7, P &lt; 0.01).	Thalidomide	62-65	vascular endothelial growth factor A	Mus musculus	18-22
15840315-9	2005	Serum VEGF level in Thd group, [(29 +/- 10) pg/ml] and Thd + CTX group [(12 +/- 6) pg/ml] was significantly lower than that in control group, [(71 +/- 16) pg/ml, P &lt; 0.01].	Thalidomide	20-23	vascular endothelial growth factor A	Mus musculus	6-10
16264875-0	2005	Does the combination of rituximab and thalidomide influence the long-term perspectives of advanced-stage MCL?	Thalidomide	38-49	C-type lectin domain family 4 member D	Homo sapiens	105-108
15654911-2	2005	Thalidomide is an immunomodulator agent of inflammatory cytokines including TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	76-85
15638853-3	2005	Specifically, we have reported that thalidomide increased serum interleukin-2 (IL-2) levels and natural killer (NK) cell numbers in the peripheral blood of responding MM patients.	Thalidomide	36-47	interleukin 2	Homo sapiens	64-77
15638853-3	2005	Specifically, we have reported that thalidomide increased serum interleukin-2 (IL-2) levels and natural killer (NK) cell numbers in the peripheral blood of responding MM patients.	Thalidomide	36-47	interleukin 2	Homo sapiens	79-83
15723633-6	2005	The suppressive effect of thalidomide on the activation of the nuclear transcription factor NF-(kappa)B may explain these effects of thalidomide.	Thalidomide	133-144	nuclear factor kappa B subunit 1	Homo sapiens	92-103
15723633-9	2005	Thalidomide, on the other hand, has been shown to selectively suppress NF-(kappa)B activation induced by inflammatory mediators.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	71-82
15723633-3	2005	So far, investigations into the mode of action of thalidomide have focused on lymphocytes and vascular endothelial cells and have shown that this agent inhibits the production of tumor necrosis factor (TNF)-alpha and is an inhibitor of tumor angiogenesis.	Thalidomide	50-61	tumor necrosis factor	Homo sapiens	179-212
15569010-4	2004	In this work we describe the effect that thalidomide had on TNF-alpha sera levels and on IL-4- and IFN gamma (IFNgamma)-producing lymphocytes of actinic prurigo (AP) patients.	Thalidomide	41-52	interferon gamma	Homo sapiens	110-118
15723633-6	2005	The suppressive effect of thalidomide on the activation of the nuclear transcription factor NF-(kappa)B may explain these effects of thalidomide.	Thalidomide	26-37	nuclear factor kappa B subunit 1	Homo sapiens	92-103
15628770-13	2004	The downregulation of bFGF, VEGF, and maybe some other angiogenesis stimulators, is one of the antiangiogenic mechanisms of thalidomide.	Thalidomide	124-135	fibroblast growth factor 2	Homo sapiens	22-26
15628770-13	2004	The downregulation of bFGF, VEGF, and maybe some other angiogenesis stimulators, is one of the antiangiogenic mechanisms of thalidomide.	Thalidomide	124-135	vascular endothelial growth factor A	Homo sapiens	28-32
15569010-4	2004	In this work we describe the effect that thalidomide had on TNF-alpha sera levels and on IL-4- and IFN gamma (IFNgamma)-producing lymphocytes of actinic prurigo (AP) patients.	Thalidomide	41-52	tumor necrosis factor	Homo sapiens	60-69
15569010-10	2004	CONCLUSIONS: Our findings confirm that AP is a disease that has an immunological component and that thalidomide clinical efficacy is exerted not only through inhibition of TNFalpha synthesis, but also through modulation of INFgamma-producing CD3+ cells.	Thalidomide	100-111	tumor necrosis factor	Homo sapiens	172-180
15569010-4	2004	In this work we describe the effect that thalidomide had on TNF-alpha sera levels and on IL-4- and IFN gamma (IFNgamma)-producing lymphocytes of actinic prurigo (AP) patients.	Thalidomide	41-52	interleukin 4	Homo sapiens	89-93
15569010-4	2004	In this work we describe the effect that thalidomide had on TNF-alpha sera levels and on IL-4- and IFN gamma (IFNgamma)-producing lymphocytes of actinic prurigo (AP) patients.	Thalidomide	41-52	interferon gamma	Homo sapiens	99-108
15345321-1	2004	Thalidomide has shown to inhibit, selectively and mainly the cytokine tumor necrosis factor-alpha (TNF-alpha), thus, thalidomide has inhibitory consequences on other cytokines; this is ascribed as an immunomodulatory effect.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	70-97
15345321-1	2004	Thalidomide has shown to inhibit, selectively and mainly the cytokine tumor necrosis factor-alpha (TNF-alpha), thus, thalidomide has inhibitory consequences on other cytokines; this is ascribed as an immunomodulatory effect.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	99-108
15345321-1	2004	Thalidomide has shown to inhibit, selectively and mainly the cytokine tumor necrosis factor-alpha (TNF-alpha), thus, thalidomide has inhibitory consequences on other cytokines; this is ascribed as an immunomodulatory effect.	Thalidomide	117-128	tumor necrosis factor	Rattus norvegicus	70-97
15345321-1	2004	Thalidomide has shown to inhibit, selectively and mainly the cytokine tumor necrosis factor-alpha (TNF-alpha), thus, thalidomide has inhibitory consequences on other cytokines; this is ascribed as an immunomodulatory effect.	Thalidomide	117-128	tumor necrosis factor	Rattus norvegicus	99-108
15377478-0	2004	Recombinant human erythropoietin and the risk of thrombosis in patients receiving thalidomide for multiple myeloma.	Thalidomide	82-93	erythropoietin	Homo sapiens	18-32
15333517-7	2004	VEGF-induced angiogenesis was inhibited after treatment with combretastatin and thalidomide.	Thalidomide	80-91	vascular endothelial growth factor A	Homo sapiens	0-4
15464241-9	2004	Expression of TNFalpha, TGFbeta1, TIMP-1, and TIMP-2 was decreased in thalidomide-treated rats compared to those treated with vehicles.	Thalidomide	70-81	tumor necrosis factor	Rattus norvegicus	14-22
15464241-9	2004	Expression of TNFalpha, TGFbeta1, TIMP-1, and TIMP-2 was decreased in thalidomide-treated rats compared to those treated with vehicles.	Thalidomide	70-81	transforming growth factor, beta 1	Rattus norvegicus	24-32
15464241-9	2004	Expression of TNFalpha, TGFbeta1, TIMP-1, and TIMP-2 was decreased in thalidomide-treated rats compared to those treated with vehicles.	Thalidomide	70-81	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	34-40
15464241-9	2004	Expression of TNFalpha, TGFbeta1, TIMP-1, and TIMP-2 was decreased in thalidomide-treated rats compared to those treated with vehicles.	Thalidomide	70-81	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	46-52
15464241-10	2004	Finally, the expression of TNFalpha and TGFbeta1 mRNA of Kupffer"s cells derived from rats treated with thalidomide were much lower than those treated with vehicle.	Thalidomide	104-115	tumor necrosis factor	Rattus norvegicus	27-35
15464241-10	2004	Finally, the expression of TNFalpha and TGFbeta1 mRNA of Kupffer"s cells derived from rats treated with thalidomide were much lower than those treated with vehicle.	Thalidomide	104-115	transforming growth factor, beta 1	Rattus norvegicus	40-48
15464241-11	2004	CONCLUSIONS: Thalidomide salvages lethal hepatic necroinflammation, accelerates recovery from cirrhosis in rats, and works by suppressing of TNFalpha and TGFbeta1 production of Kupffer"s cells.	Thalidomide	13-24	tumor necrosis factor	Rattus norvegicus	141-149
15464241-11	2004	CONCLUSIONS: Thalidomide salvages lethal hepatic necroinflammation, accelerates recovery from cirrhosis in rats, and works by suppressing of TNFalpha and TGFbeta1 production of Kupffer"s cells.	Thalidomide	13-24	transforming growth factor, beta 1	Rattus norvegicus	154-162
15235749-0	2004	Modification of thrombomodulin plasma levels in refractory myeloma patients during treatment with thalidomide and dexamethasone.	Thalidomide	98-109	thrombomodulin	Homo sapiens	16-30
15547876-3	2004	Thalidomide is an immunodulatory and antiangiogenic drug; the most pronounced effect of this drug is the inhibition of tumor necrosis factor-alpha (TNF-alpha ) production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	119-146
15547876-3	2004	Thalidomide is an immunodulatory and antiangiogenic drug; the most pronounced effect of this drug is the inhibition of tumor necrosis factor-alpha (TNF-alpha ) production.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	148-157
15205358-0	2004	The effect of thalidomide on non-small cell lung cancer (NSCLC) cell lines: possible involvement in the PPARgamma pathway.	Thalidomide	14-25	peroxisome proliferator activated receptor gamma	Mus musculus	104-113
15205358-8	2004	At the molecular level, thalidomide increased peroxisome proliferator-activated receptor gamma (PPARgamma) protein dose-dependently, and peroxisome proliferator response element activity.	Thalidomide	24-35	peroxisome proliferator activated receptor gamma	Mus musculus	46-94
15205358-8	2004	At the molecular level, thalidomide increased peroxisome proliferator-activated receptor gamma (PPARgamma) protein dose-dependently, and peroxisome proliferator response element activity.	Thalidomide	24-35	peroxisome proliferator activated receptor gamma	Mus musculus	96-105
15205358-10	2004	In our mouse xenograft model of lung cancer, we found that intratumoral thalidomide caused a 64% decrease in tumor growth; moreover, tumors from the thalidomide-treated mice expressed higher PPARgamma, than tumors from control mice.	Thalidomide	72-83	peroxisome proliferator activated receptor gamma	Mus musculus	191-200
15205358-10	2004	In our mouse xenograft model of lung cancer, we found that intratumoral thalidomide caused a 64% decrease in tumor growth; moreover, tumors from the thalidomide-treated mice expressed higher PPARgamma, than tumors from control mice.	Thalidomide	149-160	peroxisome proliferator activated receptor gamma	Mus musculus	191-200
15205358-11	2004	This study shows the antitumor activity of thalidomide against LCC tumors and suggests a model in which thalidomide exerts its antitumor effects on LCC cells through the induction of PPARgamma and subsequent downstream signaling.	Thalidomide	43-54	peroxisome proliferator activated receptor gamma	Mus musculus	183-192
15205358-11	2004	This study shows the antitumor activity of thalidomide against LCC tumors and suggests a model in which thalidomide exerts its antitumor effects on LCC cells through the induction of PPARgamma and subsequent downstream signaling.	Thalidomide	104-115	peroxisome proliferator activated receptor gamma	Mus musculus	183-192
15205358-12	2004	To our knowledge, this is the first study to show a link between thalidomide and PPARgamma.	Thalidomide	65-76	peroxisome proliferator activated receptor gamma	Mus musculus	81-90
15290170-0	2004	Thalidomide upregulates macrophage inflammatory protein-1alpha in a herpes simplex virus-induced Behcet"s disease-like animal model.	Thalidomide	0-11	chemokine (C-C motif) ligand 3	Mus musculus	24-62
15290170-9	2004	Among these, TNFalpha, MIP-1alpha, perforin and Fas were influenced by thalidomide treatment.	Thalidomide	71-82	tumor necrosis factor	Mus musculus	13-21
15290170-9	2004	Among these, TNFalpha, MIP-1alpha, perforin and Fas were influenced by thalidomide treatment.	Thalidomide	71-82	chemokine (C-C motif) ligand 3	Mus musculus	23-33
15290170-10	2004	These results suggest that thalidomide can attenuate HSV-induced BD-like symptoms in mice through the downregulation of TNFalpha (P &lt; 0.005) and the upregulation of MIP-1alpha (P &lt; 0.005), perforin (P &lt; 0.05) and FasR (P &lt; 0.1).	Thalidomide	27-38	tumor necrosis factor	Mus musculus	120-128
15290170-10	2004	These results suggest that thalidomide can attenuate HSV-induced BD-like symptoms in mice through the downregulation of TNFalpha (P &lt; 0.005) and the upregulation of MIP-1alpha (P &lt; 0.005), perforin (P &lt; 0.05) and FasR (P &lt; 0.1).	Thalidomide	27-38	chemokine (C-C motif) ligand 3	Mus musculus	168-178
15377478-1	2004	Among 199 patients treated with thalidomide for multiple myeloma, four thromboses occurred in 49 cases during erythropoietin therapy (prevalence 8.1%; annual rate 7.25%), and another 14 events occurred in patients not on erythropoietin (9.3%; 7.56%).	Thalidomide	32-43	erythropoietin	Homo sapiens	110-124
15446566-7	2004	Thalidomide decreased the stability of TNF-mRNA and COX-2 mRNA.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	39-42
15446566-7	2004	Thalidomide decreased the stability of TNF-mRNA and COX-2 mRNA.	Thalidomide	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	52-57
15329836-0	2004	Mutations in SALL4 in malformed father and daughter postulated previously due to reflect mutagenesis by thalidomide.	Thalidomide	104-115	spalt like transcription factor 4	Homo sapiens	13-18
15261258-1	2004	Thalidomide shows moderate inhibitory activity toward neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), but not toward endothelial NOS (eNOS).	Thalidomide	0-11	nitric oxide synthase 1	Homo sapiens	54-84
15261258-1	2004	Thalidomide shows moderate inhibitory activity toward neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), but not toward endothelial NOS (eNOS).	Thalidomide	0-11	nitric oxide synthase 1	Homo sapiens	86-90
15261258-1	2004	Thalidomide shows moderate inhibitory activity toward neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), but not toward endothelial NOS (eNOS).	Thalidomide	0-11	nitric oxide synthase 2	Homo sapiens	96-109
15261258-1	2004	Thalidomide shows moderate inhibitory activity toward neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS), but not toward endothelial NOS (eNOS).	Thalidomide	0-11	nitric oxide synthase 2	Homo sapiens	111-115
15288591-5	2004	High amounts of TNF-alpha were detected in the exudates, which was inhibited by dexamethasone, pentoxifylline and thalidomide.	Thalidomide	114-125	tumor necrosis factor	Rattus norvegicus	16-25
15288591-6	2004	These results suggest a specific role for TNF-alpha in this model, and the ability of pentoxifylline and thalidomide to inhibit both neutrophil influx and TNF-alpha release may have therapeutic implications in arthritis.	Thalidomide	105-116	tumor necrosis factor	Rattus norvegicus	155-164
15261445-3	2004	Clinical trials have recently been initiated to evaluate the anti-tumour activity of the VEGF inhibitors SU5416, bevacizumab and thalidomide.	Thalidomide	129-140	vascular endothelial growth factor A	Homo sapiens	89-93
15598423-3	2004	In the present study, we have investigated the effects of thalidomide, CC-5013 and CC-4047 on the expression of COX-2 by stimulated PBMC.	Thalidomide	58-69	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	112-117
15598423-4	2004	Our results show that thalidomide and IMiDs inhibited the expression of COX-2 but not the COX-1 protein in LPS-TNF-alpha and IL-1beta stimulated PBMC and shortened the half-life of COX-2 mRNA in a dose-dependent manner.	Thalidomide	22-33	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	72-77
15598423-4	2004	Our results show that thalidomide and IMiDs inhibited the expression of COX-2 but not the COX-1 protein in LPS-TNF-alpha and IL-1beta stimulated PBMC and shortened the half-life of COX-2 mRNA in a dose-dependent manner.	Thalidomide	22-33	tumor necrosis factor	Homo sapiens	111-120
15598423-4	2004	Our results show that thalidomide and IMiDs inhibited the expression of COX-2 but not the COX-1 protein in LPS-TNF-alpha and IL-1beta stimulated PBMC and shortened the half-life of COX-2 mRNA in a dose-dependent manner.	Thalidomide	22-33	interleukin 1 beta	Homo sapiens	125-133
15598423-4	2004	Our results show that thalidomide and IMiDs inhibited the expression of COX-2 but not the COX-1 protein in LPS-TNF-alpha and IL-1beta stimulated PBMC and shortened the half-life of COX-2 mRNA in a dose-dependent manner.	Thalidomide	22-33	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	181-186
15203277-0	2004	Arsenic trioxide and thalidomide combination produces multi-lineage hematological responses in myelodysplastic syndromes patients, particularly in those with high pre-therapy EVI1 expression.	Thalidomide	21-32	MDS1 and EVI1 complex locus	Homo sapiens	175-179
15221409-0	2004	Anti-angiogenic effects of thalidomide: expression of apoptosis-inducible active-caspase-3 in a three-dimensional collagen gel culture of aorta.	Thalidomide	27-38	caspase 3	Homo sapiens	81-90
15221409-7	2004	Taken together with earlier findings, our new results indicate that the thalidomide-induced inhibition of angiogenesis involves apoptosis in addition to the suppression of TNF-alpha and inhibition of cell migration from aorta explants, i.e., the factors important for capillarogenesis.	Thalidomide	72-83	tumor necrosis factor	Homo sapiens	172-181
15242253-1	2004	Celgene, in collaboration with the National Cancer Institute, is developing CC-5013, the lead compound in a series of thalidomide derivatives that inhibit TNFalpha overproduction, for the potential treatment of hematological and solid tumor cancers and inflammatory diseases.	Thalidomide	0-7	tumor necrosis factor	Homo sapiens	155-163
15226321-5	2004	RESULTS: After a median potential follow-up time of 26.4 months, the proportion of patients with a greater than 50% decline in PSA was higher in the docetaxel/thalidomide group (53% in the combined group, 37% in docetaxel-alone arm).	Thalidomide	159-170	kallikrein related peptidase 3	Homo sapiens	127-130
15226321-9	2004	CONCLUSION: In this randomized phase II trial, the addition of thalidomide to docetaxel resulted in an encouraging PSA decline rate and overall median survival rate in patients with metastatic AIPC.	Thalidomide	63-74	kallikrein related peptidase 3	Homo sapiens	115-118
15217957-10	2004	CPS45, CPS49, and thalidomide significantly reduced PC3 tumor platelet-derived growth factor (PDGF)-AA levels by 58-82% (P &lt; 0.05).	Thalidomide	18-29	chromobox 8	Homo sapiens	52-55
15244383-12	2004	Analysis of biomarker assays did not identify any biomarker associated with greater response, but a significant increase in levels of soluble intercellular adhesion molecule 1, IL-2, and interferon gamma was seen with thalidomide therapy.	Thalidomide	218-229	intercellular adhesion molecule 1	Homo sapiens	142-175
15244383-12	2004	Analysis of biomarker assays did not identify any biomarker associated with greater response, but a significant increase in levels of soluble intercellular adhesion molecule 1, IL-2, and interferon gamma was seen with thalidomide therapy.	Thalidomide	218-229	interleukin 2	Homo sapiens	177-181
15244383-12	2004	Analysis of biomarker assays did not identify any biomarker associated with greater response, but a significant increase in levels of soluble intercellular adhesion molecule 1, IL-2, and interferon gamma was seen with thalidomide therapy.	Thalidomide	218-229	interferon gamma	Homo sapiens	187-203
15069691-0	2004	Thalidomide reduces serum C-reactive protein and interleukin-6 and induces response to IL-2 in a fraction of metastatic renal cell cancer patients who failed IL-2-based therapy.	Thalidomide	0-11	C-reactive protein	Homo sapiens	26-44
15069691-0	2004	Thalidomide reduces serum C-reactive protein and interleukin-6 and induces response to IL-2 in a fraction of metastatic renal cell cancer patients who failed IL-2-based therapy.	Thalidomide	0-11	interleukin 6	Homo sapiens	49-62
15069691-0	2004	Thalidomide reduces serum C-reactive protein and interleukin-6 and induces response to IL-2 in a fraction of metastatic renal cell cancer patients who failed IL-2-based therapy.	Thalidomide	0-11	interleukin 2	Homo sapiens	87-91
15069691-0	2004	Thalidomide reduces serum C-reactive protein and interleukin-6 and induces response to IL-2 in a fraction of metastatic renal cell cancer patients who failed IL-2-based therapy.	Thalidomide	0-11	interleukin 2	Homo sapiens	158-162
15069691-3	2004	We used thalidomide to treat patients with cancer-induced cachexia and noted that the drug significantly reduced serum levels of CRP and IL-6 to normal or near normal levels in a substantial fraction of patients.	Thalidomide	8-19	C-reactive protein	Homo sapiens	129-132
15069691-3	2004	We used thalidomide to treat patients with cancer-induced cachexia and noted that the drug significantly reduced serum levels of CRP and IL-6 to normal or near normal levels in a substantial fraction of patients.	Thalidomide	8-19	interleukin 6	Homo sapiens	137-141
15069691-4	2004	We tested whether thalidomide might potentiate the response of patients with renal cell carcinoma to IL-2.	Thalidomide	18-29	interleukin 2	Homo sapiens	101-105
15069691-9	2004	Reduction of serum CRP or IL-6 levels with thalidomide may enhance the responsiveness of renal cell carcinoma to IL-2.	Thalidomide	43-54	C-reactive protein	Homo sapiens	19-22
15069691-9	2004	Reduction of serum CRP or IL-6 levels with thalidomide may enhance the responsiveness of renal cell carcinoma to IL-2.	Thalidomide	43-54	interleukin 6	Homo sapiens	26-30
15069691-9	2004	Reduction of serum CRP or IL-6 levels with thalidomide may enhance the responsiveness of renal cell carcinoma to IL-2.	Thalidomide	43-54	interleukin 2	Homo sapiens	113-117
15069691-11	2004	It is possible that the thalidomide-induced normalization of serum acute phase proteins might improve the response of other types of malignancy to IL-2 or other immune-based therapies.	Thalidomide	24-35	interleukin 2	Homo sapiens	147-151
15242253-1	2004	Celgene, in collaboration with the National Cancer Institute, is developing CC-5013, the lead compound in a series of thalidomide derivatives that inhibit TNFalpha overproduction, for the potential treatment of hematological and solid tumor cancers and inflammatory diseases.	Thalidomide	118-129	tumor necrosis factor	Homo sapiens	155-163
15222121-4	2004	Thalidomide has been shown to have antiangiogenic and immunomodulatory effects, including the inhibition of vascular endothelial growth factor, basic fibroblast growth factor and tumor necrosis factor alpha.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	108-142
15138204-10	2004	Treatment with thalidomide, dexamethasone, or fucoidin reduced gastric damage and MPO activity induced by indomethacin.	Thalidomide	15-26	myeloperoxidase	Mus musculus	82-85
15060740-13	2004	TNF mediates the effect of DMXAA on thalidomide pharmacokinetics but not that of cyclophosphamide.	Thalidomide	36-47	tumor necrosis factor	Mus musculus	0-3
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	99-133
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	170-175
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	hepatocyte growth factor	Homo sapiens	178-202
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	hepatocyte growth factor	Homo sapiens	204-207
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	interleukin 6	Homo sapiens	210-223
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	interleukin 6	Homo sapiens	225-229
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	235-262
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	264-273
15149630-1	2004	Thalidomide has antiangiogenic and immunomodulatory effects, mediated by several cytokines such as vascular endothelial growth factor (VEGF), fibroblastic growth factor (FGF-2), hepatocyte growth factor (HGF), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	135-139
15010523-11	2004	This is a possible mechanism of action with thalidomide reducing both tumor necrosis factor and the neutrophil migration.	Thalidomide	44-55	tumor necrosis factor	Homo sapiens	70-91
15086397-6	2004	In addition IgG1 antimycobacterial antibodies can reverse the effect of TNF-alpha blockers such as pentoxifylline and thalidomide.	Thalidomide	118-129	tumor necrosis factor	Homo sapiens	72-81
15182131-4	2004	Considering the involvement of IL-6 in Castleman"s disease we treated the patient with thalidomide obtaining the remission of the nephrotic syndrome.	Thalidomide	87-98	interleukin 6	Homo sapiens	31-35
15179032-9	2004	Thalidomide was found to accelerate the degradation of TNF-alpha mRNA, but had little effect on IL-1beta or IL-8.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	55-64
14988093-6	2004	In addition, arterial macrophage infiltration and local expressions of tumor necrosis factor alpha (TNF-alpha) and basic fibroblast growth factor (bFGF) in the injured arteries as measured by immunohistochemistry and immunoblot analysis were significantly reduced by thalidomide treatment.	Thalidomide	267-278	tumor necrosis factor	Rattus norvegicus	71-98
14988093-6	2004	In addition, arterial macrophage infiltration and local expressions of tumor necrosis factor alpha (TNF-alpha) and basic fibroblast growth factor (bFGF) in the injured arteries as measured by immunohistochemistry and immunoblot analysis were significantly reduced by thalidomide treatment.	Thalidomide	267-278	fibroblast growth factor 2	Rattus norvegicus	115-145
14988093-7	2004	Serum TNF-alpha, measured by ELISA, was also significantly reduced in the thalidomide-treated animals compared with controls after injury (856+/-213 versus 449+/-68 pg/mL on day 3, P=0.001; 129+/-34 versus 63+/-18 pg/mL on day 14, P=0.001), and we observed a good positive correlation between the serum TNF-alpha levels and the severity of neointimal growth.	Thalidomide	74-85	tumor necrosis factor	Rattus norvegicus	6-15
14988093-7	2004	Serum TNF-alpha, measured by ELISA, was also significantly reduced in the thalidomide-treated animals compared with controls after injury (856+/-213 versus 449+/-68 pg/mL on day 3, P=0.001; 129+/-34 versus 63+/-18 pg/mL on day 14, P=0.001), and we observed a good positive correlation between the serum TNF-alpha levels and the severity of neointimal growth.	Thalidomide	74-85	tumor necrosis factor	Rattus norvegicus	303-312
15136218-0	2004	A low serum level of soluble tumor necrosis factor receptor p55 predicts response to thalidomide in advanced multiple myeloma.	Thalidomide	85-96	tumor necrosis factor	Homo sapiens	29-50
15136218-0	2004	A low serum level of soluble tumor necrosis factor receptor p55 predicts response to thalidomide in advanced multiple myeloma.	Thalidomide	85-96	TNF receptor superfamily member 1A	Homo sapiens	60-63
15136218-1	2004	BACKGROUND AND OBJECTIVES: Thalidomide modulates the production of tumor necrosis factor (TNF-alpha).	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	67-88
15136218-1	2004	BACKGROUND AND OBJECTIVES: Thalidomide modulates the production of tumor necrosis factor (TNF-alpha).	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	90-99
15136218-6	2004	RESULTS: The pre-treatment serum level of soluble TNFR p55 in thalidomide responders was significantly lower than that in non-responders (median 1.75 ng/mL (range 1.19-2.84) vs. 2.79 ng/mL (1.36-5.51), p=0.004).	Thalidomide	62-73	TNF receptor superfamily member 1A	Homo sapiens	50-54
15136218-6	2004	RESULTS: The pre-treatment serum level of soluble TNFR p55 in thalidomide responders was significantly lower than that in non-responders (median 1.75 ng/mL (range 1.19-2.84) vs. 2.79 ng/mL (1.36-5.51), p=0.004).	Thalidomide	62-73	TNF receptor superfamily member 1A	Homo sapiens	55-58
15136218-10	2004	INTERPRETATION AND CONCLUSIONS: We conclude that soluble TNFR p55 is an adverse prognostic factor in myeloma patients with relapsed or refractory disease treated with thalidomide.	Thalidomide	167-178	TNF receptor superfamily member 1A	Homo sapiens	57-61
15136218-10	2004	INTERPRETATION AND CONCLUSIONS: We conclude that soluble TNFR p55 is an adverse prognostic factor in myeloma patients with relapsed or refractory disease treated with thalidomide.	Thalidomide	167-178	TNF receptor superfamily member 1A	Homo sapiens	62-65
15218967-4	2004	The myeloma cells decreased by thalidomide therapy were mature (MPC-1(+)/CD49e(+)) and intermediate (MPC-1(+)/CD49e(-)) types.	Thalidomide	31-42	mitochondrial pyruvate carrier 1	Homo sapiens	64-72
15218967-4	2004	The myeloma cells decreased by thalidomide therapy were mature (MPC-1(+)/CD49e(+)) and intermediate (MPC-1(+)/CD49e(-)) types.	Thalidomide	31-42	integrin subunit alpha 5	Homo sapiens	73-78
15218967-4	2004	The myeloma cells decreased by thalidomide therapy were mature (MPC-1(+)/CD49e(+)) and intermediate (MPC-1(+)/CD49e(-)) types.	Thalidomide	31-42	mitochondrial pyruvate carrier 1	Homo sapiens	101-109
15218967-4	2004	The myeloma cells decreased by thalidomide therapy were mature (MPC-1(+)/CD49e(+)) and intermediate (MPC-1(+)/CD49e(-)) types.	Thalidomide	31-42	integrin subunit alpha 5	Homo sapiens	110-115
15179032-0	2004	The effects of thalidomide on the stimulation of NF-kappaB activity and TNF-alpha production by lipopolysaccharide in a human colonic epithelial cell line.	Thalidomide	15-26	nuclear factor kappa B subunit 1	Homo sapiens	49-58
15179032-0	2004	The effects of thalidomide on the stimulation of NF-kappaB activity and TNF-alpha production by lipopolysaccharide in a human colonic epithelial cell line.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	72-81
15179032-1	2004	The immunomodulatory and anti-inflammatory effects of thalidomide are associated with inhibition of TNF-alpha levels.	Thalidomide	54-65	tumor necrosis factor	Homo sapiens	100-109
15179032-2	2004	However, the mechanism by which thalidomide reduces TNF-alpha production remains elusive.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	52-61
15179032-4	2004	We tested whether thalidomide acts through inhibiting NF-kappaB activity.	Thalidomide	18-29	nuclear factor kappa B subunit 1	Homo sapiens	54-63
15140182-2	2004	Here, male TNF-alpha (-/-) deficient mice and C57bL/6 mice were treated with MPTP (4 x 15 mg/kg, 24 h intervals) and in one series, thalidomide was administered to inhibit TNF-alpha synthesis.	Thalidomide	132-143	tumor necrosis factor	Mus musculus	172-181
15179032-10	2004	These observations suggest that the immunomodulatory effect of thalidomide in colonic epithelial cells is associated with inhibition of TNF-alpha.	Thalidomide	63-74	tumor necrosis factor	Homo sapiens	136-145
15067094-0	2004	Thalidomide induces apoptosis in human monocytes by using a cytochrome c-dependent pathway.	Thalidomide	0-11	cytochrome c, somatic	Homo sapiens	60-72
15086832-8	2004	The concentration of M-protein in the serum or urine of seven of the 11 patients was reduced by at least 30% after thalidomide treatment, and MVD in the BM decreased in three of these seven cases in response to thalidomide.	Thalidomide	115-126	myomesin 2	Homo sapiens	21-30
15086832-8	2004	The concentration of M-protein in the serum or urine of seven of the 11 patients was reduced by at least 30% after thalidomide treatment, and MVD in the BM decreased in three of these seven cases in response to thalidomide.	Thalidomide	211-222	myomesin 2	Homo sapiens	21-30
15086832-9	2004	Increased plasma concentrations of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) were observed in all 11 cases before thalidomide administration and both levels were reduced after treatment with thalidomide.	Thalidomide	157-168	fibroblast growth factor 2	Homo sapiens	67-72
15086832-9	2004	Increased plasma concentrations of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) were observed in all 11 cases before thalidomide administration and both levels were reduced after treatment with thalidomide.	Thalidomide	157-168	vascular endothelial growth factor A	Homo sapiens	114-118
15086832-9	2004	Increased plasma concentrations of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) were observed in all 11 cases before thalidomide administration and both levels were reduced after treatment with thalidomide.	Thalidomide	234-245	fibroblast growth factor 2	Homo sapiens	67-72
15086832-9	2004	Increased plasma concentrations of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) were observed in all 11 cases before thalidomide administration and both levels were reduced after treatment with thalidomide.	Thalidomide	234-245	vascular endothelial growth factor A	Homo sapiens	78-112
15086832-9	2004	Increased plasma concentrations of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) were observed in all 11 cases before thalidomide administration and both levels were reduced after treatment with thalidomide.	Thalidomide	234-245	vascular endothelial growth factor A	Homo sapiens	114-118
15086832-11	2004	It seems that thalidomide is effective in the treatment of MM through the impairment of angiogenesis by decreasing FGF-2 and VEGF production.	Thalidomide	14-25	fibroblast growth factor 2	Homo sapiens	115-120
15086832-11	2004	It seems that thalidomide is effective in the treatment of MM through the impairment of angiogenesis by decreasing FGF-2 and VEGF production.	Thalidomide	14-25	vascular endothelial growth factor A	Homo sapiens	125-129
15067094-6	2004	Monocyte apoptosis required the activation of caspases, as combined stimulation by thalidomide together with the broad caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone markedly prevented monocyte cell death.	Thalidomide	83-94	caspase 9	Homo sapiens	46-54
15016759-5	2004	After three months of thalidomide therapy, serum levels of vascular endothelial growth factor were strongly suppressed compared with pretreatment levels.	Thalidomide	22-33	vascular endothelial growth factor A	Homo sapiens	59-93
15064811-1	2004	Thalidomide is a selective inhibitor of tumor necrosis factor-alpha (TNF-alpha), a cytokine involved in mycobacterial death mechanisms.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	69-78
15056977-0	2004	Thalidomide as a nitric oxide synthase inhibitor and its structural development.	Thalidomide	0-11	nitric oxide synthase 2	Homo sapiens	17-38
15056977-1	2004	Thalidomide has been found to exhibit weak nitric oxide synthase (NOS)-inhibitory activity.	Thalidomide	0-11	nitric oxide synthase 2	Homo sapiens	43-64
15163089-3	2004	Thalidomide, a potent tumor necrosis factor alpha inhibitor, was well tolerated and possibly showed some clinical benefit in children with tuberculous meningitis during a pilot study.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	22-49
14995997-10	2004	These findings suggest that thalidomide may be procoagulant, not by enhancing doxorubicin-mediated endothelial cell injury, but by altering the expression of PAR-1 on injured endothelium and resulting in endothelial dysfunction, which may explain hypercoagulability in patients treated with chemotherapy followed by thalidomide.	Thalidomide	28-39	coagulation factor II thrombin receptor	Homo sapiens	158-163
15190511-4	2004	Thalidomide, a drug with anti-TNF, antiangiogenic, and immunomodulatory activities, and other agents with anti-TNF effects, such as pentoxifylline, etanercept, and infliximab, have produced hematologic improvement in 20% to 40% of patients.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	30-33
14995997-10	2004	These findings suggest that thalidomide may be procoagulant, not by enhancing doxorubicin-mediated endothelial cell injury, but by altering the expression of PAR-1 on injured endothelium and resulting in endothelial dysfunction, which may explain hypercoagulability in patients treated with chemotherapy followed by thalidomide.	Thalidomide	316-327	coagulation factor II thrombin receptor	Homo sapiens	158-163
14680461-1	2004	Thalidomide has several targets and mechanisms of action: a hypnosedative effect, several immunomodulatory properties with an effect on the production of TNF-alpha and the balance between the different lymphocyte subsets and an antiangiogenic action.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	154-163
15663335-7	2004	Thalidomide has been demonstrated to suppress tumor necrosis factor (TNF) release, which may be important at both the initial and chronic phases of the inflammation of sarcoidosis and appears to be crucial as part of the initial granulomatous response.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	46-67
15663335-7	2004	Thalidomide has been demonstrated to suppress tumor necrosis factor (TNF) release, which may be important at both the initial and chronic phases of the inflammation of sarcoidosis and appears to be crucial as part of the initial granulomatous response.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	69-72
15190675-0	2004	Thalidomide-based TNF-alpha inhibitors for neurodegenerative diseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	18-27
15190675-5	2004	As its clinical value in treating ENL derives from its TNF-alpha inhibitory activity, thalidomide was chosen for structural modification for the discovery of novel and more potent isosteric analogues with appropriate lipophilicity to insure high brain penetration.	Thalidomide	86-97	tumor necrosis factor	Homo sapiens	55-64
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	myeloperoxidase	Mus musculus	211-226
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	myeloperoxidase	Mus musculus	228-231
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	243-267
15581054-2	2004	Using an in vivo tumor model, we report that thalidomide (100 mg kg(-1)day(-1)) or clotrimazole (120 mg kg(-1) day(-1)), inhibit blood vessel formation (determined by hemoglobin content), leukocyte recruitment [myeloperoxidase (MPO) activity; N-acetylglucosa-minidase (NAG) activity], and vascular endothelial growth factor production.	Thalidomide	45-56	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	269-272
15581054-5	2004	Thalidomide was able to reduce the inflammatory reaction (MPO and NAG activities) by 50% to 70%, but was unable to delay tumor development.	Thalidomide	0-11	myeloperoxidase	Mus musculus	58-61
15581054-5	2004	Thalidomide was able to reduce the inflammatory reaction (MPO and NAG activities) by 50% to 70%, but was unable to delay tumor development.	Thalidomide	0-11	alpha-N-acetylglucosaminidase (Sanfilippo disease IIIB)	Mus musculus	66-69
14962263-3	2004	Current data suggest that the action of thalidomide is related to several different mechanisms, including suppression of tumor necrosis factor, effects on basic fibroblast growth factor, vascular endothelial growth factor, interleukins and interferons, downregulation of selected cell surface adhesion molecules, and changes in the lymphocyte subsets.	Thalidomide	40-51	vascular endothelial growth factor A	Homo sapiens	187-221
15479647-7	2004	However, in 2 cases in which the mean blood concentration of thalidomide was 2 microg/mL or higher, an M-protein-reducing effect was not obtained.	Thalidomide	61-72	myomesin 2	Homo sapiens	103-112
15025228-1	2004	BACKGROUND: Pentoxifylline (PTX) and thalidomide (TLD) have been shown to inhibit cytokine synthesis, mainly tumor necrosis factor (TNF)-alpha, in different inflammatory conditions.	Thalidomide	37-48	tumor necrosis factor	Rattus norvegicus	109-142
15167912-12	2004	Additionally, a dramatic decrease in Bcl-2 expression with s-thalidomide suggests a possible enhancement of cytotoxic effect if combined with other cytotoxic agents.	Thalidomide	59-72	BCL2 apoptosis regulator	Homo sapiens	37-42
29539102-1	2004	BACKGROUND: Pentoxifylline (PTX) and thalidomide (TLD) have been shown to inhibit cytokine synthesis, mainly tumor necrosis factor (TNF)-alpha, in different inflammatory conditions.	Thalidomide	37-48	tumor necrosis factor	Rattus norvegicus	109-142
14613324-0	2003	Thiothalidomides: novel isosteric analogues of thalidomide with enhanced TNF-alpha inhibitory activity.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	73-82
14693056-2	2003	The aim of this research was to observe the effect of thalidomide on tumor homograft growth in mouse H22 model and to investigate the mechanisms involved and its curative possibility to hepatoma.	Thalidomide	54-65	histocompatibility 22	Mus musculus	101-104
14693056-15	2003	CONCLUSION: Thalidomide can significantly induce apoptosis and inhibit angiogenesis in mouse H22 model when it is used at the beginning of carcinogenesis, but it has no obvious anti-angiogenic efficacy on the grown tumor.	Thalidomide	12-23	histocompatibility 22	Mus musculus	93-96
14693056-16	2003	Thalidomide cannot inhibit VEGF mRNA expression of grafted H22 tumor in mouse.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	27-31
14693056-16	2003	Thalidomide cannot inhibit VEGF mRNA expression of grafted H22 tumor in mouse.	Thalidomide	0-11	histocompatibility 22	Mus musculus	59-62
14598030-8	2003	Thalidomide, but not rosiglitazone, was associated with the inhibition of basement membrane thickening and the blockade of the increase of VEGF in ocular fluid, thus representing a potential therapeutic drug for the prevention of diabetic retinopathy.	Thalidomide	0-11	vascular endothelial growth factor A	Rattus norvegicus	139-143
14612937-13	2003	Thalidomide induced co-option of host vasculature, an effect noted previously after VEGF blockade.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	84-88
15303463-11	2004	TNF-alpha inhibitors: infliximab, CDP 571, etanercept, onercept, CNI- 1493 and thalidomide.	Thalidomide	79-90	tumor necrosis factor	Homo sapiens	0-9
14679006-6	2003	Dexamethasone and immunomodulatory derivatives of thalidomide (IMiDs), but not proteasome inhibitor PS-341, augmented MM cell apoptosis triggered by LPAAT-beta inhibitors.	Thalidomide	50-61	1-acylglycerol-3-phosphate O-acyltransferase 2	Homo sapiens	149-159
14617101-0	2003	Thalidomide inhibits UVB-induced mouse keratinocyte apoptosis by both TNF-alpha-dependent and TNF-alpha-independent pathways.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	70-79
14617101-0	2003	Thalidomide inhibits UVB-induced mouse keratinocyte apoptosis by both TNF-alpha-dependent and TNF-alpha-independent pathways.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	94-103
14617101-4	2003	PURPOSE: To test our hypothesis that thalidomide may antagonize TNF-alpha production in the skin, we used a mouse model for acute ultraviolet-B (UVB) exposure, a known stimulus for inducing this cytokine.	Thalidomide	37-48	tumor necrosis factor	Mus musculus	64-73
14617101-7	2003	RNase protection assays confirmed that high (400 mg/kg), but not low (100 mg/kg), doses of thalidomide inhibited the UVB-induced increase in steady-state TNF-alpha mRNA.	Thalidomide	91-102	tumor necrosis factor	Mus musculus	154-163
14617101-9	2003	The antiapoptotic effects of thalidomide can be reversed by the addition of exogenous recombinant mouse TNF-alpha and hence reconstituting UVB-induced programmed cell death.	Thalidomide	29-40	tumor necrosis factor	Mus musculus	104-113
14613324-3	2003	In this regard, oral thalidomide is clinically valuable in the treatment of erythema nodosum leprosum (ENL) and multiple myeloma and effectively reduces tumor necrosis factor-alpha (TNF-alpha) levels and angiogenesis in vivo.	Thalidomide	21-32	tumor necrosis factor	Homo sapiens	153-180
14613324-3	2003	In this regard, oral thalidomide is clinically valuable in the treatment of erythema nodosum leprosum (ENL) and multiple myeloma and effectively reduces tumor necrosis factor-alpha (TNF-alpha) levels and angiogenesis in vivo.	Thalidomide	21-32	tumor necrosis factor	Homo sapiens	182-191
14613324-7	2003	Two isosteric analogues of thalidomide, compounds 15 and 16, that mostly reflect the parent compound, together with the simple structure, dithioglutarimide 19, potently inhibited TNF-alpha secretion, compared to thalidomide, 1.	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	179-188
14616984-0	2003	Serum MUC-1 as a marker of disease status in multiple myeloma patients receiving thalidomide.	Thalidomide	81-92	mucin 1, cell surface associated	Homo sapiens	6-11
12930142-2	2003	Synthesis and antiangiogenic activity of the teratogenic and TNFalpha-modulatory thalidomide analogue 2-(2,6-dioxopiperidine-3-yl)phthalimidine.	Thalidomide	81-92	tumor necrosis factor	Rattus norvegicus	61-69
14682394-0	2003	Exposure to the anti-TNF-alpha drug thalidomide induces apoptotic cell death in human T leukemic cells.	Thalidomide	36-47	tumor necrosis factor	Homo sapiens	21-30
14682394-2	2003	The controversial drug thalidomide is anti-inflammatory, anti-angiogenic and a selective inhibitor of TNF-alpha that is being studied as a treatment for HIV-1-related disorders, immune disorders and cancer.	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	102-111
14682394-6	2003	Low dose thalidomide treatment of human T leukemic cells exhibited rapid increases in caspase-3 activity, annexin V-FITC binding and DNA disintegration that is characteristic of apoptosis.	Thalidomide	9-20	caspase 3	Homo sapiens	86-95
14682394-6	2003	Low dose thalidomide treatment of human T leukemic cells exhibited rapid increases in caspase-3 activity, annexin V-FITC binding and DNA disintegration that is characteristic of apoptosis.	Thalidomide	9-20	annexin A5	Homo sapiens	106-115
14505639-1	2003	Thalidomide, (1), has made a remarkable comeback from its days of a sedative with teratogenic properties due to its ability to selectively inhibit TNF-alpha, a key pro-inflammatory cytokine and its clinical benefit in the treatment of cancer.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	147-156
14505639-6	2003	On the other hand, 4 was non-cytotoxic at the tested concentrations and was found to be 830-fold more potent than thalidomide as TNF-alpha inhibitor.	Thalidomide	114-125	tumor necrosis factor	Homo sapiens	129-138
14531913-0	2003	Plasma levels of tumour necrosis factor alpha and interleukin-6 predict progression-free survival following thalidomide therapy in patients with previously untreated multiple myeloma.	Thalidomide	108-119	interleukin 6	Homo sapiens	50-63
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	22-33	fibroblast growth factor 2	Homo sapiens	84-88
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	22-33	vascular endothelial growth factor A	Homo sapiens	93-97
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	22-33	vitronectin	Homo sapiens	133-144
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	22-33	matrix metallopeptidase 2	Homo sapiens	206-211
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	22-33	C-X-C motif chemokine ligand 8	Homo sapiens	216-220
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	171-182	fibroblast growth factor 2	Homo sapiens	84-88
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	171-182	vascular endothelial growth factor A	Homo sapiens	93-97
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	171-182	vitronectin	Homo sapiens	133-144
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	171-182	matrix metallopeptidase 2	Homo sapiens	206-211
14558594-2	2003	The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug.	Thalidomide	171-182	C-X-C motif chemokine ligand 8	Homo sapiens	216-220
14577465-10	2003	In the Dhar-stimulated cells from the healthy staff thalidomide significantly suppressed TNF-alpha (P &lt; 0.05).	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	89-98
14577465-11	2003	A mixed effect was seen within and between the other groups, but there was a trend for thalidomide to suppress TNF-alpha induced by the M. leprae, Dhar and PPD antigens.	Thalidomide	87-98	tumor necrosis factor	Homo sapiens	111-120
14708607-0	2003	Thalidomide inhibits tumor necrosis factor-alpha production and antigen presentation by Langerhans cells.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	21-48
14708607-2	2003	Thalidomide is believed to exert its anti-inflammatory effects, at least in part, by inhibiting tumor necrosis factor-alpha (TNF-alpha) production by monocytes.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	96-123
14708607-2	2003	Thalidomide is believed to exert its anti-inflammatory effects, at least in part, by inhibiting tumor necrosis factor-alpha (TNF-alpha) production by monocytes.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	125-134
14708607-5	2003	Using the murine epidermis-derived dendritic cell lines, XS106A from A/J mice and XS52 from BALB/c mice as surrogates for LC, we found that thalidomide inhibited TNF-alpha production in a concentration-dependent manner.	Thalidomide	140-151	tumor necrosis factor	Mus musculus	162-171
14708607-6	2003	Northern blot analysis revealed that thalidomide significantly decreased the peak-induced mRNA level of TNF-alpha in XS106A cells and XS52 cells.	Thalidomide	37-48	tumor necrosis factor	Mus musculus	104-113
14708607-8	2003	TNF-alpha production was reduced by 67.7% at a thalidomide concentration of 200 microg per mL.	Thalidomide	47-58	tumor necrosis factor	Mus musculus	0-9
14708607-9	2003	Thalidomide also had a profound inhibitory effect on the ability of LC to present antigen to a responsive TH1 clone.	Thalidomide	0-11	negative elongation factor complex member C/D, Th1l	Mus musculus	106-109
14708607-10	2003	Thalidomide inhibits TNF-alpha production and the antigen-presenting ability of epidermal LCs.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	21-30
14551295-12	2003	CONCLUSION: The combination of frequently dosed IFN-alpha-2b and low-dose thalidomide is feasible and active in advanced RCC, but the clinical benefit may remain small compared with that of IFN alone.	Thalidomide	74-85	interferon alpha 1	Homo sapiens	190-193
12867497-0	2003	Cyp1A1-mediated activation of thalidomide and suppression of embryo fibroblast proliferation.	Thalidomide	30-41	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	0-6
12960498-2	2003	Tumor necrosis factor (TNF)-alpha is produced exclusively by the monocyte-macrophage lineage, which is mostly made up of Kupffer cells, and thalidomide has been shown to reduce TNF-alpha production from macrophages.	Thalidomide	140-151	tumor necrosis factor	Rattus norvegicus	177-186
12960498-12	2003	In isolated Kupffer cells, LPS-induced increases in [Ca2+]i and TNF-alpha production were suppressed by treatment with thalidomide.	Thalidomide	119-130	tumor necrosis factor	Rattus norvegicus	64-73
12960498-15	2003	CONCLUSIONS: Thalidomide prevents LPS-induced liver injury via mechanisms dependent on the suppression of TNF-alpha production from Kupffer cells.	Thalidomide	13-24	tumor necrosis factor	Rattus norvegicus	106-115
12736723-5	2003	In this report, we show that thalidomide downregulated the mRNA and protein expression of basic fibroblast growth factor (bFGF) in the human lung adenocarcinoma cell line A549, and that the effect of thalidomide was time and concentration-dependent.	Thalidomide	29-40	fibroblast growth factor 2	Homo sapiens	122-126
12869646-7	2003	Significant reduction of EGFP was demonstrated in cells transfected with hTERT reporter gene and treated with racemic and (S)-Thd.	Thalidomide	122-129	telomerase reverse transcriptase	Homo sapiens	73-78
12878503-1	2003	Thalidomide, an agent which inhibits biosynthesis of tumor necrosis factor alpha (TNF-alpha) and which is used to treat a variety of chronic inflammatory conditions, was investigated as therapy for experimental sepsis.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	82-91
12878503-10	2003	Pretreatment of human monocytes with thalidomide prevented the secretion of TNF-alpha and IL-1beta but not that of IL-6.	Thalidomide	37-48	tumor necrosis factor	Homo sapiens	76-85
12878503-10	2003	Pretreatment of human monocytes with thalidomide prevented the secretion of TNF-alpha and IL-1beta but not that of IL-6.	Thalidomide	37-48	interleukin 1 beta	Homo sapiens	90-98
12878503-11	2003	It is concluded that thalidomide exerts a considerable anti-inflammatory effect by preventing evolution to sepsis and by decreasing the level of production of TNF-alpha and therefore deserves to be further evaluated in research for the therapy of sepsis.	Thalidomide	21-32	tumor necrosis factor	Homo sapiens	159-168
12819930-13	2003	Hypothetical target events/molecules of thalidomide include tumor necrosis factor-alpha production, nuclear androgen receptor, cyclooxygenases, aminopeptidases, and alpha-glucosidase.	Thalidomide	40-51	sucrase-isomaltase	Homo sapiens	165-182
12843316-0	2003	Mutations at the SALL4 locus on chromosome 20 result in a range of clinically overlapping phenotypes, including Okihiro syndrome, Holt-Oram syndrome, acro-renal-ocular syndrome, and patients previously reported to represent thalidomide embryopathy.	Thalidomide	224-235	spalt like transcription factor 4	Homo sapiens	17-22
12843316-4	2003	We identified a novel SALL4 mutation in one family where the father was originally thought to have thalidomide embryopathy and had a daughter with a similar phenotype.	Thalidomide	99-110	spalt like transcription factor 4	Homo sapiens	22-27
12843316-6	2003	Our results show that some cases of "thalidomide embryopathy" might be the result of SALL4 mutations, resulting in an increased risk for similarly affected offspring.	Thalidomide	37-48	spalt like transcription factor 4	Homo sapiens	85-90
12736723-5	2003	In this report, we show that thalidomide downregulated the mRNA and protein expression of basic fibroblast growth factor (bFGF) in the human lung adenocarcinoma cell line A549, and that the effect of thalidomide was time and concentration-dependent.	Thalidomide	29-40	fibroblast growth factor 2	Homo sapiens	90-120
12736723-6	2003	In contrast, the expression of vascular endothelial growth factor (VEGF) by thalidomide in these cells was in two phases.	Thalidomide	76-87	vascular endothelial growth factor A	Homo sapiens	31-65
12736723-6	2003	In contrast, the expression of vascular endothelial growth factor (VEGF) by thalidomide in these cells was in two phases.	Thalidomide	76-87	vascular endothelial growth factor A	Homo sapiens	67-71
12736723-7	2003	The mRNA and protein expression of VEGF was increased in the lung cancer cells treated with 0.6-6 microg/ml thalidomide, while higher concentrations of thalidomide decreased VEGF levels significantly in these cells.	Thalidomide	108-119	vascular endothelial growth factor A	Homo sapiens	35-39
12736723-7	2003	The mRNA and protein expression of VEGF was increased in the lung cancer cells treated with 0.6-6 microg/ml thalidomide, while higher concentrations of thalidomide decreased VEGF levels significantly in these cells.	Thalidomide	152-163	vascular endothelial growth factor A	Homo sapiens	174-178
12789488-5	2003	The mechanism of action of thalidomide is probably based on its immunomodulatory effect, namely the suppression of production of tumor necrosis factor alpha and the modulation of interleukins.	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	129-156
12649301-0	2003	Enhancement of cytokine production and AP-1 transcriptional activity in T cells by thalidomide-related immunomodulatory drugs.	Thalidomide	83-94	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	39-43
12642474-0	2003	Thalidomide-induced suppression of embryo fibroblast proliferation requires CYP1A1-mediated activation.	Thalidomide	0-11	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	76-82
12894531-0	2003	Thalidomide down-regulates the expression of VEGF and bFGF in cisplatin-resistant human lung carcinoma cells.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	45-49
12894531-0	2003	Thalidomide down-regulates the expression of VEGF and bFGF in cisplatin-resistant human lung carcinoma cells.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	54-58
12894531-4	2003	In the current study, we showed that thalidomide suppressed the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cisplatin-resistant human A549DDP lung carcinoma cells.	Thalidomide	37-48	vascular endothelial growth factor A	Homo sapiens	78-112
12894531-4	2003	In the current study, we showed that thalidomide suppressed the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cisplatin-resistant human A549DDP lung carcinoma cells.	Thalidomide	37-48	vascular endothelial growth factor A	Homo sapiens	114-118
12894531-4	2003	In the current study, we showed that thalidomide suppressed the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cisplatin-resistant human A549DDP lung carcinoma cells.	Thalidomide	37-48	fibroblast growth factor 2	Homo sapiens	124-154
12894531-4	2003	In the current study, we showed that thalidomide suppressed the expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cisplatin-resistant human A549DDP lung carcinoma cells.	Thalidomide	37-48	fibroblast growth factor 2	Homo sapiens	156-160
12894531-5	2003	The mRNA levels of VEGF and bFGF were markedly decreased in the A549DDP cells treated with the therapeutic concentrations of thalidomide (0.6-6 micrograms/ml), as determined by RT-PCR analysis.	Thalidomide	125-136	vascular endothelial growth factor A	Homo sapiens	19-23
12894531-5	2003	The mRNA levels of VEGF and bFGF were markedly decreased in the A549DDP cells treated with the therapeutic concentrations of thalidomide (0.6-6 micrograms/ml), as determined by RT-PCR analysis.	Thalidomide	125-136	fibroblast growth factor 2	Homo sapiens	28-32
12894531-6	2003	Consistent with these results, thalidomide also significantly reduced the protein levels of VEGF and bFGF in these cells in a dose- and time-dependent manner.	Thalidomide	31-42	vascular endothelial growth factor A	Homo sapiens	92-96
12894531-6	2003	Consistent with these results, thalidomide also significantly reduced the protein levels of VEGF and bFGF in these cells in a dose- and time-dependent manner.	Thalidomide	31-42	fibroblast growth factor 2	Homo sapiens	101-105
12752784-4	2003	Inhibition of TNFalpha with thalidomide or a rat polyclonal anti-TNFalpha antibody attenuated carrageenan-induced hyperalgesia and prevented priming.	Thalidomide	28-39	tumor necrosis factor	Rattus norvegicus	14-22
12642474-8	2003	These results strongly suggest the involvement of CYP1A1 in the thalidomide-induced suppression of embryo fibroblast proliferation.	Thalidomide	64-75	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	50-56
17041438-8	2003	There are rat experiments showing that thalidomide improves neuropathic pain, probably by selectively blocking tumor necrosis factor-alpha production in activated macrophages.	Thalidomide	39-50	tumor necrosis factor	Rattus norvegicus	111-138
12644816-2	2003	Thalidomide blocks the activity of angiogenic agents including bFGF, VEGF and IL-6.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	63-67
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	tumor necrosis factor	Homo sapiens	167-194
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	tumor necrosis factor	Homo sapiens	196-204
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	interleukin 1 beta	Homo sapiens	207-229
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	interferon gamma	Homo sapiens	231-247
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	interferon gamma	Homo sapiens	249-257
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	interleukin 6	Homo sapiens	260-264
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	interleukin 10	Homo sapiens	266-271
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	284-289
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	vascular endothelial growth factor A	Homo sapiens	323-357
12720152-2	2003	Although its molecular mechanisms of action have not yet been elucidated, thalidomide and the IMiDs affect a variety of cytokines and inflammatory mediators including tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, interferon gamma (IFNgamma), IL-6, IL-10, IL-12, and COX-2 and angiogenesis factors such as vascular endothelial growth factor (VEGF) and its receptor.	Thalidomide	74-85	vascular endothelial growth factor A	Homo sapiens	359-363
12644816-2	2003	Thalidomide blocks the activity of angiogenic agents including bFGF, VEGF and IL-6.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	69-73
12644816-2	2003	Thalidomide blocks the activity of angiogenic agents including bFGF, VEGF and IL-6.	Thalidomide	0-11	interleukin 6	Homo sapiens	78-82
12874961-0	2003	Thalidomide inhibits early atherogenesis in apoE-deficient mice.	Thalidomide	0-11	apolipoprotein E	Mus musculus	44-48
12566301-0	2003	A novel subclass of thalidomide analogue with anti-solid tumor activity in which caspase-dependent apoptosis is associated with altered expression of bcl-2 family proteins.	Thalidomide	20-31	B cell leukemia/lymphoma 2	Mus musculus	150-155
12749503-9	2003	RESULTS: Thalidomide is thought to exert its therapeutic effect through the modulation of cytokines, particularly tumor necrosis factor-alpha.	Thalidomide	9-20	tumor necrosis factor	Homo sapiens	114-141
12525736-0	2003	Phase I study of thalidomide for the treatment of plexiform neurofibroma in neurofibromatosis 1.	Thalidomide	17-28	neurofibromin 1	Homo sapiens	76-95
12525736-1	2003	An open-label phase I trial of thalidomide (TL) in 20 patients with neurofibromatosis 1 (NF1) treated symptomatic plexiform neurofibroma (PNF).	Thalidomide	31-42	neurofibromin 1	Homo sapiens	68-87
12525736-1	2003	An open-label phase I trial of thalidomide (TL) in 20 patients with neurofibromatosis 1 (NF1) treated symptomatic plexiform neurofibroma (PNF).	Thalidomide	31-42	neurofibromin 1	Homo sapiens	89-92
12660941-0	2003	Thalidomide and a thalidomide analogue drug costimulate virus-specific CD8+ T cells in vitro.	Thalidomide	0-11	CD8a molecule	Homo sapiens	71-74
12660941-0	2003	Thalidomide and a thalidomide analogue drug costimulate virus-specific CD8+ T cells in vitro.	Thalidomide	18-29	CD8a molecule	Homo sapiens	71-74
12660941-3	2003	The recent finding that thalidomide acts as a T cell costimulator suggested that this drug may boost antiviral CD8(+) T cell responses.	Thalidomide	24-35	CD8a molecule	Homo sapiens	111-114
12660941-4	2003	In this in vitro study, in a human autologous CD8(+) T cell/dendritic cell (DC) coculture system, thalidomide and a potent thalidomide analogue were shown to enhance virus-specific CD8(+) T cell cytokine production and cytotoxic activity.	Thalidomide	98-109	CD8a molecule	Homo sapiens	46-49
12660941-4	2003	In this in vitro study, in a human autologous CD8(+) T cell/dendritic cell (DC) coculture system, thalidomide and a potent thalidomide analogue were shown to enhance virus-specific CD8(+) T cell cytokine production and cytotoxic activity.	Thalidomide	98-109	CD8a molecule	Homo sapiens	181-184
12660941-4	2003	In this in vitro study, in a human autologous CD8(+) T cell/dendritic cell (DC) coculture system, thalidomide and a potent thalidomide analogue were shown to enhance virus-specific CD8(+) T cell cytokine production and cytotoxic activity.	Thalidomide	123-134	CD8a molecule	Homo sapiens	181-184
12548578-4	2003	For example, immunomodulatory derivatives of thalidomide (IMiDs) and the proteasome inhibitor PS-341 both induce apoptosis of MM cell lines and patient cells refractory to melphalan, doxorubicin, and dexamethasone; abrogate MM cell binding to fibronectin and BMSCs and related protection against immune- and drug-induced apoptosis; block production of cytokines which promote MM cell growth, survival, drug resistance, and migration; inhibit angiogenesis; and stimulate host anti-tumor immunity.	Thalidomide	45-56	fibronectin 1	Homo sapiens	243-254
15040702-4	2003	Thalidomide (TH) and systemic steroids (S), both TNFa production inhibitors, are the two current effective drugs for the management of ENL.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	49-53
12874961-3	2003	To clarify the role of this cytokine, we administered thalidomide, a compound known to inhibit TNF-alpha production, to homozygous apolipoprotein E-deficient (apoE-/-) mice in order to examine the effect of thalidomide on the development of early atherosclerotic lesions.	Thalidomide	54-65	tumor necrosis factor	Mus musculus	95-104
12533164-1	2003	BACKGROUND: Thalidomide is an anti-inflammatory agent and an immunomodulator that inhibits the production of tumor necrosis factor alpha.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	109-136
12874961-7	2003	Thus, thalidomide is capable of inhibiting the early development of atherosclerosis, presumably by inhibition of TNF-alpha secretion.	Thalidomide	6-17	tumor necrosis factor	Mus musculus	113-122
12771492-5	2003	Thalidomide reduces the activity of tumor necrosis factor (TNF) alpha by accelerating the degradation of its mRNA.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	36-69
12613280-4	2003	Thalidomide mainly reduces tumor necrosis factor (TNF)-alpha production by macrophages, and its TNF alpha antagonist properties explain the beneficial effects in several TNF alpha-associated complications of severe diseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	27-60
12613280-4	2003	Thalidomide mainly reduces tumor necrosis factor (TNF)-alpha production by macrophages, and its TNF alpha antagonist properties explain the beneficial effects in several TNF alpha-associated complications of severe diseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	170-179
12560891-0	2003	Thalidomide blocking of particle-induced TNFalpha release in vitro.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	41-49
12469200-4	2003	In this study, we demonstrate increased expression and production levels of VEGF in myeloma compared to non-myelomatous hematological lines, resistance to hypoxia and enhancement of VEGF-A production by hypoxia in myeloma, and direct growth inhibition of myeloma cells due to apoptosis and G1 arrest caused by TNFalpha upregulation induced by thalidomide.	Thalidomide	343-354	vascular endothelial growth factor A	Homo sapiens	76-80
12560891-9	2003	Thalidomide treatment was found to inhibit TNFalpha production in a dose-dependent manner in human macrophages exposed to Ti particles.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	43-51
14657598-10	2003	Another 6 of the 42 patients with elevated alpha-FP levels before treatment had a more than 50% decrease in their alpha-FP levels after thalidomide treatment.	Thalidomide	136-147	alpha fetoprotein	Homo sapiens	43-51
14657598-10	2003	Another 6 of the 42 patients with elevated alpha-FP levels before treatment had a more than 50% decrease in their alpha-FP levels after thalidomide treatment.	Thalidomide	136-147	alpha fetoprotein	Homo sapiens	114-122
12422154-9	2002	CONCLUSIONS: In this pilot study, therapy with thalidomide in patients with CHF resulted in decreased TNF-alpha levels and increased cardiac performance.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	102-111
14649541-2	2003	Thalidomide inhibits TNF induction by DMXAA and also potentiates its antitumor activity.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	21-24
12520740-5	2002	Change of CD20 expression on the myeloma cells were measured by flow cytometer after and before myeloma cells were treated with thalidomide.	Thalidomide	128-139	keratin 20	Homo sapiens	10-14
12520740-7	2002	CONCLUSION: Thalidomide could enhance the inhibition of Mabthera on colony formation of MM patients" myeloma cells, which is related to that thalidomide enhances CD20 antigen expression of myeloma cells.	Thalidomide	12-23	keratin 20	Homo sapiens	162-166
12520740-7	2002	CONCLUSION: Thalidomide could enhance the inhibition of Mabthera on colony formation of MM patients" myeloma cells, which is related to that thalidomide enhances CD20 antigen expression of myeloma cells.	Thalidomide	141-152	keratin 20	Homo sapiens	162-166
16088654-9	2002	Among the new anti-tumor necrosis factor drugs are thalidomide and infliximab, an antibody to tumor necrosis factor.	Thalidomide	51-62	tumor necrosis factor	Homo sapiens	19-40
16985953-6	2003	We performed a phase II trial of docetaxel with or without thalidomide in patients with AIPC and demonstrated encouraging response rates with combination therapy.	Thalidomide	59-70	PDZ domain containing 2	Homo sapiens	88-92
15058168-2	2003	The main mechanism of action of thalidomide in these diseases is probably based on the suppression of tumor necrosis factor-alpha and the modulation of interleukins.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	102-129
12490072-10	2002	Thalidomide has no effect on tumor growth, but is also associated with increased VEGF and p53 expression.	Thalidomide	0-11	transformation related protein 53, pseudogene	Mus musculus	90-93
12485902-0	2002	Thalidomide suppresses the interleukin 1beta-induced NFkappaB signaling pathway in colon cancer cells.	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	27-44
12485902-0	2002	Thalidomide suppresses the interleukin 1beta-induced NFkappaB signaling pathway in colon cancer cells.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	53-61
12485902-3	2002	We investigated the action mechanism of thalidomide through the NFkappaB pathway.	Thalidomide	40-51	nuclear factor kappa B subunit 1	Homo sapiens	64-72
12485902-4	2002	Thalidomide inhibited interleukin (IL) 1beta-induced NFkappaB transcriptional activation and IL-8 production in Caco-2 colon cancer cells.	Thalidomide	0-11	interleukin 1 beta	Homo sapiens	22-44
12485902-4	2002	Thalidomide inhibited interleukin (IL) 1beta-induced NFkappaB transcriptional activation and IL-8 production in Caco-2 colon cancer cells.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	53-61
12485902-4	2002	Thalidomide inhibited interleukin (IL) 1beta-induced NFkappaB transcriptional activation and IL-8 production in Caco-2 colon cancer cells.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
12485902-5	2002	In addition, thalidomide suppressed NFkappaB nuclear translocation, IkappaB degradation, and NFkappaB-inducing kinase (NIK)-induced NFkappaB transcriptional activation.	Thalidomide	13-24	nuclear factor kappa B subunit 1	Homo sapiens	36-44
12485902-5	2002	In addition, thalidomide suppressed NFkappaB nuclear translocation, IkappaB degradation, and NFkappaB-inducing kinase (NIK)-induced NFkappaB transcriptional activation.	Thalidomide	13-24	nuclear factor kappa B subunit 1	Homo sapiens	93-101
12485902-5	2002	In addition, thalidomide suppressed NFkappaB nuclear translocation, IkappaB degradation, and NFkappaB-inducing kinase (NIK)-induced NFkappaB transcriptional activation.	Thalidomide	13-24	nuclear factor kappa B subunit 1	Homo sapiens	93-101
12485902-6	2002	These results suggest that the molecular target of the effects of thalidomide may be IkappaB phosphorylation by IkappaB kinase (IKK), whose activation follows NIK activation and precedes IkappaB degradation in the NFkappaB pathway.	Thalidomide	66-77	nuclear factor kappa B subunit 1	Homo sapiens	214-222
12463469-4	2002	Inhibition of NF-kappaB and/or TNFalpha is a putative mechanism for thalidomide efficacy in AS.	Thalidomide	68-79	nuclear factor kappa B subunit 1	Homo sapiens	14-23
12463469-4	2002	Inhibition of NF-kappaB and/or TNFalpha is a putative mechanism for thalidomide efficacy in AS.	Thalidomide	68-79	tumor necrosis factor	Homo sapiens	31-39
12398921-1	2002	Thalidomide has been shown to reduce the production of tumor necrosis factor-alpha (TNF-alpha), a cytokine with deleterious pathophysiologic effects in various diseases.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	55-82
12398921-1	2002	Thalidomide has been shown to reduce the production of tumor necrosis factor-alpha (TNF-alpha), a cytokine with deleterious pathophysiologic effects in various diseases.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	84-93
12398921-2	2002	In search of thalidomide analogues with improved TNF-alpha inhibiting properties, 5-ethyl-1-phenyl-5-(3,4,5,6-tetrafluorophthalimido)barbituric acid (TFBA) was found to be superior to thalidomide.	Thalidomide	13-24	tumor necrosis factor	Mus musculus	49-58
12642692-0	2002	Pharmacogenetic associations of CYP2C19 genotype with in vivo metabolisms and pharmacological effects of thalidomide.	Thalidomide	105-116	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	32-39
12642692-10	2002	The role of CYP2C19 polymorphism in thalidomide treatments remains to be elucidated.	Thalidomide	36-47	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
12490072-6	2002	RESULTS: At 6 weeks, VEGF-mAb-treated tumors were smaller (1603 +/- 296 mm(3)) than either the thalidomide-treated (6007 +/- 1498 mm(3); p = 0.008) or the control groups (4040 +/- 831 mm(3); p = 0.014) and the VEGF-mAb-treated animals maintained greater weight (30.4 +/- 0.84 g at week 6 versus thalidomide-treated, 26.0 +/- 0.94 g, p = 0.003; and control, 25.8 +/- 0.78 g, p = 0.001 animals).	Thalidomide	295-306	vascular endothelial growth factor A	Mus musculus	21-25
12490072-10	2002	Thalidomide has no effect on tumor growth, but is also associated with increased VEGF and p53 expression.	Thalidomide	0-11	vascular endothelial growth factor A	Mus musculus	81-85
12358938-0	2002	Thalidomide treatment of relapsed multiple myeloma patients and changes in circulating VEGF and bFGF.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	96-100
12242718-11	2002	Intravenous cotreatment with PBN and thalidomide (gavage) in rabbits restored normal patterns and localization of Twist, Fgf-8, and Fgf-10 expression.	Thalidomide	37-48	fibroblast growth factor 10	Oryctolagus cuniculus	132-138
12296856-1	2002	Thalidomide (Thd) is clinically useful in a number of conditions where its efficacy is probably related to its anti-TNF-alpha activity.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	116-125
12296856-1	2002	Thalidomide (Thd) is clinically useful in a number of conditions where its efficacy is probably related to its anti-TNF-alpha activity.	Thalidomide	13-16	tumor necrosis factor	Homo sapiens	116-125
12296856-3	2002	However, in contrast to their known suppressive effects during inflammatory stimuli, the effects of Thd/IMiDs on TNF-alpha and TNF receptors (TNFRs) during T cell co-stimulation are not known.	Thalidomide	100-103	tumor necrosis factor	Homo sapiens	113-122
12296856-3	2002	However, in contrast to their known suppressive effects during inflammatory stimuli, the effects of Thd/IMiDs on TNF-alpha and TNF receptors (TNFRs) during T cell co-stimulation are not known.	Thalidomide	100-103	tumor necrosis factor	Homo sapiens	113-116
12296856-5	2002	We found that co-stimulation of PBMC with Thd/IMiDs, but not CC-3052, prevented alphaCD3-induced T cell surface expression of TNFR2 and thereby reduced soluble TNFR2 (sTNFR2) levels.	Thalidomide	42-45	TNF receptor superfamily member 1B	Homo sapiens	126-131
12296856-5	2002	We found that co-stimulation of PBMC with Thd/IMiDs, but not CC-3052, prevented alphaCD3-induced T cell surface expression of TNFR2 and thereby reduced soluble TNFR2 (sTNFR2) levels.	Thalidomide	42-45	TNF receptor superfamily member 1B	Homo sapiens	160-165
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	CD69 molecule	Homo sapiens	55-59
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	interleukin 2 receptor subunit alpha	Homo sapiens	60-64
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	interleukin 2	Homo sapiens	80-84
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	CD4 molecule	Homo sapiens	125-128
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	CD8a molecule	Homo sapiens	134-137
12296856-7	2002	The extent of co-stimulation by Thd/IMiDs (assessed by CD69/CD25 expression and IL-2/sIL-2Ralpha production) was similar for CD4+ and CD8+ T lymphocytes and correlated with TNFR2 inhibition.	Thalidomide	32-35	TNF receptor superfamily member 1B	Homo sapiens	173-178
12296856-10	2002	Together, these results suggest a possible role for TNF-mediated events during co-stimulation and contrast with the TNF inhibitory effects of Thd and its analogues during inflammatory stimuli.	Thalidomide	142-145	tumor necrosis factor	Homo sapiens	116-119
12296856-0	2002	Thalidomide and its analogues have distinct and opposing effects on TNF-alpha and TNFR2 during co-stimulation of both CD4(+) and CD8(+) T cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	68-77
12296856-0	2002	Thalidomide and its analogues have distinct and opposing effects on TNF-alpha and TNFR2 during co-stimulation of both CD4(+) and CD8(+) T cells.	Thalidomide	0-11	TNF receptor superfamily member 1B	Homo sapiens	82-87
12296856-0	2002	Thalidomide and its analogues have distinct and opposing effects on TNF-alpha and TNFR2 during co-stimulation of both CD4(+) and CD8(+) T cells.	Thalidomide	0-11	CD4 molecule	Homo sapiens	118-121
12296856-0	2002	Thalidomide and its analogues have distinct and opposing effects on TNF-alpha and TNFR2 during co-stimulation of both CD4(+) and CD8(+) T cells.	Thalidomide	0-11	CD8a molecule	Homo sapiens	129-132
12242718-9	2002	In situ hybridization showed a preferential decrease in Twist, Fgf-8, and Fgf-10 expression after thalidomide treatment (400 mg/kg per day) in rabbit embryos.	Thalidomide	98-109	fibroblast growth factor 8	Oryctolagus cuniculus	63-68
12242718-9	2002	In situ hybridization showed a preferential decrease in Twist, Fgf-8, and Fgf-10 expression after thalidomide treatment (400 mg/kg per day) in rabbit embryos.	Thalidomide	98-109	fibroblast growth factor 10	Oryctolagus cuniculus	74-80
12242718-11	2002	Intravenous cotreatment with PBN and thalidomide (gavage) in rabbits restored normal patterns and localization of Twist, Fgf-8, and Fgf-10 expression.	Thalidomide	37-48	fibroblast growth factor 8	Oryctolagus cuniculus	121-126
12482346-13	2002	CONCLUSION: MVD and VEGF concentration were decreased obviously by thalidomide treatment.	Thalidomide	67-78	vascular endothelial growth factor A	Homo sapiens	20-24
12484444-3	2002	On the other hand, when the culture was treated with thalidomide plus cytochrome P-450, both types of thalidomides significantly inhibited angiogenesis.	Thalidomide	102-114	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	70-86
12484444-7	2002	The inhibition of angiogenesis by thalidomide and cytochrome P-450 takes place through a suppression of TNF-alpha and involves the metabolism of the thalidomide.	Thalidomide	34-45	tumor necrosis factor	Mus musculus	104-113
12484444-7	2002	The inhibition of angiogenesis by thalidomide and cytochrome P-450 takes place through a suppression of TNF-alpha and involves the metabolism of the thalidomide.	Thalidomide	149-160	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
12368119-12	2002	It also indicates the role of TNF-alpha upon the pathophysiology of this event based on the inhibitory action of DEXA, TAL and pentoxifylline, and on TNF-alpha secretion induced by cholera toxin.	Thalidomide	119-122	tumor necrosis factor	Rattus norvegicus	30-39
12411981-2	2002	Thalidomide has anti-inflammatory properties and selectively inhibits TNF.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	70-73
12411981-7	2002	RESULTS: Thalidomide and thalidomide analogues inhibited LPS-induced TNF biosynthesis in cardiac myocytes in a dose-dependent manner.	Thalidomide	9-20	tumor necrosis factor	Homo sapiens	69-72
12411981-7	2002	RESULTS: Thalidomide and thalidomide analogues inhibited LPS-induced TNF biosynthesis in cardiac myocytes in a dose-dependent manner.	Thalidomide	25-36	tumor necrosis factor	Homo sapiens	69-72
12411981-8	2002	Thalidomide analogues had a greater inhibitory effect on TNF production than did thalidomide.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	57-60
12200397-0	2002	Polymorphisms of the tumor necrosis factor-alpha gene promoter predict for outcome after thalidomide therapy in relapsed and refractory multiple myeloma.	Thalidomide	89-100	tumor necrosis factor	Homo sapiens	21-48
12200397-1	2002	Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) in vitro.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	145-172
12200397-1	2002	Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) in vitro.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	174-183
12200397-1	2002	Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) in vitro.	Thalidomide	0-4	tumor necrosis factor	Homo sapiens	145-172
12200397-1	2002	Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-alpha (TNF-alpha) in vitro.	Thalidomide	0-4	tumor necrosis factor	Homo sapiens	174-183
12200397-2	2002	We studied single nucleotide polymorphisms at positions -308 and -238 of the TNF-alpha gene promoter and measured the corresponding TNF-alpha cytokine levels in 81 patients (pts) with refractory and relapsed multiple myeloma (MM) who were treated with Thal.	Thalidomide	252-256	tumor necrosis factor	Homo sapiens	77-86
12380944-0	2002	PSA response to thalidomide in patients with advanced prostate cancer.	Thalidomide	16-27	aminopeptidase puromycin sensitive	Homo sapiens	0-3
12412207-2	2002	More interestingly, thalidomide has shown the ability to suppress tumor necrosis factor alpha (TNF alpha) production and to modify the expression of TNF alpha induced adhesion molecules on endothelial cells and on human leukocytes.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	66-93
12412207-2	2002	More interestingly, thalidomide has shown the ability to suppress tumor necrosis factor alpha (TNF alpha) production and to modify the expression of TNF alpha induced adhesion molecules on endothelial cells and on human leukocytes.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	95-104
12412207-2	2002	More interestingly, thalidomide has shown the ability to suppress tumor necrosis factor alpha (TNF alpha) production and to modify the expression of TNF alpha induced adhesion molecules on endothelial cells and on human leukocytes.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	149-158
12359057-11	2002	After thalidomide treatment, plasma vascular endothelial growth factor (VEGF) level was significantly reduced in responders (P = 0.025), but not in non-responders (P = 0.37).	Thalidomide	6-17	vascular endothelial growth factor A	Homo sapiens	36-70
12359057-11	2002	After thalidomide treatment, plasma vascular endothelial growth factor (VEGF) level was significantly reduced in responders (P = 0.025), but not in non-responders (P = 0.37).	Thalidomide	6-17	vascular endothelial growth factor A	Homo sapiens	72-76
12359057-12	2002	Reduction of plasma VEGF level might be an important indicator for anti-myeloma effect of thalidomide.	Thalidomide	90-101	vascular endothelial growth factor A	Homo sapiens	20-24
12349951-15	2002	Increased production of IL-2 by activated T cells may be a mechanism through which thalidomide exerts its immunomodulatory effects.	Thalidomide	83-94	interleukin 2	Homo sapiens	24-28
12190008-4	2002	Thalidomide inhibits TNF alpha production, has T-cell costimulatory properties and modulates the expression of cell surface molecules on leukocytes in vivo.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	21-30
12190011-12	2002	Thalidomide plus dexamethasone was given to 9 patients who did not respond to thalidomide alone, and in 6 of them a reduction of M-protein was then observed.	Thalidomide	0-11	myomesin 2	Homo sapiens	129-138
12167383-2	2002	AIMS: We have tried to antagonise the detrimental effects of TNFalpha on skeletal muscle apoptosis, by using thalidomide, a drug that inhibits its biosynthesis.	Thalidomide	109-120	tumor necrosis factor	Homo sapiens	61-69
12209719-2	2002	Thalidomide inhibits basic fibroblast growth factor and vascular endothelial growth factor (VEGF)-induced angiogenesis.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	56-90
12209719-2	2002	Thalidomide inhibits basic fibroblast growth factor and vascular endothelial growth factor (VEGF)-induced angiogenesis.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	92-96
12240951-2	2002	To determine whether the N-alkyl analogs of the thalidomide are active and stable, their stabilities in buffer and their abilities to inhibit tumor necrosis factor alpha (TNF-alpha) in vitro in human peripheral blood mononuclear cell cultures were investigated.	Thalidomide	48-59	tumor necrosis factor	Homo sapiens	142-169
12240951-2	2002	To determine whether the N-alkyl analogs of the thalidomide are active and stable, their stabilities in buffer and their abilities to inhibit tumor necrosis factor alpha (TNF-alpha) in vitro in human peripheral blood mononuclear cell cultures were investigated.	Thalidomide	48-59	tumor necrosis factor	Homo sapiens	171-180
12240951-7	2002	Like thalidomide, the N-alkyl analogs in this series inhibit an average of 60% of the TNF-alpha synthesis in lipopolysaccharide-stimulated peripheral blood mononuclear cell cultures.	Thalidomide	5-16	tumor necrosis factor	Homo sapiens	86-95
12371635-0	2002	Successful treatment of familial Mediterranean fever attacks with thalidomide in a colchicine resistant patient.	Thalidomide	66-77	MEFV innate immuity regulator, pyrin	Homo sapiens	24-52
12105857-0	2002	Thalidomide prevents alcoholic liver injury in rats through suppression of Kupffer cell sensitization and TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	106-115
12105857-2	2002	Thalidomide has been shown to suppress TNF-alpha production from macrophages.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	39-48
12105857-12	2002	Furthermore, thalidomide abolished the LPS-induced increase in CD14 expression and [Ca2+]i elevation in KCs.	Thalidomide	13-24	CD14 molecule	Rattus norvegicus	63-67
12105857-14	2002	Moreover, thalidomide reduced the LPS-induced TNF-alpha production by KCs by decreasing TNF-alpha messenger RNA.	Thalidomide	10-21	tumor necrosis factor	Rattus norvegicus	46-55
12105857-14	2002	Moreover, thalidomide reduced the LPS-induced TNF-alpha production by KCs by decreasing TNF-alpha messenger RNA.	Thalidomide	10-21	tumor necrosis factor	Rattus norvegicus	88-97
12105857-15	2002	CONCLUSIONS: These results collectively indicate that thalidomide prevents alcoholic liver injury through suppression of TNF-alpha production and abolishment of KC sensitization.	Thalidomide	54-65	tumor necrosis factor	Rattus norvegicus	121-130
12349951-0	2002	Thalidomide can costimulate or suppress CD4+ cells" ability to incorporate [H3]-thymidine--dependence on the primary stimulant.	Thalidomide	0-11	CD4 molecule	Homo sapiens	40-43
12349951-1	2002	Thalidomide is a drug that can enhance mitogen- and antigen-stimulated cells" ability to synthesize IL-2.	Thalidomide	0-11	interleukin 2	Homo sapiens	100-104
12349951-2	2002	To assess if thalidomide could concomitantly enhance the synthesis of IFN-gamma and incorporation of [H3]-thymidine, peripheral blood mononuclear cells (PBMC) were incubated in the presence or absence of thalidomide and staphylococcal enterotoxin A (SEA), anti-CD3, Con-A or PHA.	Thalidomide	13-24	interferon gamma	Homo sapiens	70-79
12349951-5	2002	Regardless of the mitogen used to stimulate the PBMC, the thalidomide-treated PBMC produced more IL-2 than controls.	Thalidomide	58-69	interleukin 2	Homo sapiens	97-101
12349951-6	2002	Thalidomide enhanced IFN-gamma synthesis in the Con-A and anti-CD3-stimulated PBMC.	Thalidomide	0-11	interferon gamma	Homo sapiens	21-30
11994441-0	2002	Protective antitumor immunity induced by a costimulatory thalidomide analog in conjunction with whole tumor cell vaccination is mediated by increased Th1-type immunity.	Thalidomide	57-68	negative elongation factor complex member C/D	Homo sapiens	150-153
12349951-9	2002	In the thalidomide-treated SEA-stimulated CD4+ and CD8+ cells, thalidomide acted as a costimulant to enhance the synthesis of IL-2.	Thalidomide	7-18	CD4 molecule	Homo sapiens	42-45
12349951-9	2002	In the thalidomide-treated SEA-stimulated CD4+ and CD8+ cells, thalidomide acted as a costimulant to enhance the synthesis of IL-2.	Thalidomide	7-18	interleukin 2	Homo sapiens	126-130
12349951-9	2002	In the thalidomide-treated SEA-stimulated CD4+ and CD8+ cells, thalidomide acted as a costimulant to enhance the synthesis of IL-2.	Thalidomide	63-74	CD4 molecule	Homo sapiens	42-45
12349951-9	2002	In the thalidomide-treated SEA-stimulated CD4+ and CD8+ cells, thalidomide acted as a costimulant to enhance the synthesis of IL-2.	Thalidomide	63-74	interleukin 2	Homo sapiens	126-130
12349951-10	2002	In the anti-CD3-stimulated thalidomide-treated cultures of PBMC enriched for CD4+ cells, thalidomide acted as a costimulant to enhance the incorporation [H3]-thymidine.	Thalidomide	27-38	CD4 molecule	Homo sapiens	77-80
12349951-10	2002	In the anti-CD3-stimulated thalidomide-treated cultures of PBMC enriched for CD4+ cells, thalidomide acted as a costimulant to enhance the incorporation [H3]-thymidine.	Thalidomide	89-100	CD4 molecule	Homo sapiens	77-80
12349951-11	2002	Thalidomide cooperated with all of the mitogens to enhance T-cell synthesis of IL-2.	Thalidomide	0-11	interleukin 2	Homo sapiens	79-83
12349951-13	2002	The SEA-stimulated cells targeted by thalidomide to suppress incorporation of [H3]-thymidine were CD4+.	Thalidomide	37-48	CD4 molecule	Homo sapiens	98-101
12349951-14	2002	CD4+ cells stimulated with anti-CD3 were enhanced by thalidomide in their ability to synthesize IL-2 and to incorporate [H3]-thymidine.	Thalidomide	53-64	CD4 molecule	Homo sapiens	0-3
12349951-14	2002	CD4+ cells stimulated with anti-CD3 were enhanced by thalidomide in their ability to synthesize IL-2 and to incorporate [H3]-thymidine.	Thalidomide	53-64	interleukin 2	Homo sapiens	96-100
12010810-2	2002	Several established or novel anti-multiple myeloma (anti-MM) agents, such as dexamethasone, thalidomide, and proteasome inhibitors (PS-341), inhibit NF-kappaB activity as part of their diverse actions.	Thalidomide	92-103	nuclear factor kappa B subunit 1	Homo sapiens	149-158
12060642-1	2002	PURPOSE: This research investigated the biotransformation of thalidomide by cytochrome P-450 (CYP).	Thalidomide	61-72	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	76-92
12060642-1	2002	PURPOSE: This research investigated the biotransformation of thalidomide by cytochrome P-450 (CYP).	Thalidomide	61-72	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	94-97
12060642-2	2002	EXPERIMENTAL DESIGN: We used liver microsomes from humans and/or animals and the recombinant specific CYP isozymes to investigate CYP-mediated metabolism of thalidomide.	Thalidomide	157-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	102-105
12060642-2	2002	EXPERIMENTAL DESIGN: We used liver microsomes from humans and/or animals and the recombinant specific CYP isozymes to investigate CYP-mediated metabolism of thalidomide.	Thalidomide	157-168	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	130-133
12060642-11	2002	CONCLUSIONS: We discovered that the polymorphic enzyme CYP2C19 is responsible for 5- and 5"-hydroxylation of thalidomide in humans.	Thalidomide	109-120	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	55-62
12060642-12	2002	In rats, thalidomide was hydroxylated extensively by CYP2C6 as well as the sex-specific enzyme CYP2C11.	Thalidomide	9-20	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	53-59
12060642-12	2002	In rats, thalidomide was hydroxylated extensively by CYP2C6 as well as the sex-specific enzyme CYP2C11.	Thalidomide	9-20	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	95-102
11994441-8	2002	Our results are the first to demonstrate that a costimulatory thalidomide analog can prime protective, long-lasting, tumor-specific, Th1-type responses in vivo and further support their ongoing clinical development as novel anti-cancer agents.	Thalidomide	62-73	negative elongation factor complex member C/D	Homo sapiens	133-136
12046682-1	2002	Thalidomide--removed from widespread clinical use by 1962 because of severe teratogenicity--has anti-angiogenic and immunomodulatory effects, including the inhibition of TNF alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	170-179
11972510-11	2002	Patients with PTMM and/or markedly increased circulating CD34+ cell counts might be susceptible to thalidomide-induced thrombocytosis.	Thalidomide	99-110	CD34 molecule	Homo sapiens	57-61
11909713-1	2002	Thalidomide showed cyclooxygenase (COX)-1/2 inhibitory activity with a potency comparable to that of aspirin.	Thalidomide	0-11	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	19-41
11956484-8	2002	of the selective TNF-alpha synthesis inhibitor thalidomide or 200 mg./kg.	Thalidomide	47-58	tumor necrosis factor	Mus musculus	17-26
12515619-0	2002	[Influence of thalidomide on interleukin-6 and its transmission in multiple myeloma patients].	Thalidomide	14-25	interleukin 6	Homo sapiens	29-42
12515619-1	2002	OBJECTIVE: To evaluate the mechanism and influence of thalidomide on interleukin-6 (IL-6), IL-6 receptor (IL-6R) and its transmitting chain in multiple myeloma patients.	Thalidomide	54-65	interleukin 6	Homo sapiens	69-82
12515619-1	2002	OBJECTIVE: To evaluate the mechanism and influence of thalidomide on interleukin-6 (IL-6), IL-6 receptor (IL-6R) and its transmitting chain in multiple myeloma patients.	Thalidomide	54-65	interleukin 6	Homo sapiens	84-88
12515619-1	2002	OBJECTIVE: To evaluate the mechanism and influence of thalidomide on interleukin-6 (IL-6), IL-6 receptor (IL-6R) and its transmitting chain in multiple myeloma patients.	Thalidomide	54-65	interleukin 6 receptor	Homo sapiens	91-104
12515619-1	2002	OBJECTIVE: To evaluate the mechanism and influence of thalidomide on interleukin-6 (IL-6), IL-6 receptor (IL-6R) and its transmitting chain in multiple myeloma patients.	Thalidomide	54-65	interleukin 6 receptor	Homo sapiens	106-111
12515619-3	2002	RESULTS: Serum level of IL-6 in multiple myeloma patients was 564.8 +/- 319.4 ng/L, with a positive rate on the myeloma cells of 33.6% before oral 200 mg/d thalidomide.	Thalidomide	156-167	interleukin 6	Homo sapiens	24-28
12515619-8	2002	CONCLUSION: Reduction of serum level of IL-6 in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA occur on D14 after oral 400 mg/d thalidomide.	Thalidomide	181-192	interleukin 6	Homo sapiens	40-44
12515619-8	2002	CONCLUSION: Reduction of serum level of IL-6 in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA occur on D14 after oral 400 mg/d thalidomide.	Thalidomide	181-192	interleukin 6 receptor	Homo sapiens	90-95
12515619-8	2002	CONCLUSION: Reduction of serum level of IL-6 in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA occur on D14 after oral 400 mg/d thalidomide.	Thalidomide	181-192	interleukin 6 cytokine family signal transducer	Homo sapiens	132-142
12515619-10	2002	The antitumor mechanism of thalidomide may be related to reduction of IL-6 serum level in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA.	Thalidomide	27-38	interleukin 6	Homo sapiens	70-74
12515619-10	2002	The antitumor mechanism of thalidomide may be related to reduction of IL-6 serum level in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA.	Thalidomide	27-38	interleukin 6 receptor	Homo sapiens	132-137
12515619-10	2002	The antitumor mechanism of thalidomide may be related to reduction of IL-6 serum level in multiple myeloma patients and decrease in IL-6R expression on the myeloma cells and IL-6R beta mRNA.	Thalidomide	27-38	interleukin 6 cytokine family signal transducer	Homo sapiens	174-184
11909713-2	2002	Structural development studies of thalidomide resulted in potent COX-1/2 inhibitors, and COX-1-selective and COX-2-selective inhibitors.	Thalidomide	34-45	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	65-70
11909713-2	2002	Structural development studies of thalidomide resulted in potent COX-1/2 inhibitors, and COX-1-selective and COX-2-selective inhibitors.	Thalidomide	34-45	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	89-94
11884428-0	2002	Thalidomide suppresses NF-kappa B activation induced by TNF and H2O2, but not that activated by ceramide, lipopolysaccharides, or phorbol ester.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	23-33
11995671-5	2002	In this case report, we present a patient with MRS that was treated with thalidomide because of the identification of tumor necrosis factor a in the lesion by immunohistochemical analysis.	Thalidomide	73-84	tumor necrosis factor	Homo sapiens	118-139
11942970-9	2002	There was also a trend to increased expression of FGF-2 and tumour necrosis factor-alpha in thalidomide-treated tumours.	Thalidomide	92-103	fibroblast growth factor 2	Homo sapiens	50-55
11940485-13	2002	Plasma cells from patients who responded favorably to thalidomide secreted a significantly lower amount of VEGF than plasma cells from resistant patients (126.45 165 pg/mL vs 227.11 70 pg/mL, p=0.04).	Thalidomide	54-65	vascular endothelial growth factor A	Homo sapiens	107-111
11884428-2	2002	Due to the central role of NF-kappaB in these responses, we postulated that thalidomide mediates its effects through suppression of NF-kappaB activation.	Thalidomide	76-87	nuclear factor kappa B subunit 1	Homo sapiens	27-36
11884428-2	2002	Due to the central role of NF-kappaB in these responses, we postulated that thalidomide mediates its effects through suppression of NF-kappaB activation.	Thalidomide	76-87	nuclear factor kappa B subunit 1	Homo sapiens	132-141
11884428-0	2002	Thalidomide suppresses NF-kappa B activation induced by TNF and H2O2, but not that activated by ceramide, lipopolysaccharides, or phorbol ester.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	56-59
11884428-3	2002	We investigated the effects of thalidomide on NF-kappaB activation induced by various inflammatory agents in Jurkat cells.	Thalidomide	31-42	nuclear factor kappa B subunit 1	Homo sapiens	46-55
11884428-4	2002	The treatment of these cells with thalidomide suppressed TNF-induced NF-kappaB activation, with optimum effect occurring at 50 microg/ml thalidomide.	Thalidomide	34-45	tumor necrosis factor	Homo sapiens	57-60
11788559-3	2002	Suppression of tumour necrosis factor alpha (TNF-alpha) by thalidomide has been suggested as a possible mechanism.	Thalidomide	59-70	tumor necrosis factor	Homo sapiens	45-54
11884428-4	2002	The treatment of these cells with thalidomide suppressed TNF-induced NF-kappaB activation, with optimum effect occurring at 50 microg/ml thalidomide.	Thalidomide	34-45	nuclear factor kappa B subunit 1	Homo sapiens	69-78
11884428-4	2002	The treatment of these cells with thalidomide suppressed TNF-induced NF-kappaB activation, with optimum effect occurring at 50 microg/ml thalidomide.	Thalidomide	137-148	tumor necrosis factor	Homo sapiens	57-60
11884428-4	2002	The treatment of these cells with thalidomide suppressed TNF-induced NF-kappaB activation, with optimum effect occurring at 50 microg/ml thalidomide.	Thalidomide	137-148	nuclear factor kappa B subunit 1	Homo sapiens	69-78
11884428-8	2002	Thalidomide abolished the NF-kappaB-dependent reporter gene expression activated by overexpression of TNFR1, TNFR-associated factor-2, and NF-kappaB-inducing kinase, but not that activated by the p65 subunit of NF-kappaB.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	26-35
11884428-8	2002	Thalidomide abolished the NF-kappaB-dependent reporter gene expression activated by overexpression of TNFR1, TNFR-associated factor-2, and NF-kappaB-inducing kinase, but not that activated by the p65 subunit of NF-kappaB.	Thalidomide	0-11	TNF receptor superfamily member 1A	Homo sapiens	102-107
11884428-8	2002	Thalidomide abolished the NF-kappaB-dependent reporter gene expression activated by overexpression of TNFR1, TNFR-associated factor-2, and NF-kappaB-inducing kinase, but not that activated by the p65 subunit of NF-kappaB.	Thalidomide	0-11	nuclear factor kappa B subunit 1	Homo sapiens	139-148
11884428-9	2002	Overall, our results clearly demonstrate that thalidomide suppresses NF-kappaB activation specifically induced by TNF and H(2)O(2) and that this may contribute to its role in suppression of proliferation, inflammation, angiogenesis, and the immune system.	Thalidomide	46-57	nuclear factor kappa B subunit 1	Homo sapiens	69-78
11884428-9	2002	Overall, our results clearly demonstrate that thalidomide suppresses NF-kappaB activation specifically induced by TNF and H(2)O(2) and that this may contribute to its role in suppression of proliferation, inflammation, angiogenesis, and the immune system.	Thalidomide	46-57	tumor necrosis factor	Homo sapiens	114-117
11905505-0	2002	Management of erythema nodosum leprosum by thalidomide: thalidomide analogues inhibit M. leprae-induced TNFalpha production in vitro.	Thalidomide	56-67	tumor necrosis factor	Homo sapiens	104-112
11905505-2	2002	Although the active molecules responsible for the diverse therapeutic activities of the drug and the sequence of reactions triggered inside the cells remain unclear, it was demonstrated that thalidomide (THAL) inhibits TNFalpha mRNA expression and protein production by stimulated monocytes and activated T lymphocytes.	Thalidomide	191-202	tumor necrosis factor	Homo sapiens	219-227
11905505-2	2002	Although the active molecules responsible for the diverse therapeutic activities of the drug and the sequence of reactions triggered inside the cells remain unclear, it was demonstrated that thalidomide (THAL) inhibits TNFalpha mRNA expression and protein production by stimulated monocytes and activated T lymphocytes.	Thalidomide	204-208	tumor necrosis factor	Homo sapiens	219-227
11905505-4	2002	It has been reported that thalidomide as well as some its analogues decrease M. leprae-induced TNFalpha and IL-12 mRNA in vitro.	Thalidomide	26-37	tumor necrosis factor	Homo sapiens	95-103
11905505-6	2002	The present data further support thalidomide"s effects on TNFa synthesis and the growing need to search for new specific TNFalpha inhibitors (non-teratogenic compounds) that might be potentially used in clinical disorders such as leprosy.	Thalidomide	33-44	tumor necrosis factor	Homo sapiens	58-62
11788559-11	2002	Production of TNF-alpha and IL-12 decreased during treatment with thalidomide: LPMC (TNF-alpha: 42.3 (8.3) pg/ml v 16.4 (6.3); IL-12: 9.7 (3.3) v 5.0 (2.5); p&lt;0.04) and PBMC (TNF-alpha: 62.8 (14.6) v 22.5 (9.2); p&lt;0.02).	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	14-23
11788559-11	2002	Production of TNF-alpha and IL-12 decreased during treatment with thalidomide: LPMC (TNF-alpha: 42.3 (8.3) pg/ml v 16.4 (6.3); IL-12: 9.7 (3.3) v 5.0 (2.5); p&lt;0.04) and PBMC (TNF-alpha: 62.8 (14.6) v 22.5 (9.2); p&lt;0.02).	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	85-94
11788559-11	2002	Production of TNF-alpha and IL-12 decreased during treatment with thalidomide: LPMC (TNF-alpha: 42.3 (8.3) pg/ml v 16.4 (6.3); IL-12: 9.7 (3.3) v 5.0 (2.5); p&lt;0.04) and PBMC (TNF-alpha: 62.8 (14.6) v 22.5 (9.2); p&lt;0.02).	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	85-94
11788559-13	2002	Culturing of LPMC with thalidomide showed a dose dependent decrease in TNF-alpha and IL-12 production.	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	71-80
11788559-14	2002	CONCLUSION: The clinical effects of thalidomide in Crohn"s disease may be mediated by reduction of both TNF-alpha and IL-12.	Thalidomide	36-47	tumor necrosis factor	Homo sapiens	104-113
12513842-2	2002	The level of interleukin-6 (IL-6) autosecreted by myeloma cells was tested by IL-6-dependent cell line when myeloma cells were treated with thalidomide at 200 microgram/ml, and in the same concentration of thalidomide the expression of IL-6 receptor were tested by flow cytometry.	Thalidomide	140-151	interleukin 6	Homo sapiens	13-26
12513842-2	2002	The level of interleukin-6 (IL-6) autosecreted by myeloma cells was tested by IL-6-dependent cell line when myeloma cells were treated with thalidomide at 200 microgram/ml, and in the same concentration of thalidomide the expression of IL-6 receptor were tested by flow cytometry.	Thalidomide	140-151	interleukin 6	Homo sapiens	28-32
12513842-8	2002	Inhibiting tumor cells secreting level of IL-6 and reducing the expression of IL-6 receptor on myeloma cell surface is one of the mechanisms for thalidomide to remedy multiple myeloma patients	Thalidomide	145-156	interleukin 6	Homo sapiens	42-46
12513842-8	2002	Inhibiting tumor cells secreting level of IL-6 and reducing the expression of IL-6 receptor on myeloma cell surface is one of the mechanisms for thalidomide to remedy multiple myeloma patients	Thalidomide	145-156	interleukin 6	Homo sapiens	78-82
12513842-2	2002	The level of interleukin-6 (IL-6) autosecreted by myeloma cells was tested by IL-6-dependent cell line when myeloma cells were treated with thalidomide at 200 microgram/ml, and in the same concentration of thalidomide the expression of IL-6 receptor were tested by flow cytometry.	Thalidomide	206-217	interleukin 6	Homo sapiens	13-26
12513842-2	2002	The level of interleukin-6 (IL-6) autosecreted by myeloma cells was tested by IL-6-dependent cell line when myeloma cells were treated with thalidomide at 200 microgram/ml, and in the same concentration of thalidomide the expression of IL-6 receptor were tested by flow cytometry.	Thalidomide	206-217	interleukin 6	Homo sapiens	28-32
12513842-5	2002	After treatment with thalidomide at 200 microgram/ml, the concentrations of IL-6 secreted by myeloma cells were (148.5 +/- 96.7) microgram/ml, and the levels of IL-6 receptor expressed on the cell surface were 16.7% and 20.2% in untreated and relapsed or refractory patients, respectively, and those were significantly lower than those levels in the cells before exposure to thalidomide.	Thalidomide	21-32	interleukin 6	Homo sapiens	76-80
12513842-5	2002	After treatment with thalidomide at 200 microgram/ml, the concentrations of IL-6 secreted by myeloma cells were (148.5 +/- 96.7) microgram/ml, and the levels of IL-6 receptor expressed on the cell surface were 16.7% and 20.2% in untreated and relapsed or refractory patients, respectively, and those were significantly lower than those levels in the cells before exposure to thalidomide.	Thalidomide	21-32	interleukin 6	Homo sapiens	161-165
12513842-5	2002	After treatment with thalidomide at 200 microgram/ml, the concentrations of IL-6 secreted by myeloma cells were (148.5 +/- 96.7) microgram/ml, and the levels of IL-6 receptor expressed on the cell surface were 16.7% and 20.2% in untreated and relapsed or refractory patients, respectively, and those were significantly lower than those levels in the cells before exposure to thalidomide.	Thalidomide	375-386	interleukin 6	Homo sapiens	161-165
11809002-3	2001	Recent reports of original pharmacological properties including modulation of cytokine production (mainly reduced TNF-alpha production) and inhibition of angiogenesis have led to the suggestion that thalidomide may be useful in some inflammatory and neoplastic conditions.	Thalidomide	199-210	tumor necrosis factor	Homo sapiens	114-123
11734114-3	2002	Current evidence indicates that thalidomide reduces the activity of the inflammatory cytokine tumor necrosis factor-alpha by accelerating the degradation of its messenger RNA.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	94-121
11705847-3	2001	The induction of Cox-2 protein and mRNA by LPS was also suppressed by thalidomide.	Thalidomide	70-81	prostaglandin-endoperoxide synthase 2	Mus musculus	17-22
11753617-13	2001	Finally, thalidomide (100 microM) and its immunomodulatory analog IMiD1-CC4047 (1 microM) decreased the upregulation of IL-6 and VEGF secretion in cultures of BMSCs, MM cells and co-cultures of BMSCs with MM cells.	Thalidomide	9-20	interleukin 6	Homo sapiens	120-124
11753617-13	2001	Finally, thalidomide (100 microM) and its immunomodulatory analog IMiD1-CC4047 (1 microM) decreased the upregulation of IL-6 and VEGF secretion in cultures of BMSCs, MM cells and co-cultures of BMSCs with MM cells.	Thalidomide	9-20	vascular endothelial growth factor A	Homo sapiens	129-133
11838958-0	2001	Down-regulation of cell adhesion molecules LFA-1 and ICAM-1 after in vitro treatment with the anti-TNF-alpha agent thalidomide.	Thalidomide	115-126	integrin subunit alpha L	Homo sapiens	43-48
11838958-0	2001	Down-regulation of cell adhesion molecules LFA-1 and ICAM-1 after in vitro treatment with the anti-TNF-alpha agent thalidomide.	Thalidomide	115-126	intercellular adhesion molecule 1	Homo sapiens	53-59
11838958-0	2001	Down-regulation of cell adhesion molecules LFA-1 and ICAM-1 after in vitro treatment with the anti-TNF-alpha agent thalidomide.	Thalidomide	115-126	tumor necrosis factor	Homo sapiens	99-108
11838958-1	2001	The tumor necrosis factor-alpha (TNF-alpha) inhibitor thalidomide is known to be a potent modulator of host immunity, a potential treatment for autoimmune disorders such as rheumatoid arthritis (RA) and a treatment for complications of HIV-1 infection.	Thalidomide	54-65	tumor necrosis factor	Homo sapiens	33-42
11730158-2	2001	The effects of thalidomide are at least partly mediated by down-regulation of tumour necrosis factor (TNF)-alpha, a potent proinflammatory cytokine.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	78-112
11705847-0	2001	Thalidomide and its analogues inhibit lipopolysaccharide-mediated Iinduction of cyclooxygenase-2.	Thalidomide	0-11	prostaglandin-endoperoxide synthase 2	Mus musculus	80-96
11705847-1	2001	We investigated the effect of thalidomide, a compound with immunomodulatory and antiangiogenic properties, on lipopolysaccharide (LPS)-mediated induction of cyclooxygenase-2 (Cox-2) and prostaglandin (PG) biosynthesis in murine macrophages.	Thalidomide	30-41	prostaglandin-endoperoxide synthase 2	Mus musculus	157-173
11705847-1	2001	We investigated the effect of thalidomide, a compound with immunomodulatory and antiangiogenic properties, on lipopolysaccharide (LPS)-mediated induction of cyclooxygenase-2 (Cox-2) and prostaglandin (PG) biosynthesis in murine macrophages.	Thalidomide	30-41	prostaglandin-endoperoxide synthase 2	Mus musculus	175-180
11705847-5	2001	Thalidomide decreased the stability of Cox-2 mRNA.	Thalidomide	0-11	prostaglandin-endoperoxide synthase 2	Mus musculus	39-44
11705847-6	2001	A series of structural analogues of thalidomide also inhibited LPS-mediated induction of Cox-2 and PGE(2) synthesis.	Thalidomide	36-47	prostaglandin-endoperoxide synthase 2	Mus musculus	89-94
11504824-8	2001	Thalidomide resulted in a nonsignificant decrease of CRP and SAA, but the concentrations of other inflammatory mediators, including urine neopterin, remained unchanged.	Thalidomide	0-11	C-reactive protein	Homo sapiens	53-56
11598844-4	2001	Thalidomide stimulated CD8+ T cells in peripheral blood, which increased expression of the activation markers CD38 and human leukocyte antigen DR and of the memory cell marker CD45RO.	Thalidomide	0-11	CD8a molecule	Homo sapiens	23-26
11598844-4	2001	Thalidomide stimulated CD8+ T cells in peripheral blood, which increased expression of the activation markers CD38 and human leukocyte antigen DR and of the memory cell marker CD45RO.	Thalidomide	0-11	CD38 molecule	Homo sapiens	110-114
11598844-5	2001	The frequency of HIV gag-specific CD8+ T cells in peripheral blood increased in 3 of 4 children who were evaluated during treatment with thalidomide.	Thalidomide	137-148	CD8a molecule	Homo sapiens	34-37
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	105-114
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	116-146
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	148-152
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	155-189
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	191-195
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	interleukin 6	Homo sapiens	201-214
11592764-1	2001	Thalidomide is reported to suppress levels of several cytokines, angiogenic and growth factors including TNF-alpha, basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6).	Thalidomide	0-11	interleukin 6	Homo sapiens	216-220
11555579-0	2001	High plasma basic fibroblast growth factor concentration is associated with response to thalidomide in progressive multiple myeloma.	Thalidomide	88-99	fibroblast growth factor 2	Homo sapiens	12-42
11722460-5	2001	One possible predisposing factor in AP may be tumour necrosis factor (TNF)alpha as suggested by the good response of AP to the TNFalpha inhibitor thalidomide, and by the involvement of this cytokine in many immune responses.	Thalidomide	146-157	tumor necrosis factor	Homo sapiens	70-79
11722460-5	2001	One possible predisposing factor in AP may be tumour necrosis factor (TNF)alpha as suggested by the good response of AP to the TNFalpha inhibitor thalidomide, and by the involvement of this cytokine in many immune responses.	Thalidomide	146-157	tumor necrosis factor	Homo sapiens	127-135
11574978-2	2001	Thalidomide, a non-barbiturate hypnotic, also has an anti-inflammatory effect, presumably by suppressing the production of tumor necrosis factor alpha.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	123-150
11574978-9	2001	RESULTS: Colonic wet weight, lesion area, myeloperoxidase activity and serum levels of TNF alpha were significantly lower (P &lt; 0.05) in the treatment group (iodoacetamide + thalidomide) than the control group (iodoacetamide only).	Thalidomide	176-187	tumor necrosis factor	Rattus norvegicus	87-96
11720008-0	2001	Potent inhibition of cytokine production from intestinal lamina propria T cells by phosphodiesterase-4 inhibitory thalidomide analogues.	Thalidomide	114-125	phosphodiesterase 4A	Homo sapiens	83-102
11720008-2	2001	Thalidomide influences cytokine production by leukocytes, inhibiting macrophage TNF-alpha, and is beneficial in treating Crohn"s disease.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	80-89
11504824-8	2001	Thalidomide resulted in a nonsignificant decrease of CRP and SAA, but the concentrations of other inflammatory mediators, including urine neopterin, remained unchanged.	Thalidomide	0-11	serum amyloid A1 cluster	Homo sapiens	61-64
11685731-4	2001	In a recent phase II trial of thalidomide in AIPC, 28% of patients achieved a prostate-specific antigen (PSA) decrease of &gt;40%.	Thalidomide	30-41	PDZ domain containing 2	Homo sapiens	45-49
11498529-11	2001	According to RT - PCR analysis, both thalidomide and supidimide also significantly reduced vascular cell adhesion molecule-1 mRNA expression in the affected part of the descending colon.	Thalidomide	37-48	vascular cell adhesion molecule 1	Rattus norvegicus	91-124
11448901-13	2001	Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline seen in our trial justifies further study.	Thalidomide	47-58	kallikrein related peptidase 3	Homo sapiens	69-72
11418482-4	2001	It was demonstrated that Thal/IMiDs do not induce T-cell proliferation alone but act as costimulators to trigger proliferation of anti-CD3-stimulated T cells from patients with MM, accompanied by an increase in interferon-gamma and IL-2 secretion.	Thalidomide	25-29	interferon gamma	Homo sapiens	211-227
11418482-4	2001	It was demonstrated that Thal/IMiDs do not induce T-cell proliferation alone but act as costimulators to trigger proliferation of anti-CD3-stimulated T cells from patients with MM, accompanied by an increase in interferon-gamma and IL-2 secretion.	Thalidomide	25-29	interleukin 2	Homo sapiens	232-236
11418482-6	2001	A role for natural killer (NK)- and LAK-cell-mediated killing is suggested because IL-2-primed peripheral blood mononuclear cells (PBMCs) treated with Thal/IMiDs demonstrated significantly increased lysis of MM cell lines.	Thalidomide	151-155	alpha kinase 1	Homo sapiens	36-39
11418482-6	2001	A role for natural killer (NK)- and LAK-cell-mediated killing is suggested because IL-2-primed peripheral blood mononuclear cells (PBMCs) treated with Thal/IMiDs demonstrated significantly increased lysis of MM cell lines.	Thalidomide	151-155	interleukin 2	Homo sapiens	83-87
11448901-13	2001	Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline seen in our trial justifies further study.	Thalidomide	47-58	kallikrein related peptidase 3	Homo sapiens	117-120
11302825-1	2001	Ingestion of thalidomide was associated with a reduction in the upregulation of the granulocyte activation marker CD11b and a reduced capacity to release elastase and lactoferrin after stimulation with lipopolysaccharide or lipoteichoic acid.	Thalidomide	13-24	integrin subunit alpha M	Homo sapiens	114-119
11411542-1	2001	Previous studies of alpha-glucosidase inhibitors derived from thalidomide revealed that 4,5,6,7-tetrachloro-N-alkylphthalimide derivatives are superior lead compounds.	Thalidomide	62-73	sucrase-isomaltase	Homo sapiens	20-37
12113124-4	2001	Thalidomide has antiangiogenic and immunomodulatory properties and is an effective inhibitor of TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	96-105
11297551-0	2001	Inhibition of NF-kappa B activity by thalidomide through suppression of IkappaB kinase activity.	Thalidomide	37-48	nuclear factor kappa B subunit 1	Homo sapiens	14-24
11297551-6	2001	We show here that thalidomide can block NF-kappaB activation through a mechanism that involves the inhibition of activity of the IkappaB kinase.	Thalidomide	18-29	nuclear factor kappa B subunit 1	Homo sapiens	40-49
11297551-7	2001	Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2.	Thalidomide	54-65	nuclear factor kappa B subunit 1	Homo sapiens	43-52
11297551-7	2001	Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2.	Thalidomide	54-65	nuclear factor kappa B subunit 1	Homo sapiens	109-118
11297551-7	2001	Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2.	Thalidomide	54-65	C-X-C motif chemokine ligand 8	Homo sapiens	158-171
11297551-7	2001	Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2.	Thalidomide	54-65	TNF receptor associated factor 1	Homo sapiens	173-178
11297551-7	2001	Consistent with the observed inhibition of NF-kappaB, thalidomide blocked the cytokine-induced expression of NF-kappaB-regulated genes such as those encoding interleukin-8, TRAF1, and c-IAP2.	Thalidomide	54-65	baculoviral IAP repeat containing 3	Homo sapiens	184-190
11297551-8	2001	These data indicate that the therapeutic potential for thalidomide may be based on its ability to block NF-kappaB activation through suppression of IkappaB kinase activity.	Thalidomide	55-66	nuclear factor kappa B subunit 1	Homo sapiens	104-113
11321389-3	2001	Thalidomide selectively reduces TNF-alpha production by inflammatory cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	32-41
11165754-9	2001	Thalidomide also lowered remarkably VEGF expression (P&lt;0.01) and CD31 (P&lt;0.01) as well as VEGF mRNA (P&lt;0.05), but it did not show statistically significant inhibitory effect on the tumor growth.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	36-40
11165754-9	2001	Thalidomide also lowered remarkably VEGF expression (P&lt;0.01) and CD31 (P&lt;0.01) as well as VEGF mRNA (P&lt;0.05), but it did not show statistically significant inhibitory effect on the tumor growth.	Thalidomide	0-11	platelet and endothelial cell adhesion molecule 1	Homo sapiens	68-72
11165754-9	2001	Thalidomide also lowered remarkably VEGF expression (P&lt;0.01) and CD31 (P&lt;0.01) as well as VEGF mRNA (P&lt;0.05), but it did not show statistically significant inhibitory effect on the tumor growth.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	96-100
11417421-5	2001	Thalidomide, a potent inhibitor of tumour necrosis factor alpha (TNF-alpha), was added to the treatment regimen and resulted in marked clinical improvement with resolution of the abscess within 4 months.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	65-74
11354662-0	2001	Aza analogues of thalidomide: synthesis and evaluation as inhibitors of tumor necrosis factor-alpha production in vitro.	Thalidomide	17-28	tumor necrosis factor	Homo sapiens	72-99
11354662-2	2001	These 5-phthalimidopyrimidines as well as phthalimido-2,4-difluorobenzenes were designed as analogues of thalidomide, a well known inhibitor of TNF-alpha production.	Thalidomide	105-116	tumor necrosis factor	Homo sapiens	144-153
11604049-4	2001	Effects on tumour necrosis factor-alpha (TNFalpha) release play an important role in the ability of thalidomide to affect the immune system.	Thalidomide	100-111	tumor necrosis factor	Homo sapiens	41-49
11604049-5	2001	Alteration of synthesis and release of cytokines such as interleukin (IL)-1, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12 and interferon-gamma is involved in the complex mechanisms of thalidomide.	Thalidomide	176-187	interferon gamma	Homo sapiens	118-134
11604049-11	2001	However, despite the promising findings of thalidomide at the molecular level, namely its anti-TNFalpha properties and its intercalation with DNA, and activity in clinical trials, there is still a great need for more intensive research.	Thalidomide	43-54	tumor necrosis factor	Homo sapiens	95-103
11116278-9	2001	Finally, the TNF-alpha targeting drugs, namely thalidomide and the anti-TNF-alpha mAb, infliximab, have given promising results in the treatment of severe and/or refractory AS patients, however further controlled studies are required.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	13-22
11204273-6	2001	Treatment of explants with the angiogenesis inhibitor endostatin, the chemokine IP-10, and the thalidomide derivative phatolyl glutamic acid (PG-acid) resulted in an inhibition of the formation of PECAM-1 positive tubelike structures of 48.8% (+/- 4%), 50.2% (+/- 12%), and 80.8% (+/- 3%), respectively.	Thalidomide	95-106	platelet/endothelial cell adhesion molecule 1	Mus musculus	197-204
11367517-0	2001	Differential effect of thalidomide and dexamethasone on the transcription factor NF-kappa B.	Thalidomide	23-34	nuclear factor kappa B subunit 1	Homo sapiens	81-91
11367517-2	2001	In vitro studies have shown that thalidomide inhibits tumour necrosis factor alpha (TNF-alpha) mRNA expression and protein production by mitogen-stimulated macrophages and activated T cells.	Thalidomide	33-44	tumor necrosis factor	Homo sapiens	84-93
11367517-4	2001	In the present investigations, we have examined the influence of thalidomide on nuclear levels of NF-kappa B in human peripheral blood mononuclear cells (PBMC) following activation with mitogen or phorbol myristate acetate (PMA)/ionophore.	Thalidomide	65-76	nuclear factor kappa B subunit 1	Homo sapiens	98-108
11367517-13	2001	These observations suggest that thalidomide does not act directly on NF-kappa B and therefore inhibits TNF-alpha production through another independent mechanism.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	103-112
11068114-0	2000	Thalidomide treatment in chronic constrictive neuropathy decreases endoneurial tumor necrosis factor-alpha, increases interleukin-10 and has long-term effects on spinal cord dorsal horn met-enkephalin.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	79-106
11123102-0	2000	The Th1/Th2 paradigm in the pathogenesis of scleroderma, and its modulation by thalidomide.	Thalidomide	79-90	negative elongation factor complex member C/D	Homo sapiens	4-7
11123102-5	2000	The immune modulating effects of the drug thalidomide on Th1 and Th2 immunity are also described, along with the drug"s potential application to disease processes like scleroderma.	Thalidomide	42-53	negative elongation factor complex member C/D	Homo sapiens	57-60
11121122-7	2000	An inhibitory effect on interleukin-10 mRNA was likewise seen after thalidomide and pentoxifylline, but not subsequent to prednisone treatment.	Thalidomide	68-79	interleukin 10	Homo sapiens	24-38
11204669-4	2000	Clinical experience with thalidomide (Thalomid), which inhibits angiogenesis induced by both vascular endothelial growth factor and basic fibroblast growth factor, has included observation of "clinical improvement" in patients with androgen-independent prostate cancer and anecdotal responses in patients with metastatic disease refractory to chemotherapy.	Thalidomide	25-36	vascular endothelial growth factor A	Homo sapiens	93-127
11204669-4	2000	Clinical experience with thalidomide (Thalomid), which inhibits angiogenesis induced by both vascular endothelial growth factor and basic fibroblast growth factor, has included observation of "clinical improvement" in patients with androgen-independent prostate cancer and anecdotal responses in patients with metastatic disease refractory to chemotherapy.	Thalidomide	38-46	vascular endothelial growth factor A	Homo sapiens	93-127
11079045-5	2000	Thalidomide, an oral agent with anti-TNF effects, shows promise in non-controlled experience.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	37-40
11068114-0	2000	Thalidomide treatment in chronic constrictive neuropathy decreases endoneurial tumor necrosis factor-alpha, increases interleukin-10 and has long-term effects on spinal cord dorsal horn met-enkephalin.	Thalidomide	0-11	interleukin 10	Rattus norvegicus	118-132
11068114-2	2000	Since thalidomide mainly inhibits tumor necrosis factor alpha (TNF-alpha) synthesis with less well defined effects on other cytokines, we investigated the effect of the drug on the expression of the proinflammatory cytokines TNF-alpha, interleukin-1beta (IL-1beta) and interleukin 6 (IL-6), and of the anti-inflammatory cytokine interleukin-10 (IL-10) in the lesioned rat sciatic nerve.	Thalidomide	6-17	tumor necrosis factor	Rattus norvegicus	34-61
11068114-2	2000	Since thalidomide mainly inhibits tumor necrosis factor alpha (TNF-alpha) synthesis with less well defined effects on other cytokines, we investigated the effect of the drug on the expression of the proinflammatory cytokines TNF-alpha, interleukin-1beta (IL-1beta) and interleukin 6 (IL-6), and of the anti-inflammatory cytokine interleukin-10 (IL-10) in the lesioned rat sciatic nerve.	Thalidomide	6-17	tumor necrosis factor	Rattus norvegicus	63-72
11068114-3	2000	The increase of endoneurial TNF-alpha during the first week after CCI was reduced after thalidomide treatment, as shown with immunohistochemistry and enzyme-linked-immunosorbent assay.	Thalidomide	88-99	tumor necrosis factor	Rattus norvegicus	28-37
11068114-5	2000	Recruitment of epineurial IL-10 immunoreactive macrophages as well as the recovery of injury-induced depletion of endoneurial IL-10-IR was enhanced by thalidomide treatment.	Thalidomide	151-162	interleukin 10	Rattus norvegicus	26-31
11068114-5	2000	Recruitment of epineurial IL-10 immunoreactive macrophages as well as the recovery of injury-induced depletion of endoneurial IL-10-IR was enhanced by thalidomide treatment.	Thalidomide	151-162	interleukin 10	Rattus norvegicus	126-131
11027451-5	2000	Histologic comparison of skin biopsies showed changes in skin fibrosis and an increase in epidermal and dermal infiltrating CD8(+) T cells with thalidomide treatment.	Thalidomide	144-155	CD8a molecule	Homo sapiens	124-127
11027451-8	2000	When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed.	Thalidomide	57-68	interferon gamma	Homo sapiens	126-135
11027451-6	2000	In thalidomide-treated SSc patients, plasma levels of IL-12 and TNF-alpha increased, while plasma IL-5 and IL-10 levels remained unchanged.	Thalidomide	3-14	tumor necrosis factor	Homo sapiens	64-73
11027451-8	2000	When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed.	Thalidomide	57-68	CD40 ligand	Homo sapiens	161-166
11027451-6	2000	In thalidomide-treated SSc patients, plasma levels of IL-12 and TNF-alpha increased, while plasma IL-5 and IL-10 levels remained unchanged.	Thalidomide	3-14	interleukin 5	Homo sapiens	98-102
11027451-6	2000	In thalidomide-treated SSc patients, plasma levels of IL-12 and TNF-alpha increased, while plasma IL-5 and IL-10 levels remained unchanged.	Thalidomide	3-14	interleukin 10	Homo sapiens	107-112
11027451-8	2000	When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed.	Thalidomide	57-68	interleukin 2	Homo sapiens	102-106
11027451-8	2000	When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed.	Thalidomide	57-68	interleukin 3	Homo sapiens	108-112
11027451-8	2000	When SSc PBMCs activated by anti-CD3 mAb were exposed to thalidomide, increases in both production of IL-2, IL-3, GM-CSF, and IFN-gamma and T cell expression of CD40L were observed.	Thalidomide	57-68	colony stimulating factor 2	Homo sapiens	114-120
10952569-5	2000	In all six volunteers ingestion of thalidomide was associated with enhanced SEB- and anti-CD3/CD28-induced production of the Th1 cytokine gamma interferon (P &lt; 0.05) and a decrease in the level of anti-CD3/CD28-induced interleukin-5 (IL-5) production (P &lt; 0.05).	Thalidomide	35-46	interleukin 5	Homo sapiens	222-235
10952569-5	2000	In all six volunteers ingestion of thalidomide was associated with enhanced SEB- and anti-CD3/CD28-induced production of the Th1 cytokine gamma interferon (P &lt; 0.05) and a decrease in the level of anti-CD3/CD28-induced interleukin-5 (IL-5) production (P &lt; 0.05).	Thalidomide	35-46	interleukin 5	Homo sapiens	237-241
10952569-3	2000	To obtain insight into the effect of thalidomide on the capacity of lymphocytes to produce Th1 and Th2 cytokines, six healthy volunteers received an oral dose (400 mg) of thalidomide.	Thalidomide	37-48	negative elongation factor complex member C/D	Homo sapiens	91-94
10952569-8	2000	Thus, a single oral dose of thalidomide causes a Th1-type response in healthy humans.	Thalidomide	28-39	negative elongation factor complex member C/D	Homo sapiens	49-52
10952569-5	2000	In all six volunteers ingestion of thalidomide was associated with enhanced SEB- and anti-CD3/CD28-induced production of the Th1 cytokine gamma interferon (P &lt; 0.05) and a decrease in the level of anti-CD3/CD28-induced interleukin-5 (IL-5) production (P &lt; 0.05).	Thalidomide	35-46	CD28 molecule	Homo sapiens	94-98
10952569-5	2000	In all six volunteers ingestion of thalidomide was associated with enhanced SEB- and anti-CD3/CD28-induced production of the Th1 cytokine gamma interferon (P &lt; 0.05) and a decrease in the level of anti-CD3/CD28-induced interleukin-5 (IL-5) production (P &lt; 0.05).	Thalidomide	35-46	negative elongation factor complex member C/D	Homo sapiens	125-128
10961786-7	2000	Levels of tumor necrosis factor-alpha in the cerebrospinal fluid decreased markedly during thalidomide therapy.	Thalidomide	91-102	tumor necrosis factor	Homo sapiens	10-37
10952569-5	2000	In all six volunteers ingestion of thalidomide was associated with enhanced SEB- and anti-CD3/CD28-induced production of the Th1 cytokine gamma interferon (P &lt; 0.05) and a decrease in the level of anti-CD3/CD28-induced interleukin-5 (IL-5) production (P &lt; 0.05).	Thalidomide	35-46	CD28 molecule	Homo sapiens	209-213
10937517-3	2000	RESULTS: Thalidomide reduced insulin-stimulated glucose uptake by 31% (from 27.7 to 19.2 pmol x kg(-1) x min(-1), P &lt; 0.05) compared with the prestudy and by 21% (from 24.2 to 19.2 pmol x kg(-1) x min(-1), P &lt; 0.05) compared with placebo.	Thalidomide	9-20	insulin	Homo sapiens	29-36
10937517-4	2000	Thalidomide also reduced insulin-stimulated GS by 48% (from 14.1 to 8.2 micromol x kg(-1) x min(-1), P &lt; 0.05) compared with the prestudy and by 40% (from 13.6 to 8.2 micromol x kg(-1) x min(-1), P &lt; 0.5) compared with placebo.	Thalidomide	0-11	insulin	Homo sapiens	25-32
10937517-6	2000	CONCLUSIONS: We conclude that thalidomide increased insulin resistance in obese patients with type 2 diabetes by inhibiting insulin-stimulated GS and that patients taking thalidomide should be monitored for possible deterioration in their glucose tolerance.	Thalidomide	30-41	insulin	Homo sapiens	52-59
10937517-6	2000	CONCLUSIONS: We conclude that thalidomide increased insulin resistance in obese patients with type 2 diabetes by inhibiting insulin-stimulated GS and that patients taking thalidomide should be monitored for possible deterioration in their glucose tolerance.	Thalidomide	30-41	insulin	Homo sapiens	124-131
10971513-9	2000	The results suggest a role for thalidomide analogue CC-3052 in reducing persistent activation of the TNF-alpha system in HIV without markedly impairing neutrophil viability.	Thalidomide	31-42	tumor necrosis factor	Homo sapiens	101-110
10950803-4	2000	Thalidomide treatment was found to cause potent and selective inhibition of IL-8 production in a dose-responsive manner.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	76-80
10950803-6	2000	In addition, thalidomide treatment of lipopolysaccharide-stimulated microglia inhibited the activation of protein NF-kappaB, a transcription factor known to be important for IL-8 production.	Thalidomide	13-24	nuclear factor kappa B subunit 1	Homo sapiens	114-123
10950803-6	2000	In addition, thalidomide treatment of lipopolysaccharide-stimulated microglia inhibited the activation of protein NF-kappaB, a transcription factor known to be important for IL-8 production.	Thalidomide	13-24	C-X-C motif chemokine ligand 8	Homo sapiens	174-178
10950803-7	2000	These results suggest thalidomide could have a therapeutic role in acute bacterial meningitis through inhibition of IL-8-mediated neutrophil chemotaxis.	Thalidomide	22-33	C-X-C motif chemokine ligand 8	Homo sapiens	116-120
10850856-0	2000	Modulation of hyperoxia-induced TNF-alpha expression in the newborn rat lung by thalidomide and dexamethasone.	Thalidomide	80-91	tumor necrosis factor	Rattus norvegicus	32-41
10850856-7	2000	In the lungs of animals treated with either dexamethasone or thalidomide, TNF-alpha mRNA levels were reduced, while only dexamethasone treatment also reduced IL-6 mRNA levels.	Thalidomide	61-72	tumor necrosis factor	Rattus norvegicus	74-83
10850856-7	2000	In the lungs of animals treated with either dexamethasone or thalidomide, TNF-alpha mRNA levels were reduced, while only dexamethasone treatment also reduced IL-6 mRNA levels.	Thalidomide	61-72	interleukin 6	Rattus norvegicus	158-162
10915104-0	2000	Tumor necrosis factor-alpha increased production during thalidomide treatment in patients with tuberculosis and human immunodeficiency virus coinfection.	Thalidomide	56-67	tumor necrosis factor	Homo sapiens	0-27
10799645-2	2000	We propose that thalidomide affects the following pathway during development: insulin-like growth factor I (IGF-I) and fibroblast growth factor 2 (FGF-2) stimulation of the transcription of alphav and beta3 integrin subunit genes.	Thalidomide	16-27	insulin like growth factor 1	Homo sapiens	78-106
10799645-2	2000	We propose that thalidomide affects the following pathway during development: insulin-like growth factor I (IGF-I) and fibroblast growth factor 2 (FGF-2) stimulation of the transcription of alphav and beta3 integrin subunit genes.	Thalidomide	16-27	insulin like growth factor 1	Homo sapiens	108-113
10799645-2	2000	We propose that thalidomide affects the following pathway during development: insulin-like growth factor I (IGF-I) and fibroblast growth factor 2 (FGF-2) stimulation of the transcription of alphav and beta3 integrin subunit genes.	Thalidomide	16-27	fibroblast growth factor 2	Homo sapiens	119-145
10799645-2	2000	We propose that thalidomide affects the following pathway during development: insulin-like growth factor I (IGF-I) and fibroblast growth factor 2 (FGF-2) stimulation of the transcription of alphav and beta3 integrin subunit genes.	Thalidomide	16-27	fibroblast growth factor 2	Homo sapiens	147-152
10799645-2	2000	We propose that thalidomide affects the following pathway during development: insulin-like growth factor I (IGF-I) and fibroblast growth factor 2 (FGF-2) stimulation of the transcription of alphav and beta3 integrin subunit genes.	Thalidomide	16-27	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	201-206
10799645-7	2000	Intercalation into G-rich promoter regions of DNA may explain why certain thalidomide analogs are not teratogenic while retaining their anti-tumor necrosis factor-alpha (TNF-alpha) activity, and suggests that we look elsewhere to explain the action of thalidomide on TNF-alpha.	Thalidomide	74-85	tumor necrosis factor	Homo sapiens	170-179
10816156-2	2000	After receiving thalidomide treatment, serum tumor necrosis factor (TNF) and soluble TNF receptor II levels normalized, his constitutional and gastrointestinal symptoms diminished, and the mass lesion shrunk.	Thalidomide	16-27	tumor necrosis factor	Homo sapiens	45-66
11003055-0	2000	A possible role of N-cadherin in thalidomide teratogenicity.	Thalidomide	33-44	cadherin 2	Homo sapiens	19-29
11003055-1	2000	Several experimental findings indicate that the adhesion molecule N-cadherin participates in distinct processes of embryogenesis that spatiotemporarily correlate with high sensitivity to thalidomide.	Thalidomide	187-198	cadherin 2	Homo sapiens	66-76
11003055-2	2000	Therefore, we suppose that thalidomide might interfere with N-cadherin-mediated interactions.	Thalidomide	27-38	cadherin 2	Homo sapiens	60-70
11003055-3	2000	This hypothesis is supported by protein-ligand docking studies simulating and characterizing the binding of thalidomide to N-cadherin molecules.	Thalidomide	108-119	cadherin 2	Homo sapiens	123-133
11003055-4	2000	Thalidomide was found to bind at the N-terminal domain of N-cadherin mimicking a tryptophan residue which is critical for the homodimerization of the adhesion molecule.	Thalidomide	0-11	cadherin 2	Homo sapiens	58-68
11003055-5	2000	Based on these results, we suggest that thalidomide might disturb cellular recognition and migration processes in morphogenesis by interaction with N-cadherin.	Thalidomide	40-51	cadherin 2	Homo sapiens	148-158
10816156-2	2000	After receiving thalidomide treatment, serum tumor necrosis factor (TNF) and soluble TNF receptor II levels normalized, his constitutional and gastrointestinal symptoms diminished, and the mass lesion shrunk.	Thalidomide	16-27	tumor necrosis factor	Homo sapiens	68-71
10816156-2	2000	After receiving thalidomide treatment, serum tumor necrosis factor (TNF) and soluble TNF receptor II levels normalized, his constitutional and gastrointestinal symptoms diminished, and the mass lesion shrunk.	Thalidomide	16-27	tumor necrosis factor	Homo sapiens	85-88
10849134-2	2000	The pharmacologic action involves the downregulation of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and inhibition of basic fibroblast growth factor (bFGF)-induced angiogenesis; however, not much is known about thalidomide"s effect on immunologic parameters in lupus erythematosus (LE).	Thalidomide	237-248	fibroblast growth factor 2	Homo sapiens	176-180
11249506-3	2000	Other investigational drugs that also inhibit TNF-alpha activity include new "humanised" anti-TNF-alpha antibodies (CDP571), thalidomide, new analogues of thalidomide, and TNF-alpha receptor fusion proteins.	Thalidomide	125-136	tumor necrosis factor	Homo sapiens	46-55
11249506-3	2000	Other investigational drugs that also inhibit TNF-alpha activity include new "humanised" anti-TNF-alpha antibodies (CDP571), thalidomide, new analogues of thalidomide, and TNF-alpha receptor fusion proteins.	Thalidomide	155-166	tumor necrosis factor	Homo sapiens	46-55
10781782-2	2000	Current evidence indicates that thalidomide reduces the activity of the inflammatory cytokine tumor necrosis factor (TNF)-alpha by accelerating the degradation of its messenger RNA.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	94-127
10825407-5	2000	The principle therapeutic action of thalidomide appears to be reduction of TNF-alpha levels.	Thalidomide	36-47	tumor necrosis factor	Homo sapiens	75-84
11558112-8	2000	Once the anti-inflammatory, immuno-modulatory, anti-TNF-alpha and anti-angiogenic properties of thalidomide were discovered, it was also tried in AIDS and related wasting, apthous ulcers, microsporidiosis and Kaposi"s sarcoma.	Thalidomide	96-107	tumor necrosis factor	Homo sapiens	52-61
10784439-1	2000	Previous studies on the structural development of tumor necrosis factor alpha (TNF-alpha) production regulators derived from thalidomide (N-alpha-phthalimidoglutarimide) revealed that a hydrophobic substituent at the nitrogen atom of the phthalimide ring is critical for potent activity.	Thalidomide	125-136	tumor necrosis factor	Homo sapiens	50-77
18034532-5	2000	Thalidomide produces partial inhibition of tumour necrosis factor-alpha production in vivo but recent data reveals that it can also act as a co-stimulatory molecule for T cell activation in vitro, resulting in increased production of interleukin-2 and interferon-gamma.	Thalidomide	0-11	interleukin 2	Homo sapiens	234-247
18034532-5	2000	Thalidomide produces partial inhibition of tumour necrosis factor-alpha production in vivo but recent data reveals that it can also act as a co-stimulatory molecule for T cell activation in vitro, resulting in increased production of interleukin-2 and interferon-gamma.	Thalidomide	0-11	interferon gamma	Homo sapiens	252-268
10784439-1	2000	Previous studies on the structural development of tumor necrosis factor alpha (TNF-alpha) production regulators derived from thalidomide (N-alpha-phthalimidoglutarimide) revealed that a hydrophobic substituent at the nitrogen atom of the phthalimide ring is critical for potent activity.	Thalidomide	125-136	tumor necrosis factor	Homo sapiens	79-88
10720640-10	2000	The demonstration that thalidomide is able to inhibit inflammatory hyperalgesia in rats and the writhing nociceptive response in mice suggests that these analgesic effects seem to be a consequence of the inhibition of TNF-alpha production, and indicates the need for investigations on the possibility of the use of thalidomide for the treatment of pain refractory to classical non-narcotic analgesics.	Thalidomide	23-34	tumor necrosis factor	Mus musculus	218-227
10720640-2	2000	Thalidomide has been shown to selectively inhibit TNF-alpha production.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	50-59
10647875-8	2000	The TNF-alpha secreted by the same cells incubated with thalidomide and SEA was not significantly different from that secreted by the cells incubated with SEA alone.	Thalidomide	56-67	tumor necrosis factor	Homo sapiens	4-13
10720640-5	2000	injections of carrageenin or bradykinin, which act by stimulating TNF-alpha release, but not responses to TNF-alpha or prostaglandin E(2), were inhibited in a dose-dependent manner by pretreatment of the animals with thalidomide.	Thalidomide	217-228	tumor necrosis factor	Mus musculus	66-75
10720640-8	2000	Moreover, the thalidomide pretreatment also reduced the TNF-alpha mRNA levels in the peritoneal cells induced by injection of zymosan in mice.	Thalidomide	14-25	tumor necrosis factor	Mus musculus	56-65
10720518-1	2000	Thalidomide, which inhibits monocyte tumor necrosis factor (TNF)-alpha production and costimulates T cells, was tested for immune modulation in patients with human immunodeficiency virus (HIV) infection and tuberculosis (TB) in a placebo-controlled study.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	37-70
10720518-2	2000	Thalidomide therapy resulted in increased levels of plasma interleukin (IL)-2 receptor, soluble CD8, interferon-gamma, and IL-12, indicating immune stimulation.	Thalidomide	0-11	CD8a molecule	Homo sapiens	96-99
10720518-2	2000	Thalidomide therapy resulted in increased levels of plasma interleukin (IL)-2 receptor, soluble CD8, interferon-gamma, and IL-12, indicating immune stimulation.	Thalidomide	0-11	interferon gamma	Homo sapiens	101-117
10720518-4	2000	Thalidomide treatment increased CD4+ and CD8+ T cell counts and lymphocyte proliferation to purified protein derivative.	Thalidomide	0-11	CD8a molecule	Homo sapiens	41-44
10720518-7	2000	Thalidomide-induced increased viral replication in CD4+ T cells was abrogated by adding back autologous CD8+ T cells.	Thalidomide	0-11	CD8a molecule	Homo sapiens	104-107
10661908-1	2000	We propose that thalidomide affects the following pathway during limb development: Growth factors (FGF-2 and IGF-I) attach to receptors on limb bud mesenchymal cells and initiate some second messenger system (perhaps SP-1), which activates alphav and beta3 integrin subunit genes.	Thalidomide	16-27	fibroblast growth factor 2	Homo sapiens	99-104
10661908-1	2000	We propose that thalidomide affects the following pathway during limb development: Growth factors (FGF-2 and IGF-I) attach to receptors on limb bud mesenchymal cells and initiate some second messenger system (perhaps SP-1), which activates alphav and beta3 integrin subunit genes.	Thalidomide	16-27	insulin like growth factor 1	Homo sapiens	109-114
10647875-0	2000	Thalidomide"s ability to augment the synthesis of IL-2 in vitro in HIV-infected patients is associated with the percentage of CD4+ cells in their blood.	Thalidomide	0-11	interleukin 2	Homo sapiens	50-54
10647875-0	2000	Thalidomide"s ability to augment the synthesis of IL-2 in vitro in HIV-infected patients is associated with the percentage of CD4+ cells in their blood.	Thalidomide	0-11	CD4 molecule	Homo sapiens	126-129
10647875-4	2000	We investigated the effect of thalidomide on the production of IL-2 and TNF-alpha by staphylococcal enterotoxin A (SEA) stimulated peripheral blood mononuclear cells (PBMC) from HIV-infected patients.	Thalidomide	30-41	interleukin 2	Homo sapiens	63-67
10647875-4	2000	We investigated the effect of thalidomide on the production of IL-2 and TNF-alpha by staphylococcal enterotoxin A (SEA) stimulated peripheral blood mononuclear cells (PBMC) from HIV-infected patients.	Thalidomide	30-41	tumor necrosis factor	Homo sapiens	72-81
10647875-7	2000	The PBMC incubated with thalidomide and SEA produced significantly more IL-2 than those incubated with SEA alone.	Thalidomide	24-35	interleukin 2	Homo sapiens	72-76
10732751-2	2000	Thalidomide inhibits the processing of mRNA encoding peptide molecules including tumour necrosis factor-alpha (TNF-alpha) and the angiogenic factor vascular endothelial growth factor (VEGF).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	111-120
10732751-2	2000	Thalidomide inhibits the processing of mRNA encoding peptide molecules including tumour necrosis factor-alpha (TNF-alpha) and the angiogenic factor vascular endothelial growth factor (VEGF).	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	184-188
10647875-9	2000	The amount of IL-2 produced in the thalidomide and SEA treated cultures was directly correlated with the percentage of CD4+ cells in blood, and inversely correlated with the percentage of CD8+ cells in blood.	Thalidomide	35-46	interleukin 2	Homo sapiens	14-18
10647875-9	2000	The amount of IL-2 produced in the thalidomide and SEA treated cultures was directly correlated with the percentage of CD4+ cells in blood, and inversely correlated with the percentage of CD8+ cells in blood.	Thalidomide	35-46	CD4 molecule	Homo sapiens	119-122
10647875-10	2000	No statistically significant correlations were found when comparing the amount of TNF-alpha produced in the thalidomide and SEA treated cultures with the percentage of CD4+ or CD8+ cells in the blood.	Thalidomide	108-119	tumor necrosis factor	Homo sapiens	82-91
10647875-11	2000	Thalidomide can act, in vitro, as an additional stimulant to augment the synthesis of IL-2 in HIV-infected patients.	Thalidomide	0-11	interleukin 2	Homo sapiens	86-90
10635613-13	1999	Thalidomide, another suppressor of TNF production, significantly increased the death rate when tested in a double-blind placebo controlled trial in patients with early TEN.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	35-38
10721827-1	2000	The effect of thalidomide on itch was studied in 11 patients with chronic pruritus from psoriasis, eczema, nodular prurigo, senile pruritus and primary biliary cirrhosis.	Thalidomide	14-25	itchy E3 ubiquitin protein ligase	Homo sapiens	29-33
10721827-2	2000	Itch, assessed subjectively by the patients on a 10 cm line and measured objectively as nocturnal scratch movement, was decreased by thalidomide 200 mg on the 2 nights it was given.	Thalidomide	133-144	itchy E3 ubiquitin protein ligase	Homo sapiens	0-4
11188934-3	2000	Thalidomide has been shown to block the activity of angiogenic substances like bFGF, VEGF and interleukin 6.	Thalidomide	0-11	fibroblast growth factor 2	Homo sapiens	79-83
11188934-3	2000	Thalidomide has been shown to block the activity of angiogenic substances like bFGF, VEGF and interleukin 6.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	85-89
11188934-3	2000	Thalidomide has been shown to block the activity of angiogenic substances like bFGF, VEGF and interleukin 6.	Thalidomide	0-11	interleukin 6	Homo sapiens	94-107
10632777-2	1999	Thalidomide, which inhibits TNF, is an effective drug, but has severe side-effects in pregnant women.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	28-31
10540197-2	1999	Thalidomide, and to a greater extent the new thalidomide analogue CC1069, inhibit monocyte TNF-alpha production both in vitro and in vivo.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	91-100
10540197-2	1999	Thalidomide, and to a greater extent the new thalidomide analogue CC1069, inhibit monocyte TNF-alpha production both in vitro and in vivo.	Thalidomide	45-56	tumor necrosis factor	Rattus norvegicus	91-100
10540197-13	1999	However, the development of rat AA can be blocked by the thalidomide analogue CC1069, which is an efficient inhibitor of TNF-alpha production and IL-2 in vitro.	Thalidomide	57-68	tumor necrosis factor	Rattus norvegicus	121-130
10540197-13	1999	However, the development of rat AA can be blocked by the thalidomide analogue CC1069, which is an efficient inhibitor of TNF-alpha production and IL-2 in vitro.	Thalidomide	57-68	interleukin 2	Rattus norvegicus	146-150
10870669-1	2000	The potential therapeutic utility of thalidomide (Thd), an effective inhibitor of tumor necrosis factor (TNF)-alpha in vitro, was investigated in cynomolgus monkeys (Macaca fascicularis) at 10 months after infection with simian immunodeficiency virus (SIV).	Thalidomide	37-48	tumor necrosis factor	Macaca fascicularis	82-115
10870669-1	2000	The potential therapeutic utility of thalidomide (Thd), an effective inhibitor of tumor necrosis factor (TNF)-alpha in vitro, was investigated in cynomolgus monkeys (Macaca fascicularis) at 10 months after infection with simian immunodeficiency virus (SIV).	Thalidomide	50-53	tumor necrosis factor	Macaca fascicularis	82-115
10606973-0	2000	The thalidomide analogue CC-3052 inhibits HIV-1 and tumour necrosis factor-alpha (TNF-alpha) expression in acutely and chronically infected cells in vitro.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	82-91
10711629-0	2000	Metabolism of thalidomide in human microsomes, cloned human cytochrome P-450 isozymes, and Hansen"s disease patients.	Thalidomide	14-25	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-76
10711629-1	2000	Previous in vitro studies in rat microsomal preparations suggested that thalidomide is metabolized by the cytochrome P450 system (CYP).	Thalidomide	72-83	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	130-133
10711629-2	2000	In this study, we examined the extent of thalidomide metabolism by preparations of pooled human microsomes, microsomes containing cloned human CYP isozymes (CYPIA2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4), and Hansen"s disease patients.	Thalidomide	41-52	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	143-146
10711629-2	2000	In this study, we examined the extent of thalidomide metabolism by preparations of pooled human microsomes, microsomes containing cloned human CYP isozymes (CYPIA2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4), and Hansen"s disease patients.	Thalidomide	41-52	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	157-163
10711629-2	2000	In this study, we examined the extent of thalidomide metabolism by preparations of pooled human microsomes, microsomes containing cloned human CYP isozymes (CYPIA2, CYP2A6, CYP2B6, CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4), and Hansen"s disease patients.	Thalidomide	41-52	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	181-187
10711629-3	2000	Results indicated that thalidomide was a poor substrate for CYP isozymes.	Thalidomide	23-34	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	60-63
10607376-7	2000	Results obtained indicated that thalidomide was predominantly activated by P-450 isozyne CYP2E1, although weak cross-specificity between CYP1A1/A2 may have existed.	Thalidomide	32-43	cytochrome P450 family 2 subfamily E member 1 L homeolog	Xenopus laevis	89-95
10607376-7	2000	Results obtained indicated that thalidomide was predominantly activated by P-450 isozyne CYP2E1, although weak cross-specificity between CYP1A1/A2 may have existed.	Thalidomide	32-43	cytochrome P450 family 1 subfamily A member 1 L homeolog	Xenopus laevis	137-143
10651384-8	1999	Thalidomide may have antiretroviral effects as a result of its primarily inhibitory effects on the production of tumour necrosis factor alpha (TNFalpha).	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	143-151
10651384-9	1999	TNFalpha induces expression of HIV from chronically infected cell lines by stimulating a cellular transcription factor, and blocking of TNFalpha-stimulated HIV replication by thalidomide has been shown in vitro and ex vivo.	Thalidomide	175-186	tumor necrosis factor	Homo sapiens	136-144
10579967-1	1999	BACKGROUND &amp; AIMS: Inhibition of tumor necrosis factor is a proposed mechanism for the anti-inflammatory properties of thalidomide.	Thalidomide	123-134	tumor necrosis factor	Homo sapiens	37-58
10579968-1	1999	BACKGROUND &amp; AIMS: Thalidomide decreases production of tumor necrosis factor alpha, a proinflammatory cytokine associated with Crohn"s disease (CD).	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	59-86
10499831-0	1999	Inhibition of TNF-alpha synthesis with thalidomide for prevention of acute exacerbations and altering the natural history of multiple sclerosis.	Thalidomide	39-50	tumor necrosis factor	Homo sapiens	14-23
10353884-0	1999	Protein kinase C-dependent effects on leukocyte migration of thalidomide.	Thalidomide	61-72	proline rich transmembrane protein 2	Homo sapiens	0-16
10353884-9	1999	In a cell-free assay, inhibition of PKC activation by bisindolylmaleimide could be reversed by thalidomide, indicating direct interactions of thalidomide with PKC.	Thalidomide	95-106	proline rich transmembrane protein 2	Homo sapiens	36-39
10353884-9	1999	In a cell-free assay, inhibition of PKC activation by bisindolylmaleimide could be reversed by thalidomide, indicating direct interactions of thalidomide with PKC.	Thalidomide	95-106	proline rich transmembrane protein 2	Homo sapiens	159-162
10353884-9	1999	In a cell-free assay, inhibition of PKC activation by bisindolylmaleimide could be reversed by thalidomide, indicating direct interactions of thalidomide with PKC.	Thalidomide	142-153	proline rich transmembrane protein 2	Homo sapiens	36-39
10353884-9	1999	In a cell-free assay, inhibition of PKC activation by bisindolylmaleimide could be reversed by thalidomide, indicating direct interactions of thalidomide with PKC.	Thalidomide	142-153	proline rich transmembrane protein 2	Homo sapiens	159-162
10571725-9	1999	Thalidomide did, however, induce a 2-4-fold increase in keratinocyte-derived interleukin-8, a pro-migratory cellular autocrine factor.	Thalidomide	0-11	C-X-C motif chemokine ligand 8	Homo sapiens	77-90
10480630-8	1999	When purified T cells from HIV-infected individuals were stimulated by immobilized anti-CD3 in the presence of thalidomide, a costimulatory effect of the drug was observed, resulting in increased production of IL-2 and IFN-gamma, and increased T cell-proliferative responses.	Thalidomide	111-122	interleukin 2	Homo sapiens	210-214
10480630-8	1999	When purified T cells from HIV-infected individuals were stimulated by immobilized anti-CD3 in the presence of thalidomide, a costimulatory effect of the drug was observed, resulting in increased production of IL-2 and IFN-gamma, and increased T cell-proliferative responses.	Thalidomide	111-122	interferon gamma	Homo sapiens	219-228
10384139-0	1999	Differential cytokine modulation and T cell activation by two distinct classes of thalidomide analogues that are potent inhibitors of TNF-alpha.	Thalidomide	82-93	tumor necrosis factor	Homo sapiens	134-143
10384139-2	1999	Our previous work has shown thalidomide to be a relatively selective inhibitor of TNF-alpha production in vivo and in vitro.	Thalidomide	28-39	tumor necrosis factor	Homo sapiens	82-91
10384139-4	1999	To develop thalidomide analogues with increased anti-TNF-alpha activity and reduced or absent toxicities, novel TNF-alpha inhibitors were designed and synthesized.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	53-62
10384139-4	1999	To develop thalidomide analogues with increased anti-TNF-alpha activity and reduced or absent toxicities, novel TNF-alpha inhibitors were designed and synthesized.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	112-121
10499831-4	1999	There is evidence that thalidomide is an agent which blocks production of TNF-alpha by a mechanism different from other agents.	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	74-83
10424439-1	1999	Both thalidomide and dexamethasone have been shown to inhibit the production of tumour necrosis factor alpha (TNF-alpha), but little is known of their cellular selectivity.	Thalidomide	5-16	tumor necrosis factor	Homo sapiens	110-119
10386948-1	1999	Thalidomide, (1), is a known inhibitor of TNF-alpha release in LPS stimulated human PBMC.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	42-51
10386948-2	1999	Herein we describe the TNF-alpha inhibitory activity of amino substituted analogs of thalidomide (1) and its isoindolin-1-one analog, EM-12 (2).	Thalidomide	85-96	tumor necrosis factor	Homo sapiens	23-32
10437657-0	1999	Inducer-specific bidirectional regulation of endothelial interleukin-8 production by thalidomide.	Thalidomide	85-96	C-X-C motif chemokine ligand 8	Homo sapiens	57-70
10437657-6	1999	Upon stimulation with TNFalpha or LPS, HUVEC produced increased amounts of eIL-8 and THD affected this process in a bidirectional manner, with augmentation of TNFalpha- and inhibition of LPS-effects.	Thalidomide	85-88	tumor necrosis factor	Homo sapiens	22-30
10437657-6	1999	Upon stimulation with TNFalpha or LPS, HUVEC produced increased amounts of eIL-8 and THD affected this process in a bidirectional manner, with augmentation of TNFalpha- and inhibition of LPS-effects.	Thalidomide	85-88	tumor necrosis factor	Homo sapiens	159-167
10424439-2	1999	Inhibition of monocyte TNF-alpha expression has been implicated in the clinical efficacy of thalidomide, and it has been suggested that the drug modulates only monocyte-derived cytokines.	Thalidomide	92-103	tumor necrosis factor	Homo sapiens	23-32
10424439-4	1999	In the present investigations we have examined the influence of both thalidomide and dexamethasone on mitogen-induced elaboration of TNF-alpha by CD3+ peripheral blood mononuclear cells (PBMC) and the T cell line MOLT-4.	Thalidomide	69-80	tumor necrosis factor	Homo sapiens	133-142
10424439-8	1999	Thalidomide was found to inhibit PBMC-derived TNF-alpha, but not IL-2.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	46-55
10424439-10	1999	Thalidomide and dexamethasone both suppressed intracellular levels of TNF-alpha in CD3+ PBMC, reducing percentages of double positive staining cells by 28 and 52%, respectively, compared with controls.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	70-79
10424439-11	1999	In addition, TNF-alpha production by CD3- PBMC was inhibited by 31% by thalidomide and by 47% by dexamethasone.	Thalidomide	71-82	tumor necrosis factor	Homo sapiens	13-22
10424439-13	1999	TNF-alpha secretion by PMA/ionophore activated MOLT-4 cells was reduced by 80% following thalidomide treatment and close to background levels following dexamethasone treatment.	Thalidomide	89-100	tumor necrosis factor	Homo sapiens	0-9
10336480-11	1999	A variety of well characterized angiogenesis inhibitors (including angiostatin, fumagillin, 2-methoxy estradiol, transforming growth factor-beta, and thalidomide) effectively blocked VEGF-induced down-regulation of caveolin-1 as seen by immunoblotting and immunofluorescence microscopy.	Thalidomide	150-161	vascular endothelial growth factor A	Homo sapiens	183-187
10424439-14	1999	To verify that thalidomide was acting selectively to down-regulate TNF-alpha, IL-2 production by MOLT-4 cells was also measured and found to be unaffected by the drug.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	67-76
10336480-11	1999	A variety of well characterized angiogenesis inhibitors (including angiostatin, fumagillin, 2-methoxy estradiol, transforming growth factor-beta, and thalidomide) effectively blocked VEGF-induced down-regulation of caveolin-1 as seen by immunoblotting and immunofluorescence microscopy.	Thalidomide	150-161	caveolin 1	Homo sapiens	215-225
10424439-14	1999	To verify that thalidomide was acting selectively to down-regulate TNF-alpha, IL-2 production by MOLT-4 cells was also measured and found to be unaffected by the drug.	Thalidomide	15-26	interleukin 2	Homo sapiens	78-82
10424439-16	1999	These observations suggest that thalidomide, in addition to its known inhibitory effect on monocyte-derived TNF-alpha, is capable also of down-regulating T cell-derived TNF-alpha in a direct and selective manner.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	108-117
10424439-16	1999	These observations suggest that thalidomide, in addition to its known inhibitory effect on monocyte-derived TNF-alpha, is capable also of down-regulating T cell-derived TNF-alpha in a direct and selective manner.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	169-178
10424439-17	1999	In addition, the inhibition of intracellular levels of TNF-alpha strengthens the evidence that the inhibitory effect of thalidomide is at the level of transcription and/or translation and does not reduce cellular TNF-alpha secretion.	Thalidomide	120-131	tumor necrosis factor	Homo sapiens	55-64
10080541-7	1999	Thalidomide, a drug known to inhibit TNF-alpha synthesis on monocytes, also exerted an inhibitory effect on TNF-alpha secretion in neutrophils.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	37-46
10318940-3	1999	Survival was associated with inhibition of tumor necrosis factor alpha (TNF-alpha) production by thalidomide.	Thalidomide	97-108	tumor necrosis factor	Mus musculus	72-81
10360649-4	1999	Co-administration of thalidomide with DMXAA increased anti-tumour activity and increased intra-tumoural TNF-alpha production approximately tenfold over that obtained with DMXAA alone.	Thalidomide	21-32	tumor necrosis factor	Mus musculus	104-113
10360649-5	1999	Thalidomide increased splenic TNF-alpha production slightly but significantly decreased serum and hepatic levels of TNF-alpha induced with DMXAA.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	30-39
10360649-5	1999	Thalidomide increased splenic TNF-alpha production slightly but significantly decreased serum and hepatic levels of TNF-alpha induced with DMXAA.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	116-125
10360649-7	1999	Splenic TNF-alpha activity induced with LPS was slightly increased with thalidomide, but serum and liver TNF-alpha levels were suppressed.	Thalidomide	72-83	tumor necrosis factor	Mus musculus	8-17
10360649-7	1999	Splenic TNF-alpha activity induced with LPS was slightly increased with thalidomide, but serum and liver TNF-alpha levels were suppressed.	Thalidomide	72-83	toll-like receptor 4	Mus musculus	40-43
10360649-10	1999	The increase in the anti-tumour action by thalidomide in combination with DMXAA corresponded to an increase in intra-tumoural TNF-alpha production.	Thalidomide	42-53	tumor necrosis factor	Mus musculus	126-135
10360649-11	1999	Co-administration of thalidomide may represent a novel approach to improving selective intra-tumoural TNF-alpha production and anti-tumour efficacy of DMXAA.	Thalidomide	21-32	tumor necrosis factor	Mus musculus	102-111
10229222-0	1999	Thalidomide on the comeback trail.	Thalidomide	0-11	TNF superfamily member 10	Homo sapiens	28-33
10080541-7	1999	Thalidomide, a drug known to inhibit TNF-alpha synthesis on monocytes, also exerted an inhibitory effect on TNF-alpha secretion in neutrophils.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	108-117
9780198-1	1998	The immunomodulatory drug thalidomide has been shown to be clinically useful in a number of situations due to its ability to inhibit TNF-alpha synthesis.	Thalidomide	26-37	tumor necrosis factor	Homo sapiens	133-142
10077449-1	1999	Recently, we developed novel tumor necrosis factor (TNF)-alpha production regulators with a phthalimide skeleton derived from thalidomide.	Thalidomide	126-137	tumor necrosis factor	Mus musculus	29-62
10357564-0	1999	Thalidomide up-regulates prostate-specific antigen secretion from LNCaP cells.	Thalidomide	0-11	kallikrein related peptidase 3	Homo sapiens	25-50
10357564-9	1999	Thalidomide-treated LNCaP cells demonstrated increased PSA/cell levels at all concentrations tested compared to untreated control cells.	Thalidomide	0-11	kallikrein related peptidase 3	Homo sapiens	55-58
10357564-11	1999	Comparison of cDNA expression arrays hybridized with thalidomide-treated LNCaP cDNA probes suggests that thalidomide may up- or downregulate expression of angiogenesis-related genes, i.e., vitronectin, but these differential effects require further verification.	Thalidomide	105-116	vitronectin	Homo sapiens	189-200
10357564-12	1999	Thalidomide over a range of doses has demonstrated nontoxic, cytostatic activity in LNCaP cells and significant upregulation of LNCaP cell PSA secretion in vitro.	Thalidomide	0-11	kallikrein related peptidase 3	Homo sapiens	139-142
10357564-13	1999	Furthermore, preliminary data from cDNA nucleic acid arrays of thalidomide-treated LNCaP cells suggest that thalidomide upregulates a potential angiogenic modulatory protein, the vitronectin precursor, which may eventually link thalidomide"s antiangiogenic activity with modulation of angiogenic vascular integrin pathways.	Thalidomide	63-74	vitronectin	Homo sapiens	179-190
10357564-13	1999	Furthermore, preliminary data from cDNA nucleic acid arrays of thalidomide-treated LNCaP cells suggest that thalidomide upregulates a potential angiogenic modulatory protein, the vitronectin precursor, which may eventually link thalidomide"s antiangiogenic activity with modulation of angiogenic vascular integrin pathways.	Thalidomide	108-119	vitronectin	Homo sapiens	179-190
10357564-13	1999	Furthermore, preliminary data from cDNA nucleic acid arrays of thalidomide-treated LNCaP cells suggest that thalidomide upregulates a potential angiogenic modulatory protein, the vitronectin precursor, which may eventually link thalidomide"s antiangiogenic activity with modulation of angiogenic vascular integrin pathways.	Thalidomide	108-119	vitronectin	Homo sapiens	179-190
9894629-8	1999	Thalidomide was shown to be effective for treating oral and genital ulcers and follicular lesions in Behcet"s syndrome; severe refractory Behcet"s syndrome uveitis responded to treatment with IFN-alpha.	Thalidomide	0-11	interferon alpha 1	Homo sapiens	192-201
9859910-7	1998	Meanwhile, thalidomide has been shown to possess a range of biologic actions, including inhibition of tumor necrosis factor alpha, possibly relevant to its clinical efficacy.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	102-129
10408702-7	1999	When we combined sulindac with thalidomide, we found a significantly increased inhibition of bFGF- or VEGF-induced corneal neovascularization (by 63% or 74% respectively) compared with either agent alone (P &lt; 0.01).	Thalidomide	31-42	vascular endothelial growth factor A	Oryctolagus cuniculus	102-106
15991946-3	1998	Meanwhile, immunomodulatory and anti-inflammatory activities of thalidomide, particularly its inhibition of tumour necrosis factor alpha (TNF-alpha), have been identified and elucidated.	Thalidomide	64-75	tumor necrosis factor	Homo sapiens	138-147
9877451-3	1998	TNF-alpha production in IL-1beta-stimulated or PMA-stimulated hepatocyte cultures was not altered following the addition of dihydrocortisone (&lt; or = 1 microg/ml), dibutyryl-cAMP (db-cAMP, &lt; or = 100 micromol/l), adenosine (&lt; or = 1 mmol/l), thalidomide (&lt; or = 25 microg/ml), or cyclosporine (&lt; or = 300 ng/ml).	Thalidomide	250-261	tumor necrosis factor	Homo sapiens	0-9
9843104-3	1998	Thalidomide is a potent inhibitor of TNF-alpha action.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	37-46
9843104-11	1998	Plasma TNF-alpha concentration was higher in the thalidomide group than the placebo group on day 2, though the difference was not significant (Wilcoxon rank-sum test p=0.07).	Thalidomide	49-60	tumor necrosis factor	Homo sapiens	7-16
9843104-12	1998	INTERPRETATION: Even though few patients were included, our data suggest that thalidomide is detrimental in TEN, possibly because of a paradoxical enhancement of TNF-alpha production.	Thalidomide	78-89	tumor necrosis factor	Homo sapiens	162-171
9891501-3	1998	Unexpectedly, the drug thalidomide, while reducing the serum TNF response to DMXAA, potentiates its antitumour effect.	Thalidomide	23-34	tumor necrosis factor	Mus musculus	61-64
10022026-7	1998	Thalidomide altered expression of bcl-2 (p &lt; 0.011) and tissue PSA (p &lt; 0.002).	Thalidomide	0-11	BCL2, apoptosis regulator	Rattus norvegicus	34-39
10022026-7	1998	Thalidomide altered expression of bcl-2 (p &lt; 0.011) and tissue PSA (p &lt; 0.002).	Thalidomide	0-11	aminopeptidase puromycin sensitive	Rattus norvegicus	66-69
9873600-1	1998	N-Phthaloyl 3-amino-3-arylpropionic acid analogs of thalidomide that are potent inhibitors of tumor necrosis factor-alpha are reported.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	94-121
9780198-3	1998	Recently, structural modifications of thalidomide have been designed enabling greatly enhanced anti-TNF-alpha activity in LPS-treated mice.	Thalidomide	38-49	tumor necrosis factor	Mus musculus	100-109
9692223-3	1998	The data indicates that the TNF-alpha production enhancing activity of thalidomide derivatives depends on both the electronic-state of substituents at the fused benzene ring and the stereochemistry of the glutarimide moiety.	Thalidomide	71-82	tumor necrosis factor	Homo sapiens	28-37
9790310-5	1998	This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon-gamma (IFN-gamma) mRNA-expressing cells among lymph node mononuclear cells from thalidomide-treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN.	Thalidomide	222-233	interferon gamma	Rattus norvegicus	131-147
9790310-5	1998	This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon-gamma (IFN-gamma) mRNA-expressing cells among lymph node mononuclear cells from thalidomide-treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN.	Thalidomide	222-233	interferon gamma	Rattus norvegicus	149-158
9703279-2	1998	Our previous studies have shown that thalidomide, a potent inhibitor of TNF biosynthesis that has numerous biological effects, including inhibition of tumour angiogenesis, unexpectedly augments the anti-tumour response in mice to DMXAA.	Thalidomide	37-48	tumor necrosis factor	Mus musculus	72-75
18465584-0	1998	Thalidomide Celgene Corp. Thalidomide, in development by Celgene, inhibits the effects of elevated TNFalpha and may consequently be of use in a range of diseases including cachexia, bacterial meningitis, rheumatoid arthritis, septic shock, AIDS, tuberculosis, multiple sclerosis, ulcerative colitis, graft-versus-host disease and systemic lupus erythematosus.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	99-107
18465584-0	1998	Thalidomide Celgene Corp. Thalidomide, in development by Celgene, inhibits the effects of elevated TNFalpha and may consequently be of use in a range of diseases including cachexia, bacterial meningitis, rheumatoid arthritis, septic shock, AIDS, tuberculosis, multiple sclerosis, ulcerative colitis, graft-versus-host disease and systemic lupus erythematosus.	Thalidomide	26-37	tumor necrosis factor	Homo sapiens	99-107
18465584-0	1998	Thalidomide Celgene Corp. Thalidomide, in development by Celgene, inhibits the effects of elevated TNFalpha and may consequently be of use in a range of diseases including cachexia, bacterial meningitis, rheumatoid arthritis, septic shock, AIDS, tuberculosis, multiple sclerosis, ulcerative colitis, graft-versus-host disease and systemic lupus erythematosus.	Thalidomide	12-19	tumor necrosis factor	Homo sapiens	99-107
9646092-0	1998	Thalidomide inhibits corneal angiogenesis induced by vascular endothelial growth factor.	Thalidomide	0-11	vascular endothelial growth factor A	Oryctolagus cuniculus	53-87
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	25-36	tumor necrosis factor	Homo sapiens	40-49
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	25-36	tumor necrosis factor	Homo sapiens	137-146
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	25-36	tumor necrosis factor	Homo sapiens	137-146
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	173-184	tumor necrosis factor	Homo sapiens	40-49
9776474-6	1998	Analysis of supernatants by enzyme-linked immunosorbent assay (ELISA) showed that thalidomide caused a dose-dependent inhibition of the pro-inflammatory cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha), maximally reducing production by 20 (P &lt; 0.05) and 30% (P &lt; 0.01), respectively, compared with controls.	Thalidomide	82-93	interleukin 6	Homo sapiens	163-176
9776474-6	1998	Analysis of supernatants by enzyme-linked immunosorbent assay (ELISA) showed that thalidomide caused a dose-dependent inhibition of the pro-inflammatory cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha), maximally reducing production by 20 (P &lt; 0.05) and 30% (P &lt; 0.01), respectively, compared with controls.	Thalidomide	82-93	interleukin 6	Homo sapiens	178-182
9776474-6	1998	Analysis of supernatants by enzyme-linked immunosorbent assay (ELISA) showed that thalidomide caused a dose-dependent inhibition of the pro-inflammatory cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha), maximally reducing production by 20 (P &lt; 0.05) and 30% (P &lt; 0.01), respectively, compared with controls.	Thalidomide	82-93	tumor necrosis factor	Homo sapiens	218-227
9776474-10	1998	Reverse transcription-polymerase chain reaction (RT-PCR) analyses showed that thalidomide inhibited selectively the expression of TNF-alpha and IL-6 mRNA, whereas dexamethasone inhibited mRNA levels of all cytokines examined.	Thalidomide	78-89	tumor necrosis factor	Homo sapiens	130-139
9776474-10	1998	Reverse transcription-polymerase chain reaction (RT-PCR) analyses showed that thalidomide inhibited selectively the expression of TNF-alpha and IL-6 mRNA, whereas dexamethasone inhibited mRNA levels of all cytokines examined.	Thalidomide	78-89	interleukin 6	Homo sapiens	144-148
9776474-12	1998	Conversely, thalidomide selectively inhibits the production of IL-6 and TNF-alpha.	Thalidomide	12-23	interleukin 6	Homo sapiens	63-67
9776474-12	1998	Conversely, thalidomide selectively inhibits the production of IL-6 and TNF-alpha.	Thalidomide	12-23	tumor necrosis factor	Homo sapiens	72-81
9657054-0	1998	Thalidomide promotes the release of tumor necrosis factor-alpha (TNF-alpha) and lethality by lipopolysaccharide in mice.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	36-63
9657054-0	1998	Thalidomide promotes the release of tumor necrosis factor-alpha (TNF-alpha) and lethality by lipopolysaccharide in mice.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	65-74
9657054-1	1998	We investigated the in vivo effects of thalidomide on the production of tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	39-50	tumor necrosis factor	Mus musculus	72-99
9657054-1	1998	We investigated the in vivo effects of thalidomide on the production of tumor necrosis factor-alpha (TNF-alpha).	Thalidomide	39-50	tumor necrosis factor	Mus musculus	101-110
9657054-3	1998	When thalidomide (1, 3, or 6 mg/kg) was administered intraperitoneally 3 h before the injection of LPS (0.3 mg/kg, i. p.), thalidomide markedly enhanced LPS-induced TNF-alpha release in a dose-dependent manner.	Thalidomide	5-16	tumor necrosis factor	Mus musculus	165-174
9657054-3	1998	When thalidomide (1, 3, or 6 mg/kg) was administered intraperitoneally 3 h before the injection of LPS (0.3 mg/kg, i. p.), thalidomide markedly enhanced LPS-induced TNF-alpha release in a dose-dependent manner.	Thalidomide	123-134	tumor necrosis factor	Mus musculus	165-174
9657054-6	1998	We conclude that thalidomide enhances in vivo TNF-alpha secretion and the lethality of LPS in mice.	Thalidomide	17-28	tumor necrosis factor	Mus musculus	46-55
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	173-184	tumor necrosis factor	Homo sapiens	137-146
9562600-5	1998	The regulatory effect of thalidomide on TNF-alpha production has been found to be bidirectional, depending on both the cell-type and the TNF-alpha production-inducer; i.e., thalidomide possesses both enhancing and inhibiting activities on TNF-alpha production.	Thalidomide	173-184	tumor necrosis factor	Homo sapiens	137-146
9562600-6	1998	Structural modification of thalidomide aiming at the creation of superior TNF-alpha production-regulators has afforded a number of phenyl- and benzylphthalimide analogs possessing more potent activity than thalidomide itself.	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	74-83
9562600-6	1998	Structural modification of thalidomide aiming at the creation of superior TNF-alpha production-regulators has afforded a number of phenyl- and benzylphthalimide analogs possessing more potent activity than thalidomide itself.	Thalidomide	206-217	tumor necrosis factor	Homo sapiens	74-83
9646092-5	1998	We therefore investigated the effect of thalidomide on corneal angiogenesis induced by vascular endothelial growth factor (VEGF), which has a special role among angiogenic growth factors.	Thalidomide	40-51	vascular endothelial growth factor A	Oryctolagus cuniculus	87-121
9646092-5	1998	We therefore investigated the effect of thalidomide on corneal angiogenesis induced by vascular endothelial growth factor (VEGF), which has a special role among angiogenic growth factors.	Thalidomide	40-51	vascular endothelial growth factor A	Oryctolagus cuniculus	123-127
9646092-10	1998	CONCLUSIONS: Thalidomide has a significant antiangiogenic effect against VEGF-induced neovasclar growth.	Thalidomide	13-24	vascular endothelial growth factor A	Oryctolagus cuniculus	73-77
9690766-4	1998	Evidence is presented here suggesting that the embryonic action of thalidomide was mediated by TNF-alpha, since the drug is a powerful inhibitor of the synthesis of this cytokine.	Thalidomide	67-78	tumor necrosis factor	Homo sapiens	95-104
9607928-0	1998	Thalidomide costimulates primary human T lymphocytes, preferentially inducing proliferation, cytokine production, and cytotoxic responses in the CD8+ subset.	Thalidomide	0-11	CD8a molecule	Homo sapiens	145-148
9607928-1	1998	The efficacy of thalidomide (alpha-phthalimido-glutarimide) therapy in leprosy patients with erythema nodosum leprosum is thought to be due to inhibition of tumor necrosis factor alpha.	Thalidomide	16-27	tumor necrosis factor	Homo sapiens	157-184
9607928-1	1998	The efficacy of thalidomide (alpha-phthalimido-glutarimide) therapy in leprosy patients with erythema nodosum leprosum is thought to be due to inhibition of tumor necrosis factor alpha.	Thalidomide	29-58	tumor necrosis factor	Homo sapiens	157-184
9607928-3	1998	We show that thalidomide is a potent costimulator of primary human T cells in vitro, synergizing with stimulation via the T cell receptor complex to increase interleukin 2-mediated T cell proliferation and interferon gamma production.	Thalidomide	13-24	interleukin 2	Homo sapiens	158-171
9516386-11	1998	Specific inhibition of TNF-alpha using neutralizing antibody or alpha-N-phthalimidoglutarimide (thalidomide) resulted in reversal of the hypoxia-evoked responses.	Thalidomide	64-94	tumor necrosis factor	Homo sapiens	23-32
9516386-11	1998	Specific inhibition of TNF-alpha using neutralizing antibody or alpha-N-phthalimidoglutarimide (thalidomide) resulted in reversal of the hypoxia-evoked responses.	Thalidomide	96-107	tumor necrosis factor	Homo sapiens	23-32
9607834-6	1998	When thalidomide treatment was combined with antibiotics, there was a marked reduction in TNF-alpha levels, leukocytosis, and brain pathology.	Thalidomide	5-16	tumor necrosis factor	Oryctolagus cuniculus	90-99
9623511-5	1998	TNF levels were slightly decreased after 1 month of thalidomide treatment and significantly decreased after 2 months of treatment.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	0-3
9623511-6	1998	Serum IFN-gamma was significantly lower in patients at the onset of ENL and was increased after 1 and 2 months of thalidomide treatment.	Thalidomide	114-125	interferon gamma	Homo sapiens	6-15
9598899-1	1998	OBJECTIVE: Thalidomide has been described as an inhibitor of both angiogenesis (which may account for its teratogenic effects on limb bud formation) and tumor necrosis factor-alpha (TNF-alpha) production.	Thalidomide	11-22	tumor necrosis factor	Rattus norvegicus	153-180
9598899-1	1998	OBJECTIVE: Thalidomide has been described as an inhibitor of both angiogenesis (which may account for its teratogenic effects on limb bud formation) and tumor necrosis factor-alpha (TNF-alpha) production.	Thalidomide	11-22	tumor necrosis factor	Rattus norvegicus	182-191
9493761-17	1998	Examples of human teratogens that are substrates for CYP enzymes include thalidomide, phenytoin, ethanol, and several hormonal agents.	Thalidomide	73-84	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-56
9507696-0	1998	5"-Substituted thalidomide analogs as modulators of TNF-alpha.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	52-61
9625384-2	1998	Pentoxyfylline and thalidomide are inhibitors of TNF-alpha that have been tried as rational therapeutic interventions in cachexia.	Thalidomide	19-30	tumor necrosis factor	Homo sapiens	49-58
9502617-2	1998	In addition, thalidomide has been shown to be an inhibitor of angiogenesis induced by basic fibroblast growth factor (bFGF).	Thalidomide	13-24	fibroblast growth factor 2	Cavia porcellus	86-116
9502617-2	1998	In addition, thalidomide has been shown to be an inhibitor of angiogenesis induced by basic fibroblast growth factor (bFGF).	Thalidomide	13-24	fibroblast growth factor 2	Cavia porcellus	118-122
9486396-12	1998	The amount of TNF-alpha mRNA was increased in the tissue during ENL compared with before the reaction, and decreased thereafter following treatment for reaction (either PTX or thalidomide).	Thalidomide	176-187	tumor necrosis factor	Homo sapiens	14-23
9430254-6	1997	However, a nonsignificant trend toward inhibition of mitogen-induced TNF-alpha production was observed in the thalidomide arm.	Thalidomide	110-121	tumor necrosis factor	Homo sapiens	69-78
9430254-7	1997	The lack of systemic effect and the lower tolerance of thalidomide (at this dose) in asymptomatic patients highlights the need for pharmacokinetic analysis to address possible absorption problems and the need for more potent and less toxic TNF-alpha inhibitors to be developed for use in this type of study.	Thalidomide	55-66	tumor necrosis factor	Homo sapiens	240-249
9402031-4	1997	In the present study, we investigated in vitro the effects of thalidomide (THD) on activation of endothelial cells for enhanced transmigration of neutrophils by lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF), and interleukin-1 (IL-1).	Thalidomide	75-78	tumor necrosis factor	Homo sapiens	187-214
9367395-0	1997	Thalidomide and derivatives: immunological investigations of tumour necrosis factor-alpha (TNF-alpha) inhibition suggest drugs capable of selective gene regulation.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	91-100
9402031-6	1997	Treatment of HUVEC with THD in combination with LPS, TNF, and IL-1, respectively, antagonized LPS-activated transmigration of neutrophils but stimulated the effects of TNF and IL-1.	Thalidomide	24-27	tumor necrosis factor	Homo sapiens	53-56
9402031-6	1997	Treatment of HUVEC with THD in combination with LPS, TNF, and IL-1, respectively, antagonized LPS-activated transmigration of neutrophils but stimulated the effects of TNF and IL-1.	Thalidomide	24-27	tumor necrosis factor	Homo sapiens	168-171
9402031-6	1997	Treatment of HUVEC with THD in combination with LPS, TNF, and IL-1, respectively, antagonized LPS-activated transmigration of neutrophils but stimulated the effects of TNF and IL-1.	Thalidomide	24-27	interleukin 1 alpha	Homo sapiens	176-180
9496438-10	1997	The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 micrograms to 300 micrograms in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death.	Thalidomide	47-58	toll-like receptor 4	Mus musculus	12-15
9496438-10	1997	The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 micrograms to 300 micrograms in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death.	Thalidomide	160-171	toll-like receptor 4	Mus musculus	12-15
9496438-1	1997	Thalidomide has been shown to selectively inhibit TNF-alpha production in vitro by lipopolysaccharide (LPS)-stimulated monocytes.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	50-59
9496438-10	1997	The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 micrograms to 300 micrograms in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death.	Thalidomide	160-171	toll-like receptor 4	Mus musculus	155-158
9496438-1	1997	Thalidomide has been shown to selectively inhibit TNF-alpha production in vitro by lipopolysaccharide (LPS)-stimulated monocytes.	Thalidomide	0-11	toll-like receptor 4	Mus musculus	103-106
9496438-3	1997	Using a mouse model of LPS-induced shock, we investigated the effects of thalidomide on the production of TNF-alpha and other cytokines and on animal survival.	Thalidomide	73-84	tumor necrosis factor	Mus musculus	106-115
9294124-8	1997	Consistent with these findings, thalidomide (which antagonizes TNF action) attenuates c-src induction by LPS.	Thalidomide	32-43	tumor necrosis factor	Mus musculus	63-66
9496438-5	1997	Administration of 200 mg/kg thalidomide to mice before LPS challenge modified the profile of LPS-induced cytokine secretion.	Thalidomide	28-39	toll-like receptor 4	Mus musculus	55-58
9496438-5	1997	Administration of 200 mg/kg thalidomide to mice before LPS challenge modified the profile of LPS-induced cytokine secretion.	Thalidomide	28-39	toll-like receptor 4	Mus musculus	93-96
9496438-8	1997	Thalidomide induced a two-fold increase in serum IL-10 levels.	Thalidomide	0-11	interleukin 10	Mus musculus	49-54
9197379-3	1997	The thalidomide analogs were previously shown to inhibit TNF-alpha production in vitro at much lower concentrations than thalidomide.	Thalidomide	4-15	tumor necrosis factor	Homo sapiens	57-66
15989668-0	1997	TNF-alpha antagonists: monoclonal antibodies, soluble receptors, thalidomide and other novel approaches.	Thalidomide	65-76	tumor necrosis factor	Homo sapiens	0-9
9248860-6	1997	However, neutrophils obtained from HIV-infected patients treated with thalidomide showed reduced expression of CD16, a surrogate marker for apoptosis of neutrophils.	Thalidomide	70-81	Fc gamma receptor IIIa	Homo sapiens	111-115
9278924-2	1997	Studies in marmosets and humans indicate that thalidomide, and a teratogenic analogue, decrease the expression of beta integrin subunits, most notably beta 3 and the beta 2 produced by leukocytes.	Thalidomide	46-57	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	166-172
9278924-3	1997	Since integrins are crucial for cell-matrix interactions, and the beta 2 integrins of leukocytes mediate adhesion to endothelium, it is reasonable to postulate that thalidomide inhibits cell migration in susceptible species, and that this accounts for its anti-inflammatory, anti-angiogenic, and teratogenic activity.	Thalidomide	165-176	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	66-72
9301478-1	1997	Thalidomide, when administered orally, is an inhibitor of angiogenesis in the basic fibroblast growth factor (bFGF)-induced rabbit cornea micropocket assay.	Thalidomide	0-11	fibroblast growth factor 2	Mus musculus	110-114
9301478-2	1997	We now show in the mouse that thalidomide given intraperitoneally but not orally significantly inhibits bFGF-induced and vascular endothelial growth factor (VEGF)-induced corneal neovascularization.	Thalidomide	30-41	fibroblast growth factor 2	Mus musculus	104-108
9301478-2	1997	We now show in the mouse that thalidomide given intraperitoneally but not orally significantly inhibits bFGF-induced and vascular endothelial growth factor (VEGF)-induced corneal neovascularization.	Thalidomide	30-41	vascular endothelial growth factor A	Mus musculus	121-155
9301478-2	1997	We now show in the mouse that thalidomide given intraperitoneally but not orally significantly inhibits bFGF-induced and vascular endothelial growth factor (VEGF)-induced corneal neovascularization.	Thalidomide	30-41	vascular endothelial growth factor A	Mus musculus	157-161
9301478-3	1997	We further demonstrate that this inhibition is independent from thalidomide"s ability to suppress tumor necrosis factor-alpha (TNF-alpha) production.	Thalidomide	64-75	tumor necrosis factor	Mus musculus	98-125
9301478-3	1997	We further demonstrate that this inhibition is independent from thalidomide"s ability to suppress tumor necrosis factor-alpha (TNF-alpha) production.	Thalidomide	64-75	tumor necrosis factor	Mus musculus	127-136
9301478-4	1997	Experiments examining thalidomide"s enantiomers reveal-that the S(-)-enantiomer has the strongest antiangiogenic activity in VEGF-induced and bFGF-induced corneal neovascularization.	Thalidomide	22-33	vascular endothelial growth factor A	Mus musculus	125-129
9301478-4	1997	Experiments examining thalidomide"s enantiomers reveal-that the S(-)-enantiomer has the strongest antiangiogenic activity in VEGF-induced and bFGF-induced corneal neovascularization.	Thalidomide	22-33	fibroblast growth factor 2	Mus musculus	142-146
9142912-10	1997	Inhibition of TNF-alpha synthesis/release with pentoxifylline, thalidomide, dexamethasone, or immunoneutralization of TNF-alpha (with anti-TNF-alpha) was found to significantly reduce the severity of ethanol-induced gastric mucosal damage in cirrhotic rats.	Thalidomide	63-74	tumor necrosis factor	Rattus norvegicus	14-23
9456687-8	1997	Thalidomide, which inhibits TNF alpha production, is effective treatment for RAU.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	28-37
9154767-12	1997	With thalidomide treatment there were unexpected increases in the plasma concentrations of TNF-alpha and soluble TNF-alpha receptors.	Thalidomide	5-16	tumor necrosis factor	Homo sapiens	91-100
9154767-12	1997	With thalidomide treatment there were unexpected increases in the plasma concentrations of TNF-alpha and soluble TNF-alpha receptors.	Thalidomide	5-16	tumor necrosis factor	Homo sapiens	113-122
9439767-1	1997	Thalidomide (Thd) has been shown to have interesting immunosuppressive properties and strong action against TNF-alpha.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	108-117
9439767-1	1997	Thalidomide (Thd) has been shown to have interesting immunosuppressive properties and strong action against TNF-alpha.	Thalidomide	13-16	tumor necrosis factor	Homo sapiens	108-117
9439767-4	1997	At different concentrations, both Thd and H-Thd alone inhibited the lymphocyte proliferation induced by alloantigen (MLR), mitogens (Con A, PWM) and superantigen (SEB) with an activity of 50-75% that of CsA, however, in some tests, immunosuppressive potency of H-Thd was shown to be higher than that of Thd.	Thalidomide	34-37	SET binding protein 1	Homo sapiens	163-166
9439767-4	1997	At different concentrations, both Thd and H-Thd alone inhibited the lymphocyte proliferation induced by alloantigen (MLR), mitogens (Con A, PWM) and superantigen (SEB) with an activity of 50-75% that of CsA, however, in some tests, immunosuppressive potency of H-Thd was shown to be higher than that of Thd.	Thalidomide	44-47	SET binding protein 1	Homo sapiens	163-166
9099468-3	1997	The effect of dexamethasone was most pronounced on PHA-induced T-cell proliferation and IFN-gamma secretion, whereas the effect of thalidomide was most pronounced on BPM-induced T-cell proliferation and IFN-gamma secretion.	Thalidomide	131-142	interferon gamma	Rattus norvegicus	203-212
9666962-8	1997	Thalidomide treatment resulted in a significant reduction in tumor necrosis factor-alpha, interleukin 6 (IL-6) and IL-10 protein levels (blood) and mRNA expression (lungs).	Thalidomide	0-11	tumor necrosis factor	Mus musculus	61-88
9129992-0	1997	Hydrolysis of thalidomide abrogates its ability to enhance mononuclear cell synthesis of IL-2 as well as its ability to suppress the synthesis of TNF-alpha.	Thalidomide	14-25	interleukin 2	Homo sapiens	89-93
9129992-0	1997	Hydrolysis of thalidomide abrogates its ability to enhance mononuclear cell synthesis of IL-2 as well as its ability to suppress the synthesis of TNF-alpha.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	146-155
9129992-4	1997	Unhydrolyzed thalidomide at 4.0 micrograms/ml consistently enhanced the synthesis of IL-2 in SEA-stimulated cells, and suppressed the synthesis of TNF-alpha in LPS-stimulated cells; whereas, hydrolyzed thalidomide had no enhancing effect on SEA stimulated-cell synthesis of IL-2 or suppressive effect on LPS stimulated-cell synthesis of TNF-alpha.	Thalidomide	13-24	interleukin 2	Homo sapiens	85-89
9129992-4	1997	Unhydrolyzed thalidomide at 4.0 micrograms/ml consistently enhanced the synthesis of IL-2 in SEA-stimulated cells, and suppressed the synthesis of TNF-alpha in LPS-stimulated cells; whereas, hydrolyzed thalidomide had no enhancing effect on SEA stimulated-cell synthesis of IL-2 or suppressive effect on LPS stimulated-cell synthesis of TNF-alpha.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	147-156
9129992-4	1997	Unhydrolyzed thalidomide at 4.0 micrograms/ml consistently enhanced the synthesis of IL-2 in SEA-stimulated cells, and suppressed the synthesis of TNF-alpha in LPS-stimulated cells; whereas, hydrolyzed thalidomide had no enhancing effect on SEA stimulated-cell synthesis of IL-2 or suppressive effect on LPS stimulated-cell synthesis of TNF-alpha.	Thalidomide	13-24	interleukin 2	Homo sapiens	274-278
9129992-4	1997	Unhydrolyzed thalidomide at 4.0 micrograms/ml consistently enhanced the synthesis of IL-2 in SEA-stimulated cells, and suppressed the synthesis of TNF-alpha in LPS-stimulated cells; whereas, hydrolyzed thalidomide had no enhancing effect on SEA stimulated-cell synthesis of IL-2 or suppressive effect on LPS stimulated-cell synthesis of TNF-alpha.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	337-346
9129992-5	1997	These findings demonstrate that thalidomide"s ability in vitro to enhance IL-2 and to suppress TNF-alpha in stimulated cells is dependent on the intact molecule and underscore the necessity to employ thalidomide under appropriate physicochemical conditions.	Thalidomide	32-43	interleukin 2	Homo sapiens	74-78
9129992-5	1997	These findings demonstrate that thalidomide"s ability in vitro to enhance IL-2 and to suppress TNF-alpha in stimulated cells is dependent on the intact molecule and underscore the necessity to employ thalidomide under appropriate physicochemical conditions.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	95-104
9084226-6	1997	Thalidomide is a specific inhibitor of TNF-alpha production, and this effect has been shown to be useful for the treatment of various immunodiseases.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	39-48
9084226-8	1997	We also found that in a optically active phthalimide analogues of thalidomide the inducer specific bi-directional regulation of TNF-alpha production is separated.	Thalidomide	66-77	tumor necrosis factor	Homo sapiens	128-137
9068814-3	1997	This study evaluated the effect of thalidomide on lipopolysaccharide (LPS)-induced TNF-alpha production by human alveolar macrophages obtained from patients with tuberculosis and a group of other diseases associated with macrophage activation.	Thalidomide	35-46	tumor necrosis factor	Homo sapiens	83-92
9068814-6	1997	Similarly, TNF-alpha mRNA as measured by in situ hybridization was increased following incubation with LPS (P &lt; 0.05), but this increase was prevented by addition of thalidomide (P &lt; 0.05) or dexamethasone (P &lt; 0.05).	Thalidomide	169-180	tumor necrosis factor	Homo sapiens	11-20
9068814-7	1997	The ability of thalidomide to reduce LPS-induced TNF-alpha production by alveolar macrophages was the same when cells from patients with tuberculosis (a disease associated with TNF-alpha production) and cells from patients with the other conditions were compared.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	49-58
9068814-7	1997	The ability of thalidomide to reduce LPS-induced TNF-alpha production by alveolar macrophages was the same when cells from patients with tuberculosis (a disease associated with TNF-alpha production) and cells from patients with the other conditions were compared.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	177-186
9068814-8	1997	The ability of thalidomide to reduce TNF-alpha production by human alveolar macrophages from patients with active lung disease suggests that thalidomide and its analogues may have potential as drugs to reduce TNF-alpha production in disease.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	37-46
9068814-8	1997	The ability of thalidomide to reduce TNF-alpha production by human alveolar macrophages from patients with active lung disease suggests that thalidomide and its analogues may have potential as drugs to reduce TNF-alpha production in disease.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	209-218
9068814-8	1997	The ability of thalidomide to reduce TNF-alpha production by human alveolar macrophages from patients with active lung disease suggests that thalidomide and its analogues may have potential as drugs to reduce TNF-alpha production in disease.	Thalidomide	141-152	tumor necrosis factor	Homo sapiens	37-46
9068814-8	1997	The ability of thalidomide to reduce TNF-alpha production by human alveolar macrophages from patients with active lung disease suggests that thalidomide and its analogues may have potential as drugs to reduce TNF-alpha production in disease.	Thalidomide	141-152	tumor necrosis factor	Homo sapiens	209-218
9666962-8	1997	Thalidomide treatment resulted in a significant reduction in tumor necrosis factor-alpha, interleukin 6 (IL-6) and IL-10 protein levels (blood) and mRNA expression (lungs).	Thalidomide	0-11	interleukin 6	Mus musculus	90-103
9666962-8	1997	Thalidomide treatment resulted in a significant reduction in tumor necrosis factor-alpha, interleukin 6 (IL-6) and IL-10 protein levels (blood) and mRNA expression (lungs).	Thalidomide	0-11	interleukin 6	Mus musculus	105-109
9666962-8	1997	Thalidomide treatment resulted in a significant reduction in tumor necrosis factor-alpha, interleukin 6 (IL-6) and IL-10 protein levels (blood) and mRNA expression (lungs).	Thalidomide	0-11	interleukin 10	Mus musculus	115-120
8806653-0	1996	Cell type-/inducer-specific bidirectional regulation by thalidomide and phenylphthalimides of tumor necrosis factor-alpha production and its enantio-dependence.	Thalidomide	56-67	tumor necrosis factor	Homo sapiens	94-121
8931784-1	1996	OBJECTIVE: To evaluate the efficacy of thalidomide in treating wasting syndrome in patients with advanced HIV disease, and to assess the effects of thalidomide on circulating CD4+ T cells, and on HIV viral burden in peripheral blood mononuclear cells (PBMC).	Thalidomide	148-159	CD4 molecule	Homo sapiens	175-178
8976641-2	1996	Since pentoxifylline and thalidomide inhibit endotoxin induced TNF production in vitro, these drugs were tested in an open study in rheumatoid arthritis patients to assess toxicity, the effect on TNF production, and the antiarthritic effects.	Thalidomide	25-36	tumor necrosis factor	Homo sapiens	63-66
8976641-8	1996	CONCLUSIONS: Although pentoxifylline/thalidomide reduced the production capacity of TNF, the benefit/side effects ratio was poor due to multiple adverse effects, while clinical observation suggests limited efficacy.	Thalidomide	37-48	tumor necrosis factor	Homo sapiens	84-87
8755512-0	1996	Binding of thalidomide to alpha1-acid glycoprotein may be involved in its inhibition of tumor necrosis factor alpha production.	Thalidomide	11-22	tumor necrosis factor	Homo sapiens	88-115
8862260-12	1996	Thalidomide reduces the frequency of IFN-gamma-induced ENL, but also eliminates the IFN-gamma-induced bacillary clearance.	Thalidomide	0-11	interferon gamma	Homo sapiens	37-46
8862260-12	1996	Thalidomide reduces the frequency of IFN-gamma-induced ENL, but also eliminates the IFN-gamma-induced bacillary clearance.	Thalidomide	0-11	interferon gamma	Homo sapiens	84-93
8755512-2	1996	The immunomodulatory activity of thalidomide has been ascribed to the selective inhibition of tumor necrosis factor alpha from monocytes.	Thalidomide	33-44	tumor necrosis factor	Homo sapiens	94-121
8755512-7	1996	We show that the binding of thalidomide photoaffinity label to authentic human AGP is competed with both thalidomide and the nonradioactive photoaffinity label at concentrations comparable to those required for inhibition of production of tumor necrosis factor alpha from human monocytes, suggesting that AGP may be involved in the immunomodulatory activity of thalidomide.	Thalidomide	28-39	tumor necrosis factor	Homo sapiens	239-266
8675185-11	1996	Thalidomide inhibits TNF synthesis and reduces NO production, blunts the development of the hyperdynamic circulation, and decreases portal pressure in PVL-operated rats.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	21-24
8827720-0	1996	Selection of novel analogs of thalidomide with enhanced tumor necrosis factor alpha inhibitory activity.	Thalidomide	30-41	tumor necrosis factor	Homo sapiens	56-83
8827720-2	1996	Recently, thalidomide (alpha-N-phthalimidoglutarimide) was shown to partially inhibit monocyte TNF alpha production (by 50-70%) both in vivo and in vitro.	Thalidomide	10-21	tumor necrosis factor	Homo sapiens	95-104
8827720-2	1996	Recently, thalidomide (alpha-N-phthalimidoglutarimide) was shown to partially inhibit monocyte TNF alpha production (by 50-70%) both in vivo and in vitro.	Thalidomide	23-53	tumor necrosis factor	Homo sapiens	95-104
8827720-4	1996	MATERIALS AND METHODS: Three structural analogues of thalidomide were selected for study based on increased activity against TNF alpha production.	Thalidomide	53-64	tumor necrosis factor	Homo sapiens	125-134
8827720-7	1996	RESULTS: The new compounds (two esters and one amide) showed increased inhibition of TNF alpha production by LPS-stimulated human monocytes, relative to the parent drug thalidomide.	Thalidomide	169-180	tumor necrosis factor	Homo sapiens	85-94
8827720-10	1996	CONCLUSIONS: Analogs of thalidomide designed to better inhibit TNF alpha production in vitro have correspondingly greater efficacy in vivo.	Thalidomide	24-35	tumor necrosis factor	Homo sapiens	63-72
8675185-0	1996	Thalidomide inhibits tumor necrosis factor alpha, decreases nitric oxide synthesis, and ameliorates the hyperdynamic circulatory syndrome in portal-hypertensive rats.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	21-48
8675185-3	1996	Thalidomide selectively inhibits TNF production by enhancing messenger RNA degradation.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	33-36
8702405-0	1996	Inducer-specific bidirectional regulation by thalidomide and phenylphthalimides of tumor necrosis factor-alpha production.	Thalidomide	45-56	tumor necrosis factor	Homo sapiens	83-110
8702405-1	1996	Regulation by thalidomide [N(alpha)-phthalimidoglutarimide] of tumor necrosis factor (TNF)-alpha production was found to be inducer-specific.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	63-96
8702405-2	1996	Thalidomide enhances TNF-alpha production by human leukemia HL-60 cells induced with 12-O-tetradecanoylphorbol 13-acetate (TPA), while it inhibits TNF-alpha production induced with okadaic acid (OA) in the same cell line.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	21-30
8702405-2	1996	Thalidomide enhances TNF-alpha production by human leukemia HL-60 cells induced with 12-O-tetradecanoylphorbol 13-acetate (TPA), while it inhibits TNF-alpha production induced with okadaic acid (OA) in the same cell line.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	147-156
8843588-6	1996	Stimulated lymphocytes secreted significantly more IL-2 in the presence of microsomal-treated thalidomide than did controls.	Thalidomide	94-105	interleukin 2	Rattus norvegicus	51-55
8661187-0	1996	Thalidomide inhibits TNF response and increases survival following endotoxin injection in rats.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	21-24
8661187-4	1996	Thalidomide, shown in vitro to selectively inhibit TNF production, has been used clinically in states of chronic TNF elevation with encouraging results.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	51-54
8661187-4	1996	Thalidomide, shown in vitro to selectively inhibit TNF production, has been used clinically in states of chronic TNF elevation with encouraging results.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	113-116
8661187-12	1996	Thalidomide treated rats had lower TNF levels at all time points (P = &lt;0.01 at 90 and 120 min), with the inhibition being dose dependent.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	35-38
8661187-14	1996	In conclusion, we found that thalidomide administration leads to increased survival following acute endotoxemia, which may be due to the observed TNF inhibition.	Thalidomide	29-40	tumor necrosis factor	Rattus norvegicus	146-149
8843588-13	1996	In untransplanted rats given thalidomide a decrease of CD4 positive T cells was detected on days 3 and 5.	Thalidomide	29-40	Cd4 molecule	Rattus norvegicus	55-58
8627072-4	1996	MGC formation was blocked by anti-CD14 and anti-CD18 antibodies and by thalidomide, a potent inhibitor of tumor necrosis factor-alpha (TNF-alpha) production my microglia.	Thalidomide	71-82	tumor necrosis factor	Sus scrofa	135-144
8627072-4	1996	MGC formation was blocked by anti-CD14 and anti-CD18 antibodies and by thalidomide, a potent inhibitor of tumor necrosis factor-alpha (TNF-alpha) production my microglia.	Thalidomide	71-82	tumor necrosis factor	Sus scrofa	106-133
8603261-2	1996	Thalidomide inhibits the synthesis of TNF-alpha both in vitro and in vivo and may have clinical usefulness.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	38-47
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	tumor necrosis factor	Homo sapiens	42-69
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	tumor necrosis factor	Homo sapiens	71-79
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	intercellular adhesion molecule 1	Homo sapiens	89-95
8728022-1	1996	The present study investigates synergistic effects of the TNF-alpha inhibitor thalidomide and the poly(ADP-ribose) polymerase (PARP)-inhibitor nicotinic acid amide (NAA) in male DBA/1 hybird mice suffering from type II collagen-induced arthritis.	Thalidomide	78-89	tumor necrosis factor	Mus musculus	58-67
8603261-6	1996	In patients with concomitant HIV-1 and tuberculosis infections, thalidomide therapy was associated with a reduction in both plasma TNF-alpha levels and HIV-1 levels.	Thalidomide	64-75	tumor necrosis factor	Homo sapiens	131-140
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	intercellular adhesion molecule 1	Homo sapiens	97-101
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	vascular cell adhesion molecule 1	Homo sapiens	104-110
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	vascular cell adhesion molecule 1	Homo sapiens	112-117
8603261-10	1996	The results of this pilot study suggest that thalidomide may have a clinical role in enhancing weight gain and possibly reducing TNF-alpha and HIV-1 levels in patients with HIV-1 and concomitant mycobacterial infections.	Thalidomide	45-56	tumor necrosis factor	Homo sapiens	129-138
8861747-3	1996	THD is capable of changing the density of tumor necrosis factor alpha (TNFalpha) induced ICAM-1 (CD54), VCAM-1 (CD106) and E-selectin antigens on HUVEC.	Thalidomide	0-3	selectin E	Homo sapiens	123-133
8683039-2	1996	In cultures of LPS stimulated human mononuclear cells enriched for adherent cells and in cultures of LPS stimulated human monocytes of the cell line-THP-1, thalidomide enhanced the synthesis of TNF-alpha.	Thalidomide	156-167	tumor necrosis factor	Homo sapiens	194-203
8861747-4	1996	Furthermore, modulation of L-selectin (CD62L) by THD can be demonstrated on human leukocytes in vitro.	Thalidomide	49-52	selectin L	Homo sapiens	27-37
8861747-4	1996	Furthermore, modulation of L-selectin (CD62L) by THD can be demonstrated on human leukocytes in vitro.	Thalidomide	49-52	selectin L	Homo sapiens	39-44
8683039-3	1996	When cultures of unfractionated peripheral blood mononuclear cells were stimulated with LPS, thalidomide decreased the synthesis of TNF-alpha.	Thalidomide	93-104	tumor necrosis factor	Homo sapiens	132-141
8683039-0	1996	Thalidomide can be either agonistic or antagonistic to LPS evoked synthesis of TNF-alpha by mononuclear cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	79-88
8683039-1	1996	The effect if thalidomide on tumor necrosis factor alpha (TNF-alpha) produced in vitro by lipopolysaccharide (LPS) stimulated human cells was investigated.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	29-56
8683039-4	1996	Depending on the type of cells stimulated with LPS in vitro, thalidomide, at concentrations achieved in vivo, can either enhance or suppress the synthesis of TNF-alpha.	Thalidomide	61-72	tumor necrosis factor	Homo sapiens	158-167
8683039-1	1996	The effect if thalidomide on tumor necrosis factor alpha (TNF-alpha) produced in vitro by lipopolysaccharide (LPS) stimulated human cells was investigated.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	58-67
8538367-3	1996	Treatment with low doses (20 or as little as 1 mg/kg body weight) of a highly teratogenic derivative (EM12) of thalidomide, the most notorious human teratogen, triggers a dramatic and statistically highly significant down-regulation of several surface adhesion receptors (e.g. CD11a/CD18, CD49d/CD29, CD61, etc.)	Thalidomide	111-122	integrin subunit beta 1	Felis catus	295-299
8900028-0	1996	Enantioselective inhibition of TNF-alpha release by thalidomide and thalidomide-analogues.	Thalidomide	52-63	tumor necrosis factor	Homo sapiens	31-40
8900028-0	1996	Enantioselective inhibition of TNF-alpha release by thalidomide and thalidomide-analogues.	Thalidomide	68-79	tumor necrosis factor	Homo sapiens	31-40
8900028-2	1996	The effect of the pure enantiomers of the thalidomide-analogues and also of the enantiomers of thalidomide on release of TNF-alpha was tested in vitro by using stimulated peripheral mononuclear blood cells.	Thalidomide	95-106	tumor necrosis factor	Homo sapiens	121-130
8900028-3	1996	Both enantiomers of thalidomide inhibited the release of TNF-alpha equally well at low concentrations (5 and 12.5 micrograms/ml) but at higher concentrations (25 and 50 micrograms 50 micrograms/ml) there was a weak but statistically significant selectivity towards the (-)-(S)-enantiomer.	Thalidomide	20-31	tumor necrosis factor	Homo sapiens	57-66
8900028-5	1996	The (S)-enantiomers of the thalidomide-analogues differed in their inhibitory potency from (-)-(S)-thalidomide suggesting that the introduction of the methyl-group increases the TNF-alpha-inhibitory activity while the reduction of one of the carbonyl-functions in the glutarimide-moiety to a methylene-group decreases activity.	Thalidomide	27-38	tumor necrosis factor	Homo sapiens	178-187
8900028-5	1996	The (S)-enantiomers of the thalidomide-analogues differed in their inhibitory potency from (-)-(S)-thalidomide suggesting that the introduction of the methyl-group increases the TNF-alpha-inhibitory activity while the reduction of one of the carbonyl-functions in the glutarimide-moiety to a methylene-group decreases activity.	Thalidomide	91-110	tumor necrosis factor	Homo sapiens	178-187
7590113-4	1995	A 2.1-fold increase of GOT and a 1.9-fold increase of GPT activities (P &lt; 0.001) were observed in mice treated perorally with 500 mg/kg of AAP plus 150 mg/kg of thalidomide (Thal).	Thalidomide	164-175	glutamic pyruvic transaminase, soluble	Mus musculus	54-57
8745000-6	1995	ICAM-1 expression was markedly reduced after (+)-thalidomide injection.	Thalidomide	45-60	intercellular adhesion molecule 1	Mus musculus	0-6
8745000-7	1995	Thalidomide and dexamethasone pretreatment reduced Mac-1 expression on perivascular infiltrated granulocytes.	Thalidomide	0-11	integrin alpha M	Mus musculus	51-56
8655287-0	1995	Thalidomide increases the synthesis of IL-2 in cultures of human mononuclear cells stimulated with Concanavalin-A, Staphylococcal enterotoxin A, and purified protein derivative.	Thalidomide	0-11	interleukin 2	Homo sapiens	39-43
8655287-1	1995	Thalidomide significantly increases the quantity of extracellular IL-2 in cultures of human mononuclear cells stimulated with mitogens or antigen.	Thalidomide	0-11	interleukin 2	Homo sapiens	66-70
8655287-2	1995	Cells from 7 donors exposed for 2 h to 4.0 micrograms/ml of thalidomide and stimulated for 16-18 h with 20 micrograms/ml of Concanavalin-A (Con-A) averaged producing 187 +/- 49% more IL-2 than cells stimulated with Con-A alone.	Thalidomide	60-71	interleukin 2	Homo sapiens	183-187
8655287-3	1995	In similar experimental procedures and comparisons the pg/ml of IL-2 secreted by thalidomide-treated cells from five donors stimulated with 50 ng/ml of Staphylococcal enterotoxin A (SEA) increased by 159 +/- 32%, and the pg/ml of IL-2 secreted by thalidomide-treated cells from 2 donors stimulated with 5.0 micrograms/ml of purified protein derivative of Mycobacterium tuberculosis increased by 120 +/- 4%.	Thalidomide	81-92	interleukin 2	Homo sapiens	64-68
8655287-3	1995	In similar experimental procedures and comparisons the pg/ml of IL-2 secreted by thalidomide-treated cells from five donors stimulated with 50 ng/ml of Staphylococcal enterotoxin A (SEA) increased by 159 +/- 32%, and the pg/ml of IL-2 secreted by thalidomide-treated cells from 2 donors stimulated with 5.0 micrograms/ml of purified protein derivative of Mycobacterium tuberculosis increased by 120 +/- 4%.	Thalidomide	81-92	interleukin 2	Homo sapiens	230-234
8655287-3	1995	In similar experimental procedures and comparisons the pg/ml of IL-2 secreted by thalidomide-treated cells from five donors stimulated with 50 ng/ml of Staphylococcal enterotoxin A (SEA) increased by 159 +/- 32%, and the pg/ml of IL-2 secreted by thalidomide-treated cells from 2 donors stimulated with 5.0 micrograms/ml of purified protein derivative of Mycobacterium tuberculosis increased by 120 +/- 4%.	Thalidomide	247-258	interleukin 2	Homo sapiens	64-68
8655287-4	1995	Thalidomide also significantly increases the quantity of intracellular IL-2 in cells stimulated with mitogens.	Thalidomide	0-11	interleukin 2	Homo sapiens	71-75
8655287-5	1995	Cells exposed to thalidomide and stimulated with Con-A had an increase in intracellular IL-2 of 130% after 8 h and 157% after 12 h in culture; cells stimulated with SEA had an increase in intracellular IL-2 of 120% after 8 h and 182% after 12 h in culture.	Thalidomide	17-28	interleukin 2	Homo sapiens	88-92
8655287-5	1995	Cells exposed to thalidomide and stimulated with Con-A had an increase in intracellular IL-2 of 130% after 8 h and 157% after 12 h in culture; cells stimulated with SEA had an increase in intracellular IL-2 of 120% after 8 h and 182% after 12 h in culture.	Thalidomide	17-28	interleukin 2	Homo sapiens	202-206
8634679-3	1995	In the present study, we investigated the effect of thalidomide (alpha-N-pthalimidoglutarimide), a selective inhibitor of TNF-alpha synthesis, on granuloma formation during BCG infection in Oncins France 1 (OF-1) mice.	Thalidomide	52-63	tumor necrosis factor	Mus musculus	122-131
8634679-6	1995	Serum TNF-alpha levels of thalidomide-treated mice were significantly lower (85%) than control mice on day 14 and remained lower (55%) on days 21 and 28.	Thalidomide	26-37	tumor necrosis factor	Mus musculus	6-15
8634679-8	1995	Daily administration of thalidomide for 21 to 28 days to the BCG-infected mice inhibited local TNF-alpha expression in well-developed granulomas.	Thalidomide	24-35	tumor necrosis factor	Mus musculus	95-104
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	Thalidomide	4-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	127-154
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	Thalidomide	4-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	156-160
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	Thalidomide	214-218	poly (ADP-ribose) polymerase family, member 1	Mus musculus	127-154
7590113-7	1995	The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P &lt; 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation.	Thalidomide	214-218	poly (ADP-ribose) polymerase family, member 1	Mus musculus	156-160
8825912-2	1995	Since thalidomide has been shown to inhibit TNF-alpha production, experiments were carried out to determine whether the drug can modulate the inflammatory response to either lysates of H. influenzae (gram negative) or heat killed S. pneumoniae (gram positive) in rabbits.	Thalidomide	6-17	tumor necrosis factor	Oryctolagus cuniculus	44-53
7561198-0	1995	Thalidomide inhibits tumor necrosis factor-alpha production by lipopolysaccharide- and lipoarabinomannan-stimulated human microglial cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	21-48
7561198-2	1995	The effect of thalidomide on TNF-alpha production by microglia, the resident macrophages of the brain, was evaluated.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	29-38
7561198-3	1995	In primary human fetal microglial cell cultures stimulated with lipopolysaccharide or lipoarabinomannan, thalidomide inhibited TNF-alpha release in a dose-dependent manner.	Thalidomide	105-116	tumor necrosis factor	Homo sapiens	127-136
7561198-4	1995	The inhibitory effect of thalidomide was similar to that of dexamethasone, although expression of TNF-alpha mRNA in microglial cells was reduced only by thalidomide.	Thalidomide	153-164	tumor necrosis factor	Homo sapiens	98-107
8825912-5	1995	Thalidomide treatment reduces TNF-alpha production in both experimental systems, but has a greater effect on the more indolent gram positive inflammatory response in which peak TNF-alpha levels in the CSF are reduced by &gt; 50%.	Thalidomide	0-11	tumor necrosis factor	Oryctolagus cuniculus	30-39
8825912-5	1995	Thalidomide treatment reduces TNF-alpha production in both experimental systems, but has a greater effect on the more indolent gram positive inflammatory response in which peak TNF-alpha levels in the CSF are reduced by &gt; 50%.	Thalidomide	0-11	tumor necrosis factor	Oryctolagus cuniculus	177-186
8825912-7	1995	In meningeal inflammation induced by the Gram negative lysate, treatment with thalidomide results in only a 29% inhibition of TNF-alpha release into the CSF.	Thalidomide	78-89	tumor necrosis factor	Oryctolagus cuniculus	126-135
8845811-0	1995	Benzylphthalimides and phenethylphthalimides with thalidomide-like activity on the production of tumor necrosis factor alpha.	Thalidomide	50-61	tumor necrosis factor	Homo sapiens	97-124
8845811-1	1995	Benzylphthalimide analogs (P1P"s) and phenethylphthalimide analogs (P2P"s) have been found to exhibit thalidomide-like activity on the production of tumor necrosis factor (TNF)-alpha by the human leukemia cell line, HL-60, stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA).	Thalidomide	102-113	tumor necrosis factor	Homo sapiens	149-182
7558825-7	1995	Because thalidomide has been shown to inhibit TNF-alpha production, down-modulation of this cytokine seems to be a useful treatment strategy in Langerhans" cell granulomatosis.	Thalidomide	8-19	tumor necrosis factor	Homo sapiens	46-55
7635184-0	1995	Does thalidomide affect IL-2 response and production?	Thalidomide	5-16	interleukin 2	Homo sapiens	24-28
7635184-2	1995	A common denominator in the pathogenesis of graft-vs.-host disease, graft rejection, reactional lepromatous leprosy, and autoimmune disorders modulated by thalidomide is the activation of T lymphocytes culminating in the synthesis of interleukin-2 (IL-2), the expression of high-affinity IL-2 receptors, and the induction of proliferation.	Thalidomide	155-166	interleukin 2	Homo sapiens	234-247
7635184-2	1995	A common denominator in the pathogenesis of graft-vs.-host disease, graft rejection, reactional lepromatous leprosy, and autoimmune disorders modulated by thalidomide is the activation of T lymphocytes culminating in the synthesis of interleukin-2 (IL-2), the expression of high-affinity IL-2 receptors, and the induction of proliferation.	Thalidomide	155-166	interleukin 2	Homo sapiens	249-253
7635184-2	1995	A common denominator in the pathogenesis of graft-vs.-host disease, graft rejection, reactional lepromatous leprosy, and autoimmune disorders modulated by thalidomide is the activation of T lymphocytes culminating in the synthesis of interleukin-2 (IL-2), the expression of high-affinity IL-2 receptors, and the induction of proliferation.	Thalidomide	155-166	interleukin 2	Homo sapiens	288-292
7635184-3	1995	We investigated the effect of thalidomide on the production of IL-2 by the human leukemia cell line Jurkat through induction of IL-2 gene enhancer activity and through the presence of IL-2 in supernatants.	Thalidomide	30-41	interleukin 2	Homo sapiens	63-67
7635184-4	1995	beta-galactosidase activity, encoded by a reporter lac z construct and controlled by a transcription factor in thalidomide-treated PMA- and ionomycin-stimulated Jurkat cells, was similar (97 +/- 1.33%; p &gt; 0.1) to non-thalidomide-treated controls at all drug concentrations tested.	Thalidomide	111-122	galactosidase beta 1	Homo sapiens	0-18
7635184-5	1995	IL-2 enhancer-driven beta-galactose activity of thalidomide-treated and stimulated cells was also similar to that of untreated controls (p &gt; 0.2).	Thalidomide	48-59	interleukin 2	Homo sapiens	0-4
7640215-0	1995	Effect of thalidomide on tumour necrosis factor production and anti-tumour activity induced by 5,6-dimethylxanthenone-4-acetic acid.	Thalidomide	10-21	tumor necrosis factor	Mus musculus	25-47
7640215-4	1995	Thalidomide at doses of between 8 and 250 mg kg-1 efficiently suppressed serum TNF activity in response to 5,6-MeXAA at its optimal TNF inducing dose of 55 mg kg-1.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	79-82
7640215-4	1995	Thalidomide at doses of between 8 and 250 mg kg-1 efficiently suppressed serum TNF activity in response to 5,6-MeXAA at its optimal TNF inducing dose of 55 mg kg-1.	Thalidomide	0-11	tumor necrosis factor	Mus musculus	132-135
8527011-3	1995	Recent research has shown a decrease in tumour necrosis factor-alpha (TNF alpha) during thalidomide treatment in several settings.	Thalidomide	88-99	tumor necrosis factor	Homo sapiens	70-79
7593465-4	1995	Inhibitors of TNF synthesis, pentoxifylline (PTX) and thalidomide, inhibited TNF mRNA accumulation in LPS-activated monocytes and down-regulated DR mRNA but not DP or DQ mRNA.	Thalidomide	54-65	tumor necrosis factor	Homo sapiens	77-80
7742424-9	1995	The mechanism of the effect of thalidomide is uncertain, although recent studies have suggested that thalidomide selectively inhibits the production of tumor necrosis factor alpha.	Thalidomide	101-112	tumor necrosis factor	Homo sapiens	152-179
8521296-0	1995	Thalidomide treatment reduces tumor necrosis factor alpha production and enhances weight gain in patients with pulmonary tuberculosis.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	30-57
8521296-3	1995	Thalidomide (alpha-N-phthalimidoglutarimide) has recently been shown to suppress TNF alpha production by human monocytes in vitro and to reduce serum TNF alpha in leprosy patients.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	81-90
8521296-3	1995	Thalidomide (alpha-N-phthalimidoglutarimide) has recently been shown to suppress TNF alpha production by human monocytes in vitro and to reduce serum TNF alpha in leprosy patients.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	150-159
8521296-3	1995	Thalidomide (alpha-N-phthalimidoglutarimide) has recently been shown to suppress TNF alpha production by human monocytes in vitro and to reduce serum TNF alpha in leprosy patients.	Thalidomide	13-43	tumor necrosis factor	Homo sapiens	81-90
8521296-3	1995	Thalidomide (alpha-N-phthalimidoglutarimide) has recently been shown to suppress TNF alpha production by human monocytes in vitro and to reduce serum TNF alpha in leprosy patients.	Thalidomide	13-43	tumor necrosis factor	Homo sapiens	150-159
8521296-4	1995	We have therefore conducted a two-part placebo-controlled pilot study of thalidomide in patients with active tuberculosis to determine its effects on clinical response, immune reactivity, TNF alpha levels, and weight.	Thalidomide	73-84	tumor necrosis factor	Homo sapiens	188-197
8521296-9	1995	TNF alpha production was significantly reduced during thalidomide treatment while interferon-gamma (IFN gamma) production was enhanced.	Thalidomide	54-65	tumor necrosis factor	Homo sapiens	0-9
8521296-12	1995	Thalidomide treatment reduces TNF alpha production both in vivo and in vitro and is associated with an accelerated weight gain during the study period.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	30-39
7851006-0	1995	The immunosuppressive drug thalidomide induces T helper cell type 2 (Th2) and concomitantly inhibits Th1 cytokine production in mitogen- and antigen-stimulated human peripheral blood mononuclear cell cultures.	Thalidomide	27-38	negative elongation factor complex member C/D	Homo sapiens	101-104
7851006-3	1995	In a comparative study with the immunosuppressant cyclosporin A, we have demonstrated a potent and specific effect of thalidomide on cytokine production relating to the distinct Th1 and Th2 subsets.	Thalidomide	118-129	negative elongation factor complex member C/D	Homo sapiens	178-181
7851006-6	1995	Thalidomide switched this response from a Th1 to a Th2 type.	Thalidomide	0-11	negative elongation factor complex member C/D	Homo sapiens	42-45
7851006-7	1995	The effect was most pronounced at 1000 ng/ml thalidomide, where inhibition of IFN-gamma and enhancement of IL-4 production was maximal.	Thalidomide	45-56	interferon gamma	Homo sapiens	78-87
7851006-7	1995	The effect was most pronounced at 1000 ng/ml thalidomide, where inhibition of IFN-gamma and enhancement of IL-4 production was maximal.	Thalidomide	45-56	interleukin 4	Homo sapiens	107-111
7844376-2	1995	Pentoxifylline, chlorpromazine, and thalidomide inhibit TNF-alpha production.	Thalidomide	36-47	tumor necrosis factor	Mus musculus	56-65
7851006-8	1995	In unstimulated cultures thalidomide alone induced IL-4 production.	Thalidomide	25-36	interleukin 4	Homo sapiens	51-55
7851006-10	1995	Time course data from thalidomide-treated cultures revealed that the augmented IL-4 production diminished as the culture time increased, whereas IFN-gamma production was significantly increased.	Thalidomide	22-33	interleukin 4	Homo sapiens	79-83
7851006-10	1995	Time course data from thalidomide-treated cultures revealed that the augmented IL-4 production diminished as the culture time increased, whereas IFN-gamma production was significantly increased.	Thalidomide	22-33	interferon gamma	Homo sapiens	145-154
7895307-3	1995	Among the investigated compounds, including thalidomide and methylthalidomide, N-adamantylphthalimide showed the most potent TNF-alpha production-enhancing activity.	Thalidomide	44-55	tumor necrosis factor	Homo sapiens	125-134
7851006-12	1995	The effects of thalidomide and related compounds may enhance our understanding of the mechanisms of T helper cell selection, offer the possibility of controlled therapeutic switching between Th1 and Th2 responses, and may lead to a rational approach for the treatment of some T cell-mediated immunological disorders.	Thalidomide	15-26	negative elongation factor complex member C/D	Homo sapiens	191-194
22514378-4	1995	Thalidomide, a drug used to treat reactional states in Hansen"s disease, has been reported to enhance degradation of tnf-alpha mrna.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	117-126
7830502-3	1995	Thalidomide (Thd) is capable of down-regulating the CD26 receptor on CD4+ lymphocytes after treatment of healthy volunteers.	Thalidomide	0-11	dipeptidyl peptidase 4	Homo sapiens	52-56
7830502-3	1995	Thalidomide (Thd) is capable of down-regulating the CD26 receptor on CD4+ lymphocytes after treatment of healthy volunteers.	Thalidomide	0-11	CD4 molecule	Homo sapiens	69-72
7830502-3	1995	Thalidomide (Thd) is capable of down-regulating the CD26 receptor on CD4+ lymphocytes after treatment of healthy volunteers.	Thalidomide	13-16	dipeptidyl peptidase 4	Homo sapiens	52-56
7830502-3	1995	Thalidomide (Thd) is capable of down-regulating the CD26 receptor on CD4+ lymphocytes after treatment of healthy volunteers.	Thalidomide	13-16	CD4 molecule	Homo sapiens	69-72
7516993-7	1994	After the first two doses of 7 mg Thd/kg body wt the CD18 (the common beta-chain of the beta 2-integrins) marker already decreased in surface density or was no longer detectable on granulocytes, monocytes and lymphocytes.	Thalidomide	34-37	integrin subunit beta 2	Homo sapiens	53-57
7713571-6	1994	Both the toxic symptoms and the high levels of TNF-alpha production could be inhibited by thalidomide treatment, a drug we have shown reduces the half life of TNF-alpha mRNA.	Thalidomide	90-101	tumor necrosis factor	Homo sapiens	47-56
7713571-6	1994	Both the toxic symptoms and the high levels of TNF-alpha production could be inhibited by thalidomide treatment, a drug we have shown reduces the half life of TNF-alpha mRNA.	Thalidomide	90-101	tumor necrosis factor	Homo sapiens	159-168
7713571-7	1994	In preliminary clinical trials in tuberculosis patients we have attempted to use thalidomide to reduce TNF-alpha production and toxicities.	Thalidomide	81-92	tumor necrosis factor	Homo sapiens	103-112
8069968-1	1994	The rate of racemization of N(alpha)-phthalimidoglutarimide (thalidomide) was determined as its half life to be 566 min at pH 7.4/37 degrees C. This fast racemization of thalidomide resulted in no apparent difference between (S)- and (R)-forms of the compound on enhancing activity of phorbol ester-induced tumor necrosis factor (TNF)-alpha production by human leukemia HL-60 cells.	Thalidomide	61-72	tumor necrosis factor	Homo sapiens	307-340
8069968-1	1994	The rate of racemization of N(alpha)-phthalimidoglutarimide (thalidomide) was determined as its half life to be 566 min at pH 7.4/37 degrees C. This fast racemization of thalidomide resulted in no apparent difference between (S)- and (R)-forms of the compound on enhancing activity of phorbol ester-induced tumor necrosis factor (TNF)-alpha production by human leukemia HL-60 cells.	Thalidomide	170-181	tumor necrosis factor	Homo sapiens	307-340
8069968-3	1994	Only (S)-form of methylthalidomide, but not its (R)-form, elicited TNF-alpha production-enhancing effect, suggesting that the (S)-isomer of thalidomide would be the active form in terms of thalidomidal biological response modifying effects.	Thalidomide	23-34	tumor necrosis factor	Homo sapiens	67-76
8090535-3	1994	Thalidomide reduces polyclonal hypergammaglobulinemia, that is associated with a clinical and laboratorial improvement, in a dose dependent manner as well as TNF-alpha levels.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	158-167
8135786-0	1994	Enhancement of phorbol ester-induced production of tumor necrosis factor alpha by thalidomide.	Thalidomide	82-93	tumor necrosis factor	Homo sapiens	51-78
8135786-1	1994	The effect of thalidomide [racemic (DL-) form and optically pure (D- and L-) forms] on tumor necrosis factor (TNF) alpha production by human leukemia cell lines (HL-60, K562 and U937) stimulated with 12-O-tetradecanoylphorbol-13-acetate (TPA) was investigated.	Thalidomide	14-25	tumor necrosis factor	Homo sapiens	87-120
8135786-2	1994	Though thalidomide has been regarded as a specific inhibitor of TNF-alpha production, our study indicated that all forms of thalidomide enhanced (but did not inhibit) the TPA-induced TNF-alpha production by the human leukemia cell lines investigated.	Thalidomide	124-135	tumor necrosis factor	Homo sapiens	183-192
8135786-3	1994	The effects of thalidomide on TNF-alpha production might be cell type-specific.	Thalidomide	15-26	tumor necrosis factor	Homo sapiens	30-39
7516993-7	1994	After the first two doses of 7 mg Thd/kg body wt the CD18 (the common beta-chain of the beta 2-integrins) marker already decreased in surface density or was no longer detectable on granulocytes, monocytes and lymphocytes.	Thalidomide	34-37	tubulin beta 4B class IVb	Homo sapiens	88-94
7516993-12	1994	Other markers, such as the alpha chains of the beta 1 integrins CD49b (VLA alpha 2) and CD49d (VLA alpha 4) showed contrasting reactions to the Thd-treatment.	Thalidomide	144-147	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	47-53
7516993-12	1994	Other markers, such as the alpha chains of the beta 1 integrins CD49b (VLA alpha 2) and CD49d (VLA alpha 4) showed contrasting reactions to the Thd-treatment.	Thalidomide	144-147	integrin subunit alpha 2	Homo sapiens	64-69
7516993-12	1994	Other markers, such as the alpha chains of the beta 1 integrins CD49b (VLA alpha 2) and CD49d (VLA alpha 4) showed contrasting reactions to the Thd-treatment.	Thalidomide	144-147	integrin subunit alpha 4	Homo sapiens	88-93
8327469-1	1993	Thalidomide, a selective inhibitor of tumor necrosis factor alpha (TNF-alpha) synthesis, suppresses the activation of latent human immunodeficiency virus type 1 (HIV-1) in a monocytoid (U1) line.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	67-76
8335978-3	1993	Patients with systemic ENL demonstrated the highest serum TNF alpha levels, which decreased significantly during thalidomide treatment.	Thalidomide	113-124	tumor necrosis factor	Homo sapiens	58-67
8335978-6	1993	Thalidomide therapy reduced not only serum TNF alpha levels and the clinical symptoms but also the dermal infiltration of polymorphonuclear leukocytes and T cells.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	43-52
8335978-8	1993	These results indicate that the thalidomide-induced alleviation of clinical symptoms of ENL was associated with a reduction of TNF alpha levels.	Thalidomide	32-43	tumor necrosis factor	Homo sapiens	127-136
8177242-0	1993	Inhibition of tumor necrosis factor-alpha by thalidomide in magnesium deficiency.	Thalidomide	45-56	tumor necrosis factor	Rattus norvegicus	14-41
8177242-3	1993	Thalidomide (1 mg/day) caused a complete inhibition of the increase in circulating tumor necrosis factor-alpha levels, without having an effect on interleukin 1.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	83-110
8327469-4	1993	Thalidomide inhibition of virus replication in the phorbol myristate acetate- and recombinant TNF-alpha-stimulated T-cell line ACH-2 is not observed.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	94-103
8327469-4	1993	Thalidomide inhibition of virus replication in the phorbol myristate acetate- and recombinant TNF-alpha-stimulated T-cell line ACH-2 is not observed.	Thalidomide	0-11	acyl-CoA thioesterase 1	Homo sapiens	127-132
8327469-6	1993	These results suggest the use of thalidomide in a clinical setting to inhibit both virus replication and the TNF-alpha-induced systemic toxicity of HIV-1 and opportunistic infections.	Thalidomide	33-44	tumor necrosis factor	Homo sapiens	109-118
8452474-11	1993	(c) The most significant effect, reduction in the reactivity of CD2+, was detectable subsequent to daily oral doses as low as 10 mg Thd/kg or 1 mg EM12/kg bw.	Thalidomide	132-135	T-cell surface antigen CD2	Callithrix jacchus	64-67
8496685-0	1993	Thalidomide exerts its inhibitory action on tumor necrosis factor alpha by enhancing mRNA degradation.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	44-71
8496685-1	1993	We have examined the mechanism of thalidomide inhibition of lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production and found that the drug enhances the degradation of TNF-alpha mRNA.	Thalidomide	34-45	tumor necrosis factor	Homo sapiens	93-120
8496685-1	1993	We have examined the mechanism of thalidomide inhibition of lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production and found that the drug enhances the degradation of TNF-alpha mRNA.	Thalidomide	34-45	tumor necrosis factor	Homo sapiens	122-131
8496685-1	1993	We have examined the mechanism of thalidomide inhibition of lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) production and found that the drug enhances the degradation of TNF-alpha mRNA.	Thalidomide	34-45	tumor necrosis factor	Homo sapiens	196-205
8496685-6	1993	The selective inhibition of TNF-alpha production makes thalidomide an ideal candidate for the treatment of inflammatory conditions where TNF-alpha-induced toxicities are observed and where immunity must remain intact.	Thalidomide	55-66	tumor necrosis factor	Homo sapiens	28-37
8496685-6	1993	The selective inhibition of TNF-alpha production makes thalidomide an ideal candidate for the treatment of inflammatory conditions where TNF-alpha-induced toxicities are observed and where immunity must remain intact.	Thalidomide	55-66	tumor necrosis factor	Homo sapiens	137-146
8433015-8	1993	Cytokine treatment induced large amounts of tumor necrosis factor-alpha, which is toxic in this context but can be selectively down-regulated by thalidomide without interfering with other monocyte cytokines necessary for normal immune function.	Thalidomide	145-156	tumor necrosis factor	Homo sapiens	44-71
8452474-16	1993	(f) A rough estimate of the relative potency to reduce the CD2 receptor in the marmoset suggests EM12 to be five to ten times more potent than Thd.	Thalidomide	143-146	T-cell surface antigen CD2	Callithrix jacchus	59-62
1466907-1	1992	Four agents, thalidomide, oxpentifylline, dexamethasone and a polyclonal anti-TNF-alpha antibody, were all shown by specific Elisa to block endogenous TNF-alpha production by Bacillus Calmette Guerin (BCG)-infected human monocyte-derived macrophages in in vitro culture.	Thalidomide	13-24	tumor necrosis factor	Homo sapiens	151-160
1588290-9	1992	Control of toxic symptoms with thalidomide was associated with a 50-80% reduction in agonist-stimulated monocyte TNF-alpha secretion.	Thalidomide	31-42	tumor necrosis factor	Homo sapiens	113-122
1588290-10	1992	IFN-gamma enhanced the monocyte release of TNF-alpha by 3-7.5-fold (agonist dependent) when added to patient"s cells in vitro, and this could be suppressed by the in vitro addition of 10 micrograms/ml of thalidomide.	Thalidomide	204-215	interferon gamma	Homo sapiens	0-9
1588290-10	1992	IFN-gamma enhanced the monocyte release of TNF-alpha by 3-7.5-fold (agonist dependent) when added to patient"s cells in vitro, and this could be suppressed by the in vitro addition of 10 micrograms/ml of thalidomide.	Thalidomide	204-215	tumor necrosis factor	Homo sapiens	43-52
15508726-3	2004	In the 1990s, the biological activities of thalidomide were determined to include the control of tumor necrosis factor-alpha production and inhibition of angiogenesis.	Thalidomide	43-54	tumor necrosis factor	Homo sapiens	97-124
1548069-6	1992	Treatment of ENL patients with thalidomide reduced TNF secretion by more than 90%.	Thalidomide	31-42	tumor necrosis factor	Homo sapiens	51-54
1569817-4	1992	Thalidomide has been shown to cause a decrease in the ratio of CD4+ to CD8+ lymphocytes in the blood of healthy males.	Thalidomide	0-11	CD8a molecule	Homo sapiens	71-74
2262716-1	1990	A clinical experience of using thalidomide in type-2 lepra reaction (ENL) in 90 male patients--57 with lepromatous leprosy (LL) and 33 with borderline lepromatous leprosy (BL)--is described.	Thalidomide	31-42	MLLT1 super elongation complex subunit	Homo sapiens	69-72
33773263-0	2021	In pursuit of a selective hepatocellular carcinoma therapeutic agent: Novel thalidomide derivatives with antiproliferative, antimigratory and STAT3 inhibitory properties.	Thalidomide	76-87	signal transducer and activator of transcription 3	Homo sapiens	142-147
1569817-0	1992	Thalidomide"s effectiveness in erythema nodosum leprosum is associated with a decrease in CD4+ cells in the peripheral blood.	Thalidomide	0-11	CD4 molecule	Homo sapiens	90-93
1569817-4	1992	Thalidomide has been shown to cause a decrease in the ratio of CD4+ to CD8+ lymphocytes in the blood of healthy males.	Thalidomide	0-11	CD4 molecule	Homo sapiens	63-66
1569817-6	1992	In this study, thalidomide"s effectiveness in halting chronic ENL and arresting a relapse into ENL was consistently associated with a decrease in the numbers of CD4+ lymphocytes in the blood of 2 male lepromatous leprosy patients.	Thalidomide	15-26	CD4 molecule	Homo sapiens	161-164
1997652-0	1991	Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	33-60
1997652-1	1991	Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	66-93
1997652-1	1991	Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture.	Thalidomide	0-11	tumor necrosis factor	Homo sapiens	95-104
2397633-0	1990	Behcet"s disease, palmoplantar pustulosis and HLA-B27 treatment with thalidomide.	Thalidomide	69-80	major histocompatibility complex, class I, B	Homo sapiens	46-53
33763605-9	2021	Moreover, thalidomide altered the expression of the genes involved in TGF-beta signaling, limb formation, and multiple myeloma, which are related to thalidomide-induced malformations and medication.	Thalidomide	10-21	transforming growth factor alpha	Homo sapiens	70-78
33763605-9	2021	Moreover, thalidomide altered the expression of the genes involved in TGF-beta signaling, limb formation, and multiple myeloma, which are related to thalidomide-induced malformations and medication.	Thalidomide	149-160	transforming growth factor alpha	Homo sapiens	70-78
33777938-2	2021	We had previously demonstrated that cereblon (CRBN) is the target of thalidomide embryopathy and acts as a substrate receptor for the E3 ubiquitin ligase complex, Cullin-Ring ligase 4 (CRL4CRBN) in zebrafish and chicks.	Thalidomide	69-80	cereblon	Danio rerio	46-50
33777938-4	2021	Fetuses exposed to thalidomide in early pregnancy were at risk of neurodevelopmental disorders such as autism, suggesting that CRBN is involved in prenatal brain development.	Thalidomide	19-30	cereblon	Homo sapiens	127-131
33777938-7	2021	Accumulating evidence shows that CRBN is essential not only for the teratogenic effects but also for the therapeutic effects of thalidomide.	Thalidomide	128-139	cereblon	Homo sapiens	33-37
33777938-9	2021	Investigation of the molecular mechanisms underlying the therapeutic effects of thalidomide and its derivatives, CRBN E3 ligase modulators (CELMoDs), reveals that these modulators provide CRBN the ability to recognize neosubstrates depending on their structure.	Thalidomide	80-91	cereblon	Homo sapiens	113-117
33777938-9	2021	Investigation of the molecular mechanisms underlying the therapeutic effects of thalidomide and its derivatives, CRBN E3 ligase modulators (CELMoDs), reveals that these modulators provide CRBN the ability to recognize neosubstrates depending on their structure.	Thalidomide	80-91	cereblon	Homo sapiens	188-192
26159874-5	2015	The incidence of PM status by phenotype following administration of omeprazole/esomeprazole (known inhibitors of CYP2C19) was 10-fold higher than those who are genetically PMs in the general population, which could have critical clinical implications for personalizing medications primarily metabolized by CYP2C19, such as clopidogrel, PPI, cyclophosphamide, thalidomide, citalopram, clonazepam, diazepam, phenytoin, etc.	Thalidomide	359-370	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	113-120
34704527-9	2022	EXPERT OPINION: The chemical space of CRBN ligands which is related to the classical IMiDs (thalidomide/lenalidomide/pomalidomide) is comprehensively covered by the current patent literature.	Thalidomide	92-103	cereblon	Homo sapiens	38-42
34932796-7	2021	Drinking alcohol and the fT3/fT4 ratio (<= 0.24) were independent risk factors, and thalidomide was an independent protective factor, for NCR in intestinal BS patients treated by IFX.	Thalidomide	84-95	Neutrophil migration (granulocyte glycoprotein)	Homo sapiens	138-141
34834536-8	2021	As all these chemotypes-thalidomide, IMiDs, CELMoDs and PROTACs-engage CRBN and modify its functions, we describe them here in aggregate as "CRBN-interacting small molecules" (CISMs).	Thalidomide	24-35	cereblon	Homo sapiens	71-75
34834536-8	2021	As all these chemotypes-thalidomide, IMiDs, CELMoDs and PROTACs-engage CRBN and modify its functions, we describe them here in aggregate as "CRBN-interacting small molecules" (CISMs).	Thalidomide	24-35	cereblon	Homo sapiens	141-145
34838332-3	2022	Here, we aimed to develop a MYC PROTAC based on the MYC-MAX dimerization inhibitor 10058-F4 derivative 28RH and Thalidomide, called MDEG-541.	Thalidomide	112-123	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	28-31
34838332-3	2022	Here, we aimed to develop a MYC PROTAC based on the MYC-MAX dimerization inhibitor 10058-F4 derivative 28RH and Thalidomide, called MDEG-541.	Thalidomide	112-123	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	52-55
34967303-11	2021	In vitro, compared with the HG group, MC apoptosis reduced dramatically with Thd treatment along with upregulation of Bcl-2 and downregulation of Bax.	Thalidomide	77-80	B cell leukemia/lymphoma 2	Mus musculus	118-123
34967303-11	2021	In vitro, compared with the HG group, MC apoptosis reduced dramatically with Thd treatment along with upregulation of Bcl-2 and downregulation of Bax.	Thalidomide	77-80	BCL2-associated X protein	Mus musculus	146-149
34967303-12	2021	At the same time, ER stress markers GRP78, C/EBP homologous protein (CHOP), and Caspase-12 were also mitigated following the Thd treatment.	Thalidomide	125-128	heat shock protein 5	Mus musculus	36-41
34967303-12	2021	At the same time, ER stress markers GRP78, C/EBP homologous protein (CHOP), and Caspase-12 were also mitigated following the Thd treatment.	Thalidomide	125-128	DNA-damage inducible transcript 3	Mus musculus	43-67
34967303-12	2021	At the same time, ER stress markers GRP78, C/EBP homologous protein (CHOP), and Caspase-12 were also mitigated following the Thd treatment.	Thalidomide	125-128	DNA-damage inducible transcript 3	Mus musculus	69-73
34967303-12	2021	At the same time, ER stress markers GRP78, C/EBP homologous protein (CHOP), and Caspase-12 were also mitigated following the Thd treatment.	Thalidomide	125-128	caspase 12	Mus musculus	80-90
34967303-13	2021	CONCLUSION: The present study indicates that Thd might reduce the ER stress in DN via downregulating of GRP78, CHOP, and Caspase12 expression, ultimately mitigating MCs apoptosis.	Thalidomide	45-48	heat shock protein 5	Mus musculus	104-109
34967303-13	2021	CONCLUSION: The present study indicates that Thd might reduce the ER stress in DN via downregulating of GRP78, CHOP, and Caspase12 expression, ultimately mitigating MCs apoptosis.	Thalidomide	45-48	DNA-damage inducible transcript 3	Mus musculus	111-115
34967303-13	2021	CONCLUSION: The present study indicates that Thd might reduce the ER stress in DN via downregulating of GRP78, CHOP, and Caspase12 expression, ultimately mitigating MCs apoptosis.	Thalidomide	45-48	caspase 12	Mus musculus	121-130
34944673-0	2021	Thalidomide Exerts Anti-Inflammatory Effects in Cutaneous Lupus by Inhibiting the IRF4/NF-kB and AMPK1/mTOR Pathways.	Thalidomide	0-11	interferon regulatory factor 4	Homo sapiens	82-86
34944673-0	2021	Thalidomide Exerts Anti-Inflammatory Effects in Cutaneous Lupus by Inhibiting the IRF4/NF-kB and AMPK1/mTOR Pathways.	Thalidomide	0-11	mechanistic target of rapamycin kinase	Homo sapiens	103-107
34944673-5	2021	Integrating RNA-seq data, public databases, and literature, TMPS analysis generated mathematical models which predicted that thalidomide acts via two CRBN-CRL4A- (CRL4CRBN) dependent pathways: IRF4/NF-kB and AMPK1/mTOR.	Thalidomide	125-136	cereblon	Homo sapiens	150-154
34944673-5	2021	Integrating RNA-seq data, public databases, and literature, TMPS analysis generated mathematical models which predicted that thalidomide acts via two CRBN-CRL4A- (CRL4CRBN) dependent pathways: IRF4/NF-kB and AMPK1/mTOR.	Thalidomide	125-136	interleukin 17 receptor B	Homo sapiens	163-171
34944673-5	2021	Integrating RNA-seq data, public databases, and literature, TMPS analysis generated mathematical models which predicted that thalidomide acts via two CRBN-CRL4A- (CRL4CRBN) dependent pathways: IRF4/NF-kB and AMPK1/mTOR.	Thalidomide	125-136	interferon regulatory factor 4	Homo sapiens	193-197
34944673-5	2021	Integrating RNA-seq data, public databases, and literature, TMPS analysis generated mathematical models which predicted that thalidomide acts via two CRBN-CRL4A- (CRL4CRBN) dependent pathways: IRF4/NF-kB and AMPK1/mTOR.	Thalidomide	125-136	mechanistic target of rapamycin kinase	Homo sapiens	214-218
34944673-7	2021	In vitro experiments confirmed the effect of thalidomide downregulating IRF4 in PBMCs and mTOR in keratinocytes, which converged in an NF-kB reduction that led to a resolution of the inflammatory lesion.	Thalidomide	45-56	interferon regulatory factor 4	Homo sapiens	72-76
34944673-7	2021	In vitro experiments confirmed the effect of thalidomide downregulating IRF4 in PBMCs and mTOR in keratinocytes, which converged in an NF-kB reduction that led to a resolution of the inflammatory lesion.	Thalidomide	45-56	mechanistic target of rapamycin kinase	Homo sapiens	90-94
34764413-2	2021	Cereblon (CRBN) is a common direct target of thalidomide and related compounds and works as a Cullin Ring 4 E3 ubiquitin ligase (CRL4) with DDB1, CUL4, and ROC1.	Thalidomide	45-56	cereblon	Homo sapiens	10-14
34764413-2	2021	Cereblon (CRBN) is a common direct target of thalidomide and related compounds and works as a Cullin Ring 4 E3 ubiquitin ligase (CRL4) with DDB1, CUL4, and ROC1.	Thalidomide	45-56	interleukin 17 receptor B	Homo sapiens	129-133
34764413-2	2021	Cereblon (CRBN) is a common direct target of thalidomide and related compounds and works as a Cullin Ring 4 E3 ubiquitin ligase (CRL4) with DDB1, CUL4, and ROC1.	Thalidomide	45-56	damage specific DNA binding protein 1	Homo sapiens	140-144
34764413-2	2021	Cereblon (CRBN) is a common direct target of thalidomide and related compounds and works as a Cullin Ring 4 E3 ubiquitin ligase (CRL4) with DDB1, CUL4, and ROC1.	Thalidomide	45-56	ring-box 1	Homo sapiens	156-160
34764413-3	2021	The substrate specificity of CRL4CRBN is modulated by thalidomide-related compounds.	Thalidomide	54-65	interleukin 17 receptor B	Homo sapiens	29-37
34704527-10	2022	The promising area of research is in the identification of non-thalidomide-like chemotypes capable of binding to CRBN.	Thalidomide	63-74	cereblon	Homo sapiens	113-117
34455300-6	2021	Collectively, a substitution position, an alkyne-azide cyclization and a liker type significantly affect the ability of ANF-thalidomide conjugates in eliminating drug resistance of CYP1B1-expressing DU145 (DU145/CY) cells to docetaxel via targeted CYP1B1 degradation.	Thalidomide	124-135	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	181-187
34455300-6	2021	Collectively, a substitution position, an alkyne-azide cyclization and a liker type significantly affect the ability of ANF-thalidomide conjugates in eliminating drug resistance of CYP1B1-expressing DU145 (DU145/CY) cells to docetaxel via targeted CYP1B1 degradation.	Thalidomide	124-135	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	248-254
34085173-2	2021	The TNF-alpha inhibitor thalidomide is reported to be effective for inducing remission in pediatric Crohn"s disease (CD) and adults with refractory CD.	Thalidomide	24-35	tumor necrosis factor	Mus musculus	4-13
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	FYVE, RhoGEF and PH domain containing 5	Homo sapiens	66-70
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	prostaglandin D2 receptor	Homo sapiens	71-74
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	microRNA 454	Homo sapiens	75-82
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	zinc finger E-box binding homeobox 1	Homo sapiens	86-90
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	105-110
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	programmed cell death 1	Homo sapiens	126-130
34520751-0	2021	Thalidomide suppresses angiogenesis and immune evasion via lncRNA FGD5-AS1/miR-454-3p/ZEB1 axis-mediated VEGFA expression and PD-1/PD-L1 checkpoint in NSCLC.	Thalidomide	0-11	CD274 molecule	Homo sapiens	131-136
34520751-11	2021	RESULTS: Thalidomide reduced tumor growth and angiogenesis and increased CD8+ T cell ratio in a mouse model.	Thalidomide	9-20	CD8a molecule	Homo sapiens	73-76
34520751-14	2021	Thalidomide targeted FGD5-AS1 to exert its anti-tumor activity in NSCLC.	Thalidomide	0-11	FYVE, RhoGEF and PH domain containing 5	Homo sapiens	21-25
34520751-14	2021	Thalidomide targeted FGD5-AS1 to exert its anti-tumor activity in NSCLC.	Thalidomide	0-11	prostaglandin D2 receptor	Homo sapiens	26-29
34520751-16	2021	Simultaneous overexpression of FGD5-AS1 and silencing of miR-454-3p reversed thalidomide-mediated anti-tumor effects in NSCLC.	Thalidomide	77-88	FGD5 antisense RNA 1	Homo sapiens	31-39
34520751-16	2021	Simultaneous overexpression of FGD5-AS1 and silencing of miR-454-3p reversed thalidomide-mediated anti-tumor effects in NSCLC.	Thalidomide	77-88	microRNA 454	Homo sapiens	57-64
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	FYVE, RhoGEF and PH domain containing 5	Homo sapiens	75-79
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	prostaglandin D2 receptor	Homo sapiens	80-83
34085173-0	2021	Thalidomide Attenuates Colitis and Is Associated with the Suppression of M1 Macrophage Polarization by Targeting the Transcription Factor IRF5.	Thalidomide	0-11	interferon regulatory factor 5	Mus musculus	138-142
34085173-11	2021	Mechanistically, we observed that thalidomide could increase epithelial cell self-renewal capacity and modulate M1/M2 polarization by decreasing M1 markers CD86 and CCR7 and increasing M2 protein signatures CD206 and Arg-1.	Thalidomide	34-45	CD86 antigen	Mus musculus	156-160
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	microRNA 454	Homo sapiens	84-91
34085173-11	2021	Mechanistically, we observed that thalidomide could increase epithelial cell self-renewal capacity and modulate M1/M2 polarization by decreasing M1 markers CD86 and CCR7 and increasing M2 protein signatures CD206 and Arg-1.	Thalidomide	34-45	chemokine (C-C motif) receptor 7	Mus musculus	165-169
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	zinc finger E-box binding homeobox 1	Homo sapiens	95-99
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	vascular endothelial growth factor A	Homo sapiens	128-133
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	programmed cell death 1	Homo sapiens	149-153
34520751-17	2021	CONCLUSION: Thalidomide inhibits NSCLC angiogenesis and immune evasion via FGD5-AS1/miR-454-3p/ZEB1 axis-mediated regulation of VEGFA expression and PD-1/PD-L1 checkpoint.	Thalidomide	12-23	CD274 molecule	Homo sapiens	154-159
34085173-11	2021	Mechanistically, we observed that thalidomide could increase epithelial cell self-renewal capacity and modulate M1/M2 polarization by decreasing M1 markers CD86 and CCR7 and increasing M2 protein signatures CD206 and Arg-1.	Thalidomide	34-45	mannose receptor, C type 1	Mus musculus	207-212
34085173-11	2021	Mechanistically, we observed that thalidomide could increase epithelial cell self-renewal capacity and modulate M1/M2 polarization by decreasing M1 markers CD86 and CCR7 and increasing M2 protein signatures CD206 and Arg-1.	Thalidomide	34-45	arginase, liver	Mus musculus	217-222
34085173-12	2021	Thalidomide controls M1 macrophage polarization by targeting the transcription factor IRF5.	Thalidomide	0-11	interferon regulatory factor 5	Mus musculus	86-90
34583995-3	2021	CRBN, a substrate receptor of CUL4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase, is a direct target for thalidomide teratogenicity and antitumor activity of IMiDs (now known as Cereblon E3 ligase modulators: CELMoDs).	Thalidomide	105-116	cereblon	Homo sapiens	0-4
34339726-0	2021	Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLCgamma dependent autophagy pathways in human umbilical vein endothelial cells.	Thalidomide	27-38	protein tyrosine kinase 2	Homo sapiens	84-87
34339726-0	2021	Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLCgamma dependent autophagy pathways in human umbilical vein endothelial cells.	Thalidomide	27-38	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	88-91
34339726-0	2021	Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLCgamma dependent autophagy pathways in human umbilical vein endothelial cells.	Thalidomide	27-38	mitogen-activated protein kinase 1	Homo sapiens	96-99
34339726-0	2021	Palladium (II) complex and thalidomide intercept angiogenic signaling via targeting FAK/Src and Erk/Akt/PLCgamma dependent autophagy pathways in human umbilical vein endothelial cells.	Thalidomide	27-38	AKT serine/threonine kinase 1	Homo sapiens	100-103
34339726-2	2021	The viability was assessed after treatment with palladium (II) complex (1.56-100 muM) and thalidomide (0.1-400 muM) alone by using ATP assay for 48 h. Palladium (II) complex was found to inhibit growth statistically significant in a dose-dependent manner in HUVECs and promoted PARP-1 cleavage through the production of ROS.	Thalidomide	90-101	poly(ADP-ribose) polymerase 1	Homo sapiens	278-284
34339726-8	2021	We also showed that being treated with thalidomide and palladium (II) complex inhibited phosphorylation of the signaling regulators downstream of the VEGFR2.	Thalidomide	39-50	kinase insert domain receptor	Homo sapiens	150-156
34339726-11	2021	Hence, we demonstrated that palladium (II) and thalidomide can induce cell death via the Erk/Akt/PLCgamma signaling pathway and that this pathway might be a novel mechanism.	Thalidomide	47-58	mitogen-activated protein kinase 1	Homo sapiens	89-92
34339726-11	2021	Hence, we demonstrated that palladium (II) and thalidomide can induce cell death via the Erk/Akt/PLCgamma signaling pathway and that this pathway might be a novel mechanism.	Thalidomide	47-58	AKT serine/threonine kinase 1	Homo sapiens	93-96
34583995-3	2021	CRBN, a substrate receptor of CUL4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase, is a direct target for thalidomide teratogenicity and antitumor activity of IMiDs (now known as Cereblon E3 ligase modulators: CELMoDs).	Thalidomide	105-116	ring-box 1	Homo sapiens	35-39
34583995-3	2021	CRBN, a substrate receptor of CUL4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase, is a direct target for thalidomide teratogenicity and antitumor activity of IMiDs (now known as Cereblon E3 ligase modulators: CELMoDs).	Thalidomide	105-116	damage specific DNA binding protein 1	Homo sapiens	40-44
34583995-3	2021	CRBN, a substrate receptor of CUL4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase, is a direct target for thalidomide teratogenicity and antitumor activity of IMiDs (now known as Cereblon E3 ligase modulators: CELMoDs).	Thalidomide	105-116	cereblon	Homo sapiens	45-49
34583995-3	2021	CRBN, a substrate receptor of CUL4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase, is a direct target for thalidomide teratogenicity and antitumor activity of IMiDs (now known as Cereblon E3 ligase modulators: CELMoDs).	Thalidomide	105-116	interleukin 17 receptor B	Homo sapiens	51-59
34641286-0	2021	Isotretinoin and Thalidomide Down-Regulate c-MYC Gene Expression and Modify Proteins Associated with Cancer in Hepatic Cells.	Thalidomide	17-28	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	43-48
34312685-0	2021	Combined use of interferon alpha-1b, interleukin-2, and thalidomide to reverse the AML1-ETO fusion gene in acute myeloid leukemia.	Thalidomide	56-67	RUNX family transcription factor 1	Homo sapiens	83-87
34312685-0	2021	Combined use of interferon alpha-1b, interleukin-2, and thalidomide to reverse the AML1-ETO fusion gene in acute myeloid leukemia.	Thalidomide	56-67	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	88-91
34312685-1	2021	This study aims to explore the effect of the ITI (interferon alpha-1b, thalidomide, and interleukin-2) regimen on the AML1-ETO fusion gene in patients with t(8;21) acute myeloid leukemia (AML) who were in hematologic remission but positive for the AML1-ETO fusion gene.	Thalidomide	71-82	RUNX family transcription factor 1	Homo sapiens	118-122
34312685-1	2021	This study aims to explore the effect of the ITI (interferon alpha-1b, thalidomide, and interleukin-2) regimen on the AML1-ETO fusion gene in patients with t(8;21) acute myeloid leukemia (AML) who were in hematologic remission but positive for the AML1-ETO fusion gene.	Thalidomide	71-82	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	123-126
34312685-1	2021	This study aims to explore the effect of the ITI (interferon alpha-1b, thalidomide, and interleukin-2) regimen on the AML1-ETO fusion gene in patients with t(8;21) acute myeloid leukemia (AML) who were in hematologic remission but positive for the AML1-ETO fusion gene.	Thalidomide	71-82	RUNX family transcription factor 1	Homo sapiens	248-252
34312685-1	2021	This study aims to explore the effect of the ITI (interferon alpha-1b, thalidomide, and interleukin-2) regimen on the AML1-ETO fusion gene in patients with t(8;21) acute myeloid leukemia (AML) who were in hematologic remission but positive for the AML1-ETO fusion gene.	Thalidomide	71-82	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	253-256
34390739-8	2021	Particularly, thalidomide specifically stimulated IL-10 and beta-endorphin expressions in microglia but not astrocytes or neurons.	Thalidomide	14-25	interleukin 10	Rattus norvegicus	50-55
34390739-10	2021	Importantly, pretreatment with intrathecal injection of the microglial metabolic inhibitor minocycline, IL-10 antibody, beta-endorphin antiserum, and preferred or selective mu-opioid receptor antagonist naloxone or CTAP entirely blocked thalidomide gavage-induced mechanical antiallodynia.	Thalidomide	237-248	interleukin 10	Rattus norvegicus	104-109
34390739-11	2021	Our results demonstrate that thalidomide, but not lenalidomide or pomalidomide, alleviates neuropathic pain, which is mediated by upregulation of spinal microglial IL-10/beta-endorphin expression, rather than downregulation of TNFalpha expression.	Thalidomide	29-40	interleukin 10	Rattus norvegicus	164-169
34390739-0	2021	Thalidomide alleviates neuropathic pain through microglial IL-10/beta-endorphin signaling pathway.	Thalidomide	0-11	interleukin 10	Rattus norvegicus	59-64
34390739-6	2021	Treatment with thalidomide, lenalidomide and pomalidomide reduced peripheral nerve injury-induced proinflammatory cytokines (TNFalpha, IL-1beta and IL-6) in the ipsilateral spinal cords of neuropathic rats and LPS-treated primary microglial cells.	Thalidomide	15-26	tumor necrosis factor	Rattus norvegicus	125-133
34390739-6	2021	Treatment with thalidomide, lenalidomide and pomalidomide reduced peripheral nerve injury-induced proinflammatory cytokines (TNFalpha, IL-1beta and IL-6) in the ipsilateral spinal cords of neuropathic rats and LPS-treated primary microglial cells.	Thalidomide	15-26	interleukin 1 alpha	Rattus norvegicus	135-143
34390739-6	2021	Treatment with thalidomide, lenalidomide and pomalidomide reduced peripheral nerve injury-induced proinflammatory cytokines (TNFalpha, IL-1beta and IL-6) in the ipsilateral spinal cords of neuropathic rats and LPS-treated primary microglial cells.	Thalidomide	15-26	interleukin 6	Rattus norvegicus	148-152
34390739-7	2021	In contrast, treatment with thalidomide, but not lenalidomide or pomalidomide, stimulated spinal expressions of IL-10 and beta-endorphin in neuropathic rats.	Thalidomide	28-39	interleukin 10	Rattus norvegicus	112-117
34584130-9	2021	Thalidomide treatment significantly reduced serum levels of hepatic enzymes and TNF-alpha, IL-1-beta, and IL-6.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	80-89
34584130-9	2021	Thalidomide treatment significantly reduced serum levels of hepatic enzymes and TNF-alpha, IL-1-beta, and IL-6.	Thalidomide	0-11	interleukin 1 alpha	Rattus norvegicus	91-100
34584130-9	2021	Thalidomide treatment significantly reduced serum levels of hepatic enzymes and TNF-alpha, IL-1-beta, and IL-6.	Thalidomide	0-11	interleukin 6	Rattus norvegicus	106-110
34251884-6	2021	These data might have also implications for cancer, as frequently occurring mutations of MEKK1 might have an impact on genome stability and the therapeutic efficacy of CRL4-dependent immunomodulatory drugs such as thalidomide-derivatives.	Thalidomide	214-225	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	89-94
34251884-6	2021	These data might have also implications for cancer, as frequently occurring mutations of MEKK1 might have an impact on genome stability and the therapeutic efficacy of CRL4-dependent immunomodulatory drugs such as thalidomide-derivatives.	Thalidomide	214-225	interleukin 17 receptor B	Homo sapiens	168-172
34641286-5	2021	The objective of this work was to evaluate the effect of the drugs isotretinoin and thalidomide on c-MYC expression and cancer-related proteins in an HCC cellular model.	Thalidomide	84-95	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	99-104
34641286-10	2021	We demonstrated that in HepG2 cells, isotretinoin and thalidomide reduced c-MYC mRNA expression levels, but this decrease in expression was linked to the regulation of P1 and P1-P2 c-MYC promoter activity in isotretinoin only.	Thalidomide	54-65	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	74-79
34641286-13	2021	In conclusion, isotretinoin and thalidomide down-regulate c-MYC mRNA expression and this is partially due to P1 or P2 promoter activity, suggesting that these drugs could be promising options for modulating the expression of oncogenes and tumor suppressor genes in HCC.	Thalidomide	32-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
34522548-4	2021	She had several stigmata of thalidomide embryopathy.	Thalidomide	28-39	Src homology 2 domain containing E	Homo sapiens	0-3
34530760-6	2021	The antiangiogenic and immunomodulatory drug thalidomide is a cereblon-based molecular glue that can induce the degradation of the IKAROS family transcription factors IKZF1 and IKZF3.	Thalidomide	45-56	IKAROS family zinc finger 1	Homo sapiens	167-172
34530760-6	2021	The antiangiogenic and immunomodulatory drug thalidomide is a cereblon-based molecular glue that can induce the degradation of the IKAROS family transcription factors IKZF1 and IKZF3.	Thalidomide	45-56	IKAROS family zinc finger 3	Homo sapiens	177-182
34530760-14	2021	DISCUSSION: The addition of thalidomide to pyrotinib is expected to increase the clinical benefit in advanced NSCLC patients with HER2 exon 20 insertions, and reduce the incidence of pyrotinib-related diarrhea.	Thalidomide	28-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	130-134
34650759-0	2021	Effect of thalidomide combined with TP chemotherapy on serum VEGF and NRP-1 levels advanced esophageal cancer patients.	Thalidomide	10-21	vascular endothelial growth factor A	Homo sapiens	61-65
34650759-0	2021	Effect of thalidomide combined with TP chemotherapy on serum VEGF and NRP-1 levels advanced esophageal cancer patients.	Thalidomide	10-21	neuropilin 1	Homo sapiens	70-75
34650759-1	2021	OBJECTIVE: This study aimed to investigate the effect of thalidomide combined with pacilitaxel plus cisplatin (TP) chemotherapy on serum vascular endothelial growth factor (VEGF) and neuropilin-1 (NRP-1) levels in advanced esophageal cancer patients.	Thalidomide	57-68	vascular endothelial growth factor A	Homo sapiens	137-171
34650759-1	2021	OBJECTIVE: This study aimed to investigate the effect of thalidomide combined with pacilitaxel plus cisplatin (TP) chemotherapy on serum vascular endothelial growth factor (VEGF) and neuropilin-1 (NRP-1) levels in advanced esophageal cancer patients.	Thalidomide	57-68	vascular endothelial growth factor A	Homo sapiens	173-177
34650759-1	2021	OBJECTIVE: This study aimed to investigate the effect of thalidomide combined with pacilitaxel plus cisplatin (TP) chemotherapy on serum vascular endothelial growth factor (VEGF) and neuropilin-1 (NRP-1) levels in advanced esophageal cancer patients.	Thalidomide	57-68	neuropilin 1	Homo sapiens	183-195
34650759-1	2021	OBJECTIVE: This study aimed to investigate the effect of thalidomide combined with pacilitaxel plus cisplatin (TP) chemotherapy on serum vascular endothelial growth factor (VEGF) and neuropilin-1 (NRP-1) levels in advanced esophageal cancer patients.	Thalidomide	57-68	neuropilin 1	Homo sapiens	197-202
34539435-2	2021	Thalidomide has been confirmed to inhibit angiogenesis by inhibiting the secretion of vascular endothelial growth factor (VEGF), but the exact mechanism by which thalidomide inhibits vascular proliferation during PD is still unclear.	Thalidomide	0-11	vascular endothelial growth factor A	Homo sapiens	122-126
34539435-2	2021	Thalidomide has been confirmed to inhibit angiogenesis by inhibiting the secretion of vascular endothelial growth factor (VEGF), but the exact mechanism by which thalidomide inhibits vascular proliferation during PD is still unclear.	Thalidomide	162-173	vascular endothelial growth factor A	Homo sapiens	122-126
34539435-3	2021	Here, the objective of the present study was to investigate whether the reduction in VEGF production by human peritoneal mesothelial cells (HPMCs) was controlled by thalidomide.	Thalidomide	165-176	vascular endothelial growth factor A	Homo sapiens	85-89
34539435-4	2021	Stimulation of HPMCs with IL-6 in combination with soluble IL-6 receptor (sIL-6R) promoted VEGF expression and secretion, but these effects were attenuated by thalidomide treatment through a transcriptional mechanism that involved signal transducer and activator of transcription 3 (STAT3) and SP4.	Thalidomide	159-170	interleukin 6	Rattus norvegicus	26-30
34539435-4	2021	Stimulation of HPMCs with IL-6 in combination with soluble IL-6 receptor (sIL-6R) promoted VEGF expression and secretion, but these effects were attenuated by thalidomide treatment through a transcriptional mechanism that involved signal transducer and activator of transcription 3 (STAT3) and SP4.	Thalidomide	159-170	vascular endothelial growth factor A	Homo sapiens	91-95
34539435-4	2021	Stimulation of HPMCs with IL-6 in combination with soluble IL-6 receptor (sIL-6R) promoted VEGF expression and secretion, but these effects were attenuated by thalidomide treatment through a transcriptional mechanism that involved signal transducer and activator of transcription 3 (STAT3) and SP4.	Thalidomide	159-170	signal transducer and activator of transcription 3	Rattus norvegicus	231-281
34539435-4	2021	Stimulation of HPMCs with IL-6 in combination with soluble IL-6 receptor (sIL-6R) promoted VEGF expression and secretion, but these effects were attenuated by thalidomide treatment through a transcriptional mechanism that involved signal transducer and activator of transcription 3 (STAT3) and SP4.	Thalidomide	159-170	signal transducer and activator of transcription 3	Homo sapiens	283-288
34539435-4	2021	Stimulation of HPMCs with IL-6 in combination with soluble IL-6 receptor (sIL-6R) promoted VEGF expression and secretion, but these effects were attenuated by thalidomide treatment through a transcriptional mechanism that involved signal transducer and activator of transcription 3 (STAT3) and SP4.	Thalidomide	159-170	Sp4 transcription factor	Homo sapiens	294-297
34539435-5	2021	Conditioned medium from HPMCs cultured with thalidomide inhibited angiogenic endothelial tube formation, which could be further blocked by silencing SP4 and promoted by overexpressing SP4.	Thalidomide	44-55	Sp4 transcription factor	Homo sapiens	149-152
34539435-5	2021	Conditioned medium from HPMCs cultured with thalidomide inhibited angiogenic endothelial tube formation, which could be further blocked by silencing SP4 and promoted by overexpressing SP4.	Thalidomide	44-55	Sp4 transcription factor	Homo sapiens	184-187
34539435-7	2021	Taken together, these findings identify a novel mechanism that links thalidomide, STAT3/SP4 signaling, and angiogenesis in the peritoneal membrane.	Thalidomide	69-80	Sp4 transcription factor	Rattus norvegicus	88-91
34431670-3	2021	Employing thalidomide to recruit cereblon/cullin 4A E3 ligase and through the rigidification of the linker, we discovered highly potent AR degraders with good oral pharmacokinetic properties in mice with ARD-2128 being the best compound.	Thalidomide	10-21	androgen receptor	Mus musculus	136-138
34539435-0	2021	Thalidomide Suppresses Angiogenesis Through the Signal Transducer and Activator of Transcription 3/SP4 Signaling Pathway in the Peritoneal Membrane.	Thalidomide	0-11	signal transducer and activator of transcription 3	Rattus norvegicus	48-98
34539435-0	2021	Thalidomide Suppresses Angiogenesis Through the Signal Transducer and Activator of Transcription 3/SP4 Signaling Pathway in the Peritoneal Membrane.	Thalidomide	0-11	Sp4 transcription factor	Rattus norvegicus	99-102
34512420-8	2021	Administration of TNF-alpha synthesis blocker, thalidomide (THL), immediately after SPS prevented increased TNF-alpha and development of allodynia and hyperalgesia.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	18-27
34512420-8	2021	Administration of TNF-alpha synthesis blocker, thalidomide (THL), immediately after SPS prevented increased TNF-alpha and development of allodynia and hyperalgesia.	Thalidomide	47-58	tumor necrosis factor	Homo sapiens	108-117
34512420-8	2021	Administration of TNF-alpha synthesis blocker, thalidomide (THL), immediately after SPS prevented increased TNF-alpha and development of allodynia and hyperalgesia.	Thalidomide	60-63	tumor necrosis factor	Homo sapiens	18-27
34512420-8	2021	Administration of TNF-alpha synthesis blocker, thalidomide (THL), immediately after SPS prevented increased TNF-alpha and development of allodynia and hyperalgesia.	Thalidomide	60-63	tumor necrosis factor	Homo sapiens	108-117
34512420-10	2021	THL also prevented SPS-induced increases in serum N/OFQ and reversed regional N/OFQ mRNA expression changes in the CNS.	Thalidomide	0-3	prepronociceptin	Homo sapiens	50-55
34512420-10	2021	THL also prevented SPS-induced increases in serum N/OFQ and reversed regional N/OFQ mRNA expression changes in the CNS.	Thalidomide	0-3	prepronociceptin	Homo sapiens	78-83
34150160-0	2021	The effect of TACE in combination with thalidomide-mediated adjuvant therapy on the levels of VEGF and bFGF in patients with hepatocellular carcinoma.	Thalidomide	39-50	vascular endothelial growth factor A	Homo sapiens	94-98
34128013-3	2021	To compare the structure of the bound CRBN thalidomide enantiomers with that of the isolated molecule, the rotational spectrum of laser-ablated thalidomide has been studied by chirp-pulsed Fourier transform microwave spectroscopy in supersonic jets complemented by theoretical computations.	Thalidomide	43-54	cereblon	Homo sapiens	38-42
34128013-9	2021	This is consistent with a less stable (R)-enantiomer and the known preference of (S)-thalidomide to bind CRBN, which starts the process leading to teratogenic effects.	Thalidomide	81-96	cereblon	Homo sapiens	105-109
34207079-4	2021	Here, we evaluated the expression of CRL4-CRBN complex proteins and their downstream targets with immunohistochemistry (IHC) staining in 130 bone marrow samples from MM patients treated with thalidomide or lenalidomide-based regimens.	Thalidomide	191-202	interleukin 17 receptor B	Homo sapiens	37-41
34207079-4	2021	Here, we evaluated the expression of CRL4-CRBN complex proteins and their downstream targets with immunohistochemistry (IHC) staining in 130 bone marrow samples from MM patients treated with thalidomide or lenalidomide-based regimens.	Thalidomide	191-202	cereblon	Homo sapiens	42-46
34306363-6	2021	The caspase 3, 8, and 9 immunoreactivities were increased in all treatment groups and TUNEL positive cells were the highest in the Wortmannin and Thalidomide group.	Thalidomide	146-157	caspase 3	Mus musculus	4-13
34073624-4	2021	However, the effect of thalidomide on the function of CRBN as a negative regulator of AMPK through interaction with the alpha subunit remains unclear.	Thalidomide	23-34	cereblon	Homo sapiens	54-58
34249098-0	2021	Comparative Genomics Identifies Putative Interspecies Mechanisms Underlying Crbn-Sall4-Linked Thalidomide Embryopathy.	Thalidomide	94-105	cereblon	Mus musculus	76-80
34249098-0	2021	Comparative Genomics Identifies Putative Interspecies Mechanisms Underlying Crbn-Sall4-Linked Thalidomide Embryopathy.	Thalidomide	94-105	spalt like transcription factor 4	Mus musculus	81-86
34249098-1	2021	The identification of thalidomide-Cereblon-induced SALL4 degradation has brought new understanding for thalidomide embryopathy (TE) differences across species.	Thalidomide	22-33	spalt like transcription factor 4	Mus musculus	51-56
34249098-1	2021	The identification of thalidomide-Cereblon-induced SALL4 degradation has brought new understanding for thalidomide embryopathy (TE) differences across species.	Thalidomide	103-114	spalt like transcription factor 4	Mus musculus	51-56
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	cereblon	Mus musculus	27-31
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	T-box 5	Mus musculus	180-184
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	establishment of sister chromatid cohesion N-acetyltransferase 2	Mus musculus	186-191
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	RecQ protein-like 4	Mus musculus	193-199
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	spalt like transcription factor 4	Mus musculus	205-210
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	cereblon	Mus musculus	212-216
34249098-9	2021	In co-expression analysis, Crbn was a gene identified as a driver of the co-expression of other genes implicated in genetic, non-teratogenic, limb reduction defects (LRD), such as Tbx5, Esco2, Recql4, and Sall4; Crbn and Sall4 were shown to have a moderate co-expression correlation, which is affected after thalidomide exposure.	Thalidomide	308-319	spalt like transcription factor 4	Mus musculus	221-226
34150160-0	2021	The effect of TACE in combination with thalidomide-mediated adjuvant therapy on the levels of VEGF and bFGF in patients with hepatocellular carcinoma.	Thalidomide	39-50	fibroblast growth factor 2	Homo sapiens	103-107
34150160-1	2021	OBJECTIVE: To investigate the efficacy of transcatheter arterial chemoembolization (TACE) combined with thalidomide-mediated adjuvant therapy on the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in hepatocellular carcinoma (HCC) patients.	Thalidomide	104-115	vascular endothelial growth factor A	Homo sapiens	170-204
34150160-1	2021	OBJECTIVE: To investigate the efficacy of transcatheter arterial chemoembolization (TACE) combined with thalidomide-mediated adjuvant therapy on the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in hepatocellular carcinoma (HCC) patients.	Thalidomide	104-115	vascular endothelial growth factor A	Homo sapiens	206-210
34150160-1	2021	OBJECTIVE: To investigate the efficacy of transcatheter arterial chemoembolization (TACE) combined with thalidomide-mediated adjuvant therapy on the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in hepatocellular carcinoma (HCC) patients.	Thalidomide	104-115	fibroblast growth factor 2	Homo sapiens	216-246
34150160-1	2021	OBJECTIVE: To investigate the efficacy of transcatheter arterial chemoembolization (TACE) combined with thalidomide-mediated adjuvant therapy on the expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in hepatocellular carcinoma (HCC) patients.	Thalidomide	104-115	fibroblast growth factor 2	Homo sapiens	248-252
34150160-13	2021	CONCLUSION: TACE in combination with thalidomide-mediated adjuvant treatment has revealed a promising clinical outcome on HCC patients by downregulating the levels of VEGF and bFGF.	Thalidomide	37-48	vascular endothelial growth factor A	Homo sapiens	167-171
34150160-13	2021	CONCLUSION: TACE in combination with thalidomide-mediated adjuvant treatment has revealed a promising clinical outcome on HCC patients by downregulating the levels of VEGF and bFGF.	Thalidomide	37-48	fibroblast growth factor 2	Homo sapiens	176-180
34853241-7	2021	These results suggest that metabolic activation of thalidomide may be dependent on rabbit liver enzymes just it was for cytochrome P450 enzymes in humanized-liver mice; in contrast, rodent livers predominantly mediate biotransformation of thalidomide to 5"-hydroxythalidomide.	Thalidomide	51-62	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	120-135
34162559-0	2021	Thalidomide Reduces Activation of Murine Pancreatic Stellate Cells by Inhibiting the TGF-beta/Smad Pathway.	Thalidomide	0-11	transforming growth factor alpha	Mus musculus	85-93
34162559-0	2021	Thalidomide Reduces Activation of Murine Pancreatic Stellate Cells by Inhibiting the TGF-beta/Smad Pathway.	Thalidomide	0-11	SMAD family member 7	Mus musculus	94-98
34162559-3	2021	We measured the effects of thalidomide on PSC activation by detecting the expression of alpha-SMA, collagen type I, and the TGF-beta/Smad pathway through quantitative real-time PCR and Western blot analysis.	Thalidomide	27-38	actin alpha 2, smooth muscle, aorta	Mus musculus	88-97
34162559-3	2021	We measured the effects of thalidomide on PSC activation by detecting the expression of alpha-SMA, collagen type I, and the TGF-beta/Smad pathway through quantitative real-time PCR and Western blot analysis.	Thalidomide	27-38	transforming growth factor alpha	Mus musculus	124-132
34162559-4	2021	RESULTS: Compared with TGF-beta1 alone, thalidomide significantly inhibited PSC activation by reducing alpha-SMA expression (P<0.05) and decreasing collagen type I deposition (P<0.05).	Thalidomide	40-51	actin alpha 2, smooth muscle, aorta	Mus musculus	103-112
34162559-5	2021	PSCs treated with thalidomide alone showed lower expression of alpha-SMA and collagen type I than those treated with thalidomide and TGF-beta1 at random order (P<0.01).	Thalidomide	18-29	corneal susceptibility to P. aeruginosa	Mus musculus	0-4
34162559-5	2021	PSCs treated with thalidomide alone showed lower expression of alpha-SMA and collagen type I than those treated with thalidomide and TGF-beta1 at random order (P<0.01).	Thalidomide	18-29	actin alpha 2, smooth muscle, aorta	Mus musculus	63-72
34162559-5	2021	PSCs treated with thalidomide alone showed lower expression of alpha-SMA and collagen type I than those treated with thalidomide and TGF-beta1 at random order (P<0.01).	Thalidomide	117-128	actin alpha 2, smooth muscle, aorta	Mus musculus	63-72
34162559-6	2021	Thalidomide downregulated TGF-beta1 and Smad3 and upregulated Smad7 (P<0.05).	Thalidomide	0-11	transforming growth factor, beta 1	Mus musculus	26-35
34162559-6	2021	Thalidomide downregulated TGF-beta1 and Smad3 and upregulated Smad7 (P<0.05).	Thalidomide	0-11	SMAD family member 3	Mus musculus	40-45
34162559-6	2021	Thalidomide downregulated TGF-beta1 and Smad3 and upregulated Smad7 (P<0.05).	Thalidomide	0-11	SMAD family member 7	Mus musculus	62-67
34162559-7	2021	CONCLUSION: Thalidomide could repress PSC activation and alleviate fibrosis by regulating the TGF-beta/Smad pathway.	Thalidomide	12-23	transforming growth factor alpha	Mus musculus	94-102
34162559-7	2021	CONCLUSION: Thalidomide could repress PSC activation and alleviate fibrosis by regulating the TGF-beta/Smad pathway.	Thalidomide	12-23	SMAD family member 7	Mus musculus	103-107
35413617-3	2022	It was found that thalidomide and its analogs could bind to CRBN E3 ubiquitin ligase and modulate CRBN.	Thalidomide	18-29	cereblon	Homo sapiens	98-102
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	CD274 molecule	Homo sapiens	149-179
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	CD274 molecule	Homo sapiens	181-186
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	nuclear factor kappa B subunit 1	Homo sapiens	236-245
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	hypoxia inducible factor 1 subunit alpha	Homo sapiens	248-279
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	hypoxia inducible factor 1 subunit alpha	Homo sapiens	281-291
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	epidermal growth factor receptor	Homo sapiens	294-326
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	epidermal growth factor receptor	Homo sapiens	328-332
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	signal transducer and activator of transcription 3	Homo sapiens	339-389
35472743-2	2022	Food and Drug Administration (FDA)-approved immune-modulatory agent, thalidomide, can modulate the related proteins of upstream signaling pathway of programmed cell death-ligand 1 (PD-L1), including nuclear transcription factor kappaB (NF-kappaB), hypoxia inducible factor-1alpha (HIF-1alpha), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3), all acting as key antitumor target proteins.	Thalidomide	69-80	signal transducer and activator of transcription 3	Homo sapiens	391-396
35472743-6	2022	Fluorescent confocal and western blotting experiments proved that 6 significantly regulated NF-kappaB, EGFR, HIF-1alpha and phosphor-signal transducer and activator of transcription 3 (p-STAT3), and simultaneously inhibited PD-L1 expression to interrupt programmed cell death 1 (PD-1)/PD-L1 signaling pathway, suggesting a synergistic action of cisplatin and thalidomide.	Thalidomide	359-370	signal transducer and activator of transcription 3	Homo sapiens	187-192
35628464-0	2022	Thalidomide Alleviates Pulmonary Fibrosis Induced by Silica in Mice by Inhibiting ER Stress and the TLR4-NF-kappaB Pathway.	Thalidomide	0-11	toll-like receptor 4	Mus musculus	100-104
35384188-0	2022	Cutaneous involvement in DOCK8 related immunodeficiency syndrome responding to thalidomide.	Thalidomide	79-90	dedicator of cytokinesis 8	Homo sapiens	25-30
35495588-0	2022	Targeting TNFalpha-mediated cytotoxicity using thalidomide after experimental cardiac arrest in rats: An exploratory study.	Thalidomide	47-58	tumor necrosis factor	Rattus norvegicus	10-18
35495588-2	2022	Thalidomide has been reported to be neuroprotective by selectively decreasing TNFalpha synthesis.	Thalidomide	0-11	tumor necrosis factor	Rattus norvegicus	78-86
35495588-3	2022	We hypothesized that thalidomide would decrease the systemic and organ-specific TNFalpha/cytokine response and biomarkers of injury in rats subjected to 10 min CA.	Thalidomide	21-32	tumor necrosis factor	Rattus norvegicus	80-88
35628464-0	2022	Thalidomide Alleviates Pulmonary Fibrosis Induced by Silica in Mice by Inhibiting ER Stress and the TLR4-NF-kappaB Pathway.	Thalidomide	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	105-114
35628464-9	2022	Treating both silicotic mice and silica-stimulated MH-S cells with thalidomide inhibited ER stress and the TLR4-NF-kappaB pathway as well as the inflammatory response.	Thalidomide	67-78	toll-like receptor 4	Mus musculus	107-111
35628464-9	2022	Treating both silicotic mice and silica-stimulated MH-S cells with thalidomide inhibited ER stress and the TLR4-NF-kappaB pathway as well as the inflammatory response.	Thalidomide	67-78	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-121
34768284-5	2022	We validated the predictive role of MCT1 for IMiD-based maintenance in an independent cohort of patients receiving thalidomide (OS 83.6 months vs. NR in MCT1high vs. MCT1low; P=.03).	Thalidomide	115-126	solute carrier family 16 member 1	Homo sapiens	36-40
35595613-6	2022	On the other hand, the efficiency of Thalidomide derivates in myelodysplastic syndromes (MDS), such as Lenalidomide, acted as the starting point for the development of targeted leukemia-associated protein degradation molecules.	Thalidomide	37-48	ribosomal protein L34	Homo sapiens	177-204
35512188-3	2022	In a systematic analysis of 416 patients with t-MN and detailed prior exposure history, we found that TP53 mutations were significantly associated with prior treatment with thalidomide analogs, specifically lenalidomide.	Thalidomide	173-184	tumor protein p53	Homo sapiens	102-106
35143878-7	2022	Most strikingly, burn injury-induced pain symptoms and the activation of astrocytes were significantly suppressed by TNF inhibitor Thalidomide.	Thalidomide	131-142	tumor necrosis factor	Mus musculus	117-120
34989322-0	2022	Esco2 and cohesin regulate CRL4 ubiquitin ligase ddb1 expression and thalidomide teratogenicity.	Thalidomide	69-80	establishment of sister chromatid cohesion N-acetyltransferase 2	Homo sapiens	0-5
34989322-4	2022	Our results reveal that Esco2 and cohesin co-regulate the transcription of a component of CRL4 ubiquitin ligase through which thalidomide exerts teratogenic effects.	Thalidomide	126-137	establishment of sister chromatid cohesion N-acetyltransferase 2	Homo sapiens	24-29
34989322-4	2022	Our results reveal that Esco2 and cohesin co-regulate the transcription of a component of CRL4 ubiquitin ligase through which thalidomide exerts teratogenic effects.	Thalidomide	126-137	interleukin 17 receptor B	Homo sapiens	90-94
35045330-1	2022	Cereblon (CRBN) mediates the teratogenic effect of thalidomide in zebrafish, chicken, and humans.	Thalidomide	51-62	cereblon	Danio rerio	10-14
35083901-8	2022	The TM/DX treatment affected the CD4+ T cell subsets without suppressing the total CD4+ T cell population.	Thalidomide	4-6	CD4 molecule	Homo sapiens	33-36
35083901-10	2022	Increase in cell counts and median fluorescence intensity on CD11c+CD85k+ with TM/DX were observed.	Thalidomide	79-81	integrin subunit alpha X	Homo sapiens	61-66
35083901-10	2022	Increase in cell counts and median fluorescence intensity on CD11c+CD85k+ with TM/DX were observed.	Thalidomide	79-81	leukocyte immunoglobulin-like receptor, subfamily B, member 4A	Mus musculus	67-72
35141236-9	2021	We found an association between polymorphisms in TLR1/rs4833095, TLR2/rs3804099, TLR4/rs1927914, and TLR6/rs5783810 with the dose variation of thalidomide in a time-dependent manner, i.e., the association with the genetic variant and the dose of the drug was different depending on the moment of the treatment evaluated.	Thalidomide	143-154	toll like receptor 1	Homo sapiens	49-53
35141236-9	2021	We found an association between polymorphisms in TLR1/rs4833095, TLR2/rs3804099, TLR4/rs1927914, and TLR6/rs5783810 with the dose variation of thalidomide in a time-dependent manner, i.e., the association with the genetic variant and the dose of the drug was different depending on the moment of the treatment evaluated.	Thalidomide	143-154	toll like receptor 2	Homo sapiens	65-69
35141236-9	2021	We found an association between polymorphisms in TLR1/rs4833095, TLR2/rs3804099, TLR4/rs1927914, and TLR6/rs5783810 with the dose variation of thalidomide in a time-dependent manner, i.e., the association with the genetic variant and the dose of the drug was different depending on the moment of the treatment evaluated.	Thalidomide	143-154	toll like receptor 4	Homo sapiens	81-85
35141236-9	2021	We found an association between polymorphisms in TLR1/rs4833095, TLR2/rs3804099, TLR4/rs1927914, and TLR6/rs5783810 with the dose variation of thalidomide in a time-dependent manner, i.e., the association with the genetic variant and the dose of the drug was different depending on the moment of the treatment evaluated.	Thalidomide	143-154	toll like receptor 6	Homo sapiens	101-105
34978798-1	2022	The thalidomide analogue lenalidomide (Len) is a clinical therapeutic that alters the substrate engagement of cereblon (CRBN), a substrate receptor for the CRL4 E3 ubiquitin ligase.	Thalidomide	4-15	cereblon	Homo sapiens	120-124
34978798-1	2022	The thalidomide analogue lenalidomide (Len) is a clinical therapeutic that alters the substrate engagement of cereblon (CRBN), a substrate receptor for the CRL4 E3 ubiquitin ligase.	Thalidomide	4-15	interleukin 17 receptor B	Homo sapiens	156-160
34978798-3	2022	pLen preserves the substrate degradation profile, phenotypic antiproliferative and immunomodulatory properties of Len, and enhances interactions with the thalidomide-binding domain of CRBN, as revealed by binding site mapping and molecular modeling.	Thalidomide	154-165	cereblon	Homo sapiens	184-188