PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33907421-0	2021	Downregulation of Chemokine CCL20 Involved in Myeloma Cells Resistant to Elotuzumab and Lenalidomide.	Lenalidomide	88-100	C-C motif chemokine ligand 20	Homo sapiens	28-33
33839882-0	2021	Cereblon expression is a prognostic marker in newly diagnosed POEMS syndrome treated with lenalidomide plus dexamethasone.	Lenalidomide	90-102	cereblon	Homo sapiens	0-8
33839882-3	2021	Cereblon has been identified as the direct target of lenalidomide, and high cereblon expression is associated with better response and outcome to lenalidomide therapy in multiple myeloma patients.	Lenalidomide	53-65	cereblon	Homo sapiens	0-8
33839882-3	2021	Cereblon has been identified as the direct target of lenalidomide, and high cereblon expression is associated with better response and outcome to lenalidomide therapy in multiple myeloma patients.	Lenalidomide	146-158	cereblon	Homo sapiens	76-84
34025681-3	2021	Objective: To evaluate skin responses after treatment with low-dose lenalidomide plus dexamethasone and determine their relationship with vascular endothelial growth factor (VEGF) and hematological responses.	Lenalidomide	68-80	vascular endothelial growth factor A	Homo sapiens	138-172
34025681-3	2021	Objective: To evaluate skin responses after treatment with low-dose lenalidomide plus dexamethasone and determine their relationship with vascular endothelial growth factor (VEGF) and hematological responses.	Lenalidomide	68-80	vascular endothelial growth factor A	Homo sapiens	174-178
33989279-1	2021	Single-agent lenalidomide has modest activity in diffuse large B-cell lymphoma (DLBCL) and is thought to be more potent in activated B-cell (ABC) lymphomas, which are more treatment-resistant.	Lenalidomide	13-25	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	141-144
33989279-2	2021	However, the addition of lenalidomide to rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in randomized clinical trials has shown equivocal benefit, despite phase 2 studies that suggested otherwise.	Lenalidomide	25-37	DNA damage inducible transcript 3	Homo sapiens	118-122
33839882-7	2021	In conclusion, our results emphasized the role of cereblon mRNA expression as a unique biomarker for predicting the clinical response and outcome of lenalidomide-based therapy in newly diagnosed POEMS syndrome patients.	Lenalidomide	149-161	cereblon	Homo sapiens	50-58
34013974-8	2021	Interestingly, lenalidomide enhanced the expression of IRF4 and the co-stimulatory molecule CD86.	Lenalidomide	15-27	interferon regulatory factor 4	Homo sapiens	55-59
34013974-8	2021	Interestingly, lenalidomide enhanced the expression of IRF4 and the co-stimulatory molecule CD86.	Lenalidomide	15-27	CD86 molecule	Homo sapiens	92-96
34013974-10	2021	CD49d-negative CLL cases were more sensitive to lenalidomide treatment.	Lenalidomide	48-60	integrin subunit alpha 4	Homo sapiens	0-5
34003300-0	2022	Lenalidomide enhances the efficacy of anti-BCMA CAR-T treatment in relapsed/refractory multiple myeloma: a case report and revies of the literature.	Lenalidomide	0-12	TNF receptor superfamily member 17	Homo sapiens	43-47
34003300-0	2022	Lenalidomide enhances the efficacy of anti-BCMA CAR-T treatment in relapsed/refractory multiple myeloma: a case report and revies of the literature.	Lenalidomide	0-12	CXADR pseudogene 1	Homo sapiens	48-51
34003300-1	2022	We report successful clinical experience using anti-BCMA CAR-T combined with lenalidomide in a patient who was refractory to a previous CAR-T treatment.	Lenalidomide	77-89	CXADR pseudogene 1	Homo sapiens	136-139
33980611-7	2021	Genetic and pharmacological inhibition of EGR1 synergizes with the BRD4 inhibitor JQ1 or the type I interferon inducer lenalidomide in growth inhibition of ABC DLBCL both in cell cultures and xenograft mouse models.	Lenalidomide	119-131	early growth response 1	Mus musculus	42-46
33972500-0	2021	Lenalidomide downregulates ACE2 protein abundance to alleviate infection by SARS-CoV-2 spike protein conditioned pseudoviruses.	Lenalidomide	0-12	angiotensin converting enzyme 2	Homo sapiens	27-31
33972500-0	2021	Lenalidomide downregulates ACE2 protein abundance to alleviate infection by SARS-CoV-2 spike protein conditioned pseudoviruses.	Lenalidomide	0-12	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	87-92
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.	Lenalidomide	180-192	ALK receptor tyrosine kinase	Homo sapiens	91-94
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.	Lenalidomide	180-192	cereblon	Homo sapiens	124-128
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.	Lenalidomide	32-44	cereblon	Homo sapiens	131-135
33704530-7	2021	A slight increase of T-bet-positive TH1-equivalents was identifiable under lenalidomide.	Lenalidomide	75-87	T-box transcription factor 21	Homo sapiens	21-26
33704530-7	2021	A slight increase of T-bet-positive TH1-equivalents was identifiable under lenalidomide.	Lenalidomide	75-87	negative elongation factor complex member C/D	Homo sapiens	36-39
33623139-7	2021	We modulated IKAROS protein levels both by genetic manipulation and pharmacologically by treating CLL cells with lenalidomide and avadomide (IMIDs).	Lenalidomide	113-125	IKAROS family zinc finger 1	Homo sapiens	13-19
33877296-4	2021	Lenalidomide rapidly and transiently induced an activated T-cell phenotype, including HLA-DR, Tim-3, CD137, and programmed cell death protein 1 (PD-1) upregulation.	Lenalidomide	0-12	hepatitis A virus cellular receptor 2	Homo sapiens	94-99
33877296-4	2021	Lenalidomide rapidly and transiently induced an activated T-cell phenotype, including HLA-DR, Tim-3, CD137, and programmed cell death protein 1 (PD-1) upregulation.	Lenalidomide	0-12	TNF receptor superfamily member 9	Homo sapiens	101-106
33877296-4	2021	Lenalidomide rapidly and transiently induced an activated T-cell phenotype, including HLA-DR, Tim-3, CD137, and programmed cell death protein 1 (PD-1) upregulation.	Lenalidomide	0-12	programmed cell death 1	Homo sapiens	112-143
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	43-46
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33885752-12	2021	Lenalidomide also synergized with HexaBody-DR5/DR5, but only via its immunomodulatory effects, presumably by enhancing the antibody-dependent cellular cytotoxicity activity of HexaBody-DR5/DR5.	Lenalidomide	0-12	TNF receptor superfamily member 10b	Homo sapiens	47-50
33925565-9	2021	Moreover, combination of LAG-3 with the immunomodulatory drug (IMiD) lenalidomide significantly increased IL-2 production by T cells and antibody-dependent cytotoxicity (ADCC) mediated by NK cells.	Lenalidomide	69-81	lymphocyte activating 3	Homo sapiens	25-30
33925565-9	2021	Moreover, combination of LAG-3 with the immunomodulatory drug (IMiD) lenalidomide significantly increased IL-2 production by T cells and antibody-dependent cytotoxicity (ADCC) mediated by NK cells.	Lenalidomide	69-81	interleukin 2	Homo sapiens	106-110
33907421-9	2021	Conclusion: The expression of CCL20 was decreased in lenalidomide and Elotuzumab resistant U266 cells and in RRMM patients.	Lenalidomide	53-65	C-C motif chemokine ligand 20	Homo sapiens	30-35
33907421-10	2021	CCL20 could therefore possibly increase the sensitivity of lenalidomide and Elotuzumab.	Lenalidomide	59-71	C-C motif chemokine ligand 20	Homo sapiens	0-5
33621109-2	2021	Phase II studies demonstrated that adding the immunomodulatory agent lenalidomide to R-CHOP improved outcomes in ABC-type DLBCL.	Lenalidomide	69-81	DNA damage inducible transcript 3	Homo sapiens	87-91
33555941-1	2021	PURPOSE: Lenalidomide combined with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) (R2CHOP) in untreated diffuse large B-cell lymphoma (DLBCL) has shown promising activity, particularly in the activated B-cell-like (ABC) subtype.	Lenalidomide	9-21	DNA damage inducible transcript 3	Homo sapiens	113-117
33621109-3	2021	The goal of the global, phase III ROBUST study was to compare lenalidomide plus R-CHOP (R2-CHOP) with placebo/R-CHOP in previously untreated, ABC-type DLBCL.	Lenalidomide	62-74	ribonucleotide reductase regulatory subunit M2	Homo sapiens	88-95
33444079-3	2021	In combination with R-CHOP (R2-CHOP), lenalidomide has an acceptable level of toxicity and may mitigate the negative prognosis of the non-germinal center B-cell-like phenotype.	Lenalidomide	38-50	DNA damage inducible transcript 3	Homo sapiens	31-35
33856277-2	2021	Ibrutinib and lenalidomide are synergistic in vitro in ABC DLBCL and may augment salvage chemotherapy.	Lenalidomide	14-26	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	55-58
33733978-6	2021	The combination of lenalidomide plus dexamethasone with an anti-CD38 MoAb such as daratumumab and a proteasome inhibitor such as bortezomib is currently one of the most potent first line treatment regimens for MM.	Lenalidomide	19-31	CD38 molecule	Homo sapiens	64-68
34007370-10	2021	Due to MYC-positivity, lenalidomide was added to the therapy regimen.	Lenalidomide	23-35	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	7-10
34007370-12	2021	Lenalidomide is an oral immunomodulatory drug that downregulates MYC gene and is commonly used in patients with multiple myeloma.	Lenalidomide	0-12	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	65-68
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	39-51	erythropoietin receptor	Homo sapiens	74-97
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	39-51	erythropoietin	Homo sapiens	165-172
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	39-51	erythropoietin	Homo sapiens	174-177
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	39-51	erythropoietin	Homo sapiens	74-88
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	53-56	erythropoietin receptor	Homo sapiens	74-97
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	53-56	erythropoietin	Homo sapiens	165-172
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	53-56	erythropoietin	Homo sapiens	174-177
33439748-2	2021	We investigated whether treatment with lenalidomide (LEN), which augments erythropoietin receptor signaling in vitro, can restore and improve hemoglobin response to epoetin (EPO) alfa in patients with lower-risk, non-del(5q) MDS who have anemia that is refractory to or have low probability of benefit from treatment with recombinant erythropoietin.	Lenalidomide	53-56	erythropoietin	Homo sapiens	74-88
33139584-6	2021	The anti-PD-L1 effects on multiple myeloma may be related to a decrease in the immunosuppressive myeloidderived suppressor cells (MDSCs), but there were no changes in the splenic MDSCs after combined treatment with lenalidomide and the anti-PD-L1 antibody.	Lenalidomide	215-227	CD274 antigen	Mus musculus	9-14
33757580-3	2021	Cereblon (CRBN) is a key mediator of the bioactivities of IMiDs such as lenalidomide.	Lenalidomide	72-84	cereblon	Homo sapiens	10-14
33757580-7	2021	METHODS: We established lenalidomide-resistant cells by knocking down CRBN with RNAi-mediated downregulation or knocking out CRBN using CRISPR-Cas9 in MM cells.	Lenalidomide	24-36	cereblon	Homo sapiens	70-74
33757580-12	2021	CRBN-deficient cells showed lenalidomide-induced upregulation of phosphorylated glycogen synthase kinase-3 (p-GSK-3) and c-Myc phosphorylation.	Lenalidomide	28-40	cereblon	Homo sapiens	0-4
33757580-12	2021	CRBN-deficient cells showed lenalidomide-induced upregulation of phosphorylated glycogen synthase kinase-3 (p-GSK-3) and c-Myc phosphorylation.	Lenalidomide	28-40	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	121-126
33757580-15	2021	The dual HDAC and PI3K inhibitor, CUDC-907, exhibited cytotoxic and immunotherapy-enhancing effects in MM cells, including multi-drug-resistant lines and primary cells from lenalidomide-resistant patients.	Lenalidomide	173-185	histone deacetylase 9	Homo sapiens	9-13
33746969-3	2021	In the absence of myeloma cells, lenalidomide and pomalidomide induce CD4+ T cell secretion of IL-2 and indirect activation of Natural Killer (NK) cells.	Lenalidomide	33-45	CD4 molecule	Homo sapiens	70-73
33746969-3	2021	In the absence of myeloma cells, lenalidomide and pomalidomide induce CD4+ T cell secretion of IL-2 and indirect activation of Natural Killer (NK) cells.	Lenalidomide	33-45	interleukin 2	Homo sapiens	95-99
33534410-2	2021	Lenalidomide prevents the proliferation of multiple myeloma cells through binding to cereblon and promoting the ubiquitinational degradation of IKZF1 (Ikaros)/IKZF3 (Aiolos).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	144-149
33534410-2	2021	Lenalidomide prevents the proliferation of multiple myeloma cells through binding to cereblon and promoting the ubiquitinational degradation of IKZF1 (Ikaros)/IKZF3 (Aiolos).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	151-157
33534410-2	2021	Lenalidomide prevents the proliferation of multiple myeloma cells through binding to cereblon and promoting the ubiquitinational degradation of IKZF1 (Ikaros)/IKZF3 (Aiolos).	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	159-164
33534410-2	2021	Lenalidomide prevents the proliferation of multiple myeloma cells through binding to cereblon and promoting the ubiquitinational degradation of IKZF1 (Ikaros)/IKZF3 (Aiolos).	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	166-172
33563611-8	2021	Lenalidomide is known to exert its beneficial effects by modulating the CRBN-CRL4 E3 ligase to ubiquitinate and degrade the transcription factor IKAROS family zinc finger 1 (IKZF1).	Lenalidomide	0-12	cereblon	Homo sapiens	72-76
33563611-8	2021	Lenalidomide is known to exert its beneficial effects by modulating the CRBN-CRL4 E3 ligase to ubiquitinate and degrade the transcription factor IKAROS family zinc finger 1 (IKZF1).	Lenalidomide	0-12	interleukin 17 receptor B	Homo sapiens	77-81
33563611-8	2021	Lenalidomide is known to exert its beneficial effects by modulating the CRBN-CRL4 E3 ligase to ubiquitinate and degrade the transcription factor IKAROS family zinc finger 1 (IKZF1).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	145-172
33563611-8	2021	Lenalidomide is known to exert its beneficial effects by modulating the CRBN-CRL4 E3 ligase to ubiquitinate and degrade the transcription factor IKAROS family zinc finger 1 (IKZF1).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	174-179
33563611-9	2021	In M2-like MAMs, we observed enhanced IKZF1 levels that vanished through treatment with lenalidomide, yielding MAMs with a bioenergetic profile, T-cell stimulatory properties, and loss of tumor-promoting capabilities that resemble M1 cells.	Lenalidomide	88-100	IKAROS family zinc finger 1	Homo sapiens	38-43
32779949-5	2020	Here we report the design, synthesis, and evaluation of a proteolysis targeting chimaera (PROTAC) based on the combination of PARP-1 inhibitor olaparib and the CRBN (cereblon) ligand lenalidomide.	Lenalidomide	183-195	cereblon	Homo sapiens	160-164
33408186-4	2021	We developed ON and OFF switches for CAR T cells using the clinically approved drug lenalidomide, which mediates the proteasomal degradation of several target proteins by inducing interactions between the CRL4CRBN E3 ubiquitin ligase and a C2H2 zinc finger degron motif.	Lenalidomide	84-96	nuclear receptor subfamily 1 group I member 3	Homo sapiens	37-40
33408186-7	2021	Subtherapeutic lenalidomide concentrations controlled the effector functions of ON- and OFF-switch CAR T cells.	Lenalidomide	15-27	nuclear receptor subfamily 1 group I member 3	Homo sapiens	99-102
33357426-9	2020	PC4 knockdown in human B cell lymphoma and myeloma cells reduces IKAROS protein as an anticancer drug, lenalidomide.	Lenalidomide	103-115	SUB1 regulator of transcription	Homo sapiens	0-3
33357426-9	2020	PC4 knockdown in human B cell lymphoma and myeloma cells reduces IKAROS protein as an anticancer drug, lenalidomide.	Lenalidomide	103-115	IKAROS family zinc finger 1	Homo sapiens	65-71
33284947-4	2020	The 5 analyzed proteins involved in lenalidomide"s mode of action were associated with time to progression (TTP); low levels of cereblon and IRF4 protein and high levels of Ikaros, AGO2, and Aiolos were significantly associated with shorter TTP.	Lenalidomide	36-48	interferon regulatory factor 4	Homo sapiens	141-145
33284947-4	2020	The 5 analyzed proteins involved in lenalidomide"s mode of action were associated with time to progression (TTP); low levels of cereblon and IRF4 protein and high levels of Ikaros, AGO2, and Aiolos were significantly associated with shorter TTP.	Lenalidomide	36-48	IKAROS family zinc finger 1	Homo sapiens	173-179
33284947-4	2020	The 5 analyzed proteins involved in lenalidomide"s mode of action were associated with time to progression (TTP); low levels of cereblon and IRF4 protein and high levels of Ikaros, AGO2, and Aiolos were significantly associated with shorter TTP.	Lenalidomide	36-48	argonaute RISC catalytic component 2	Homo sapiens	181-185
33284947-4	2020	The 5 analyzed proteins involved in lenalidomide"s mode of action were associated with time to progression (TTP); low levels of cereblon and IRF4 protein and high levels of Ikaros, AGO2, and Aiolos were significantly associated with shorter TTP.	Lenalidomide	36-48	IKAROS family zinc finger 3	Homo sapiens	191-197
33273169-7	2020	Agents such as the Bruton tyrosine kinase (BTK) inhibitor ibrutinib or immunomodulatory drugs such as lenalidomide and pomalidomide have shown promising response rates in the relapsed setting.	Lenalidomide	102-114	Bruton tyrosine kinase	Homo sapiens	43-46
33256379-0	2020	Treatment of patients with MYC rearrangement positive large B-cell lymphoma with R-CHOP plus lenalidomide: results of a multicenter HOVON phase II trial.	Lenalidomide	93-105	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-30
33256379-3	2020	Lenalidomide is an oral immunomodulatory drug which downregulates MYC and its target genes thereby providing support using lenalidomide as additional therapeutic option for MYC+ LBCL.	Lenalidomide	0-12	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	66-69
33256379-3	2020	Lenalidomide is an oral immunomodulatory drug which downregulates MYC and its target genes thereby providing support using lenalidomide as additional therapeutic option for MYC+ LBCL.	Lenalidomide	0-12	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	173-176
33256379-3	2020	Lenalidomide is an oral immunomodulatory drug which downregulates MYC and its target genes thereby providing support using lenalidomide as additional therapeutic option for MYC+ LBCL.	Lenalidomide	123-135	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	66-69
33256379-3	2020	Lenalidomide is an oral immunomodulatory drug which downregulates MYC and its target genes thereby providing support using lenalidomide as additional therapeutic option for MYC+ LBCL.	Lenalidomide	123-135	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	173-176
33256379-4	2020	A phase II trial was conducted evaluating the efficacy of lenalidomide (15 mg day 1-14) in combination with R-CHOP (R2CHOP) in newly diagnosed MYC+ LBCL patients identified through a nationwide MYC-FISH screening program.	Lenalidomide	58-70	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	143-146
33085797-1	2021	Carfilzomib-lenalidomide-dexamethasone (KRd) has been approved for the treatment of relapsed/refractory multiple myeloma (RRMM).	Lenalidomide	12-24	calcium responsive transcription factor	Homo sapiens	0-11
33375215-4	2020	Personalized low dose rIL-2 in combination with either lenalidomide or venetoclax mediates natural killer stimulation and is an effective non-toxic immunotherapy administered in the outpatient setting for poor prognosis CLL.	Lenalidomide	55-67	interleukin 2	Rattus norvegicus	22-27
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	caspase 8	Homo sapiens	100-106
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	cereblon	Homo sapiens	177-181
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	IKAROS family zinc finger 1	Homo sapiens	218-223
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	145-157	IKAROS family zinc finger 3	Homo sapiens	228-233
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	caspase 8	Homo sapiens	100-106
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	cereblon	Homo sapiens	177-181
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	IKAROS family zinc finger 1	Homo sapiens	218-223
33392195-7	2020	Using myeloma as a model system, we further revealed that either inhibition or genetic depletion of CASP-8 enhances the anti-myeloma activity of lenalidomide (Len) by impairing CRBN cleavage, leading to the attenuated IKZF1 and IKZF3 protein levels and the reduced viability of myeloma cell lines and primary myeloma cells from patients.	Lenalidomide	159-162	IKAROS family zinc finger 3	Homo sapiens	228-233
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	110-116
33392195-8	2020	The present study discovered that the stability of the substrate receptor of an E3 ligase can be modulated by CASP-8 and suggested that administration of CASP-8 inhibitors enhances the overall effectiveness of Len-based combination therapy in myeloma.	Lenalidomide	210-213	caspase 8	Homo sapiens	154-160
32779949-5	2020	Here we report the design, synthesis, and evaluation of a proteolysis targeting chimaera (PROTAC) based on the combination of PARP-1 inhibitor olaparib and the CRBN (cereblon) ligand lenalidomide.	Lenalidomide	183-195	cereblon	Homo sapiens	166-174
33227124-1	2020	The immunomodulatory drugs lenalidomide and pomalidomide enhance the potency of AMG 701 in multiple myeloma preclinical models.	Lenalidomide	27-39	amelogenin X-linked	Homo sapiens	80-83
32852308-4	2020	Also the SLAMF7-targeting antibody, elotuzumab, improves the survival of relapsed/refractory multiple myeloma patients, when it is combined with either lenalidomide or pomalidomide.	Lenalidomide	152-164	SLAM family member 7	Homo sapiens	9-15
33124184-9	2020	Lenalidomide non-significantly decreased the level of CD8+ T cells but increased CD4+ T cells leading to increased CD4+ /CD8+ T cell ratio.	Lenalidomide	0-12	CD8a molecule	Homo sapiens	54-57
33124184-9	2020	Lenalidomide non-significantly decreased the level of CD8+ T cells but increased CD4+ T cells leading to increased CD4+ /CD8+ T cell ratio.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	81-84
33124184-9	2020	Lenalidomide non-significantly decreased the level of CD8+ T cells but increased CD4+ T cells leading to increased CD4+ /CD8+ T cell ratio.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	115-118
33124184-9	2020	Lenalidomide non-significantly decreased the level of CD8+ T cells but increased CD4+ T cells leading to increased CD4+ /CD8+ T cell ratio.	Lenalidomide	0-12	CD8a molecule	Homo sapiens	121-124
32932183-9	2020	Our data shows that lenalidomide alleviated rotenone-induced motor impairments and deficits in dopamine-related behaviors and resulted in increased levels of tumor necrosis factor-alpha and calcium-binding protein B in the SNpc.	Lenalidomide	20-32	tumor necrosis factor	Rattus norvegicus	158-185
32958952-6	2020	Pomalidomide is more effective than lenalidomide in degrading ARID2 and is capable of inhibiting MYC expression and proliferation in lenalidomide-resistant cell lines.	Lenalidomide	36-48	AT-rich interaction domain 2	Homo sapiens	62-67
32958952-6	2020	Pomalidomide is more effective than lenalidomide in degrading ARID2 and is capable of inhibiting MYC expression and proliferation in lenalidomide-resistant cell lines.	Lenalidomide	133-145	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	97-100
32958952-8	2020	These findings suggest that ARID2 is a promising target for overcoming lenalidomide resistance in patients with multiple myeloma.	Lenalidomide	71-83	AT-rich interaction domain 2	Homo sapiens	28-33
32932183-10	2020	Moreover, chronic lenalidomide treatment resulted increase in transforming growth factor immunoreactivity and brain derived neurotrophic factor expression in the SNPc.	Lenalidomide	18-30	brain-derived neurotrophic factor	Rattus norvegicus	110-143
32350909-0	2020	Clinical benefit of ixazomib plus lenalidomide-dexamethasone in myeloma patients with non-canonical NF-kappaB pathway activation.	Lenalidomide	34-46	nuclear factor kappa B subunit 1	Homo sapiens	100-109
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.	Lenalidomide	119-131	cereblon	Homo sapiens	0-8
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.	Lenalidomide	119-131	cereblon	Homo sapiens	10-14
33190445-0	2020	[Lenalidomide for myelodysplastic syndrome with excess blasts with germline DDX41 mutation: a case report and literatures review].	Lenalidomide	1-13	DEAD-box helicase 41	Homo sapiens	76-81
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.	Lenalidomide	187-199	mitogen-activated protein kinase kinase kinase 12	Homo sapiens	9-12
32704173-1	2020	BACKGROUND: Purpose: The combination of a mammalian target of rapamycin inhibitor and lenalidomide showed enhanced preclinical cytotoxicity.	Lenalidomide	86-98	mechanistic target of rapamycin kinase	Homo sapiens	42-71
32669063-5	2020	In RRMM, the annual budget savings of lenalidomide entry were estimated at EGP-(-1,103,969, -3,362,793 and -5,949,228) at year 1, year 2 and year 3 respectively.	Lenalidomide	38-50	tumor associated calcium signal transducer 2	Homo sapiens	75-82
32843459-4	2020	Given how aggressive and difficult to treat ALK+ LBCL is, further research is warranted to more completely elucidate the mechanism of action of lenalidomide in ALK+ LBCL and its role in treatment.	Lenalidomide	144-156	ALK receptor tyrosine kinase	Homo sapiens	44-47
32982239-0	2020	Nanomicellar Lenalidomide-Fenretinide Combination Suppresses Tumor Growth in an MYCN Amplified Neuroblastoma Tumor.	Lenalidomide	13-25	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	80-84
32982239-1	2020	Purpose: In a previous study, we demonstrated that the combination of fenretinide with lenalidomide, administered by a novel nanomicellar formulation (FLM), provided a strong antitumor effect in a neuroblastoma TrkB-expressing tumor.	Lenalidomide	87-99	neurotrophic receptor tyrosine kinase 2	Homo sapiens	211-215
32761232-4	2020	Both lenalidomide and pomalidomide dose-dependently inhibited interleukin-12 (IL-12) and TNF production and STAT4 expression, and enhanced IL-10 production in response to LPS.	Lenalidomide	5-17	tumor necrosis factor	Homo sapiens	89-92
32761232-4	2020	Both lenalidomide and pomalidomide dose-dependently inhibited interleukin-12 (IL-12) and TNF production and STAT4 expression, and enhanced IL-10 production in response to LPS.	Lenalidomide	5-17	signal transducer and activator of transcription 4	Homo sapiens	108-113
32761232-4	2020	Both lenalidomide and pomalidomide dose-dependently inhibited interleukin-12 (IL-12) and TNF production and STAT4 expression, and enhanced IL-10 production in response to LPS.	Lenalidomide	5-17	interleukin 10	Homo sapiens	139-144
32761232-6	2020	In 46 myeloma patients, serum CCL17 levels at the onset of lenalidomide-associated rash were significantly higher than those without rashes during lenalidomide treatment and those before treatment.	Lenalidomide	59-71	C-C motif chemokine ligand 17	Homo sapiens	30-35
32761232-6	2020	In 46 myeloma patients, serum CCL17 levels at the onset of lenalidomide-associated rash were significantly higher than those without rashes during lenalidomide treatment and those before treatment.	Lenalidomide	147-159	C-C motif chemokine ligand 17	Homo sapiens	30-35
32761232-7	2020	Furthermore, serum CCL17 levels in patients who achieved a very good partial response (VGPR) were significantly higher compared with a less than VGPR during lenalidomide treatment.	Lenalidomide	157-169	C-C motif chemokine ligand 17	Homo sapiens	19-24
32618603-0	2020	A Case of Lenalidomide-Associated Papulopustular Rash: Beyond the Epidermal Growth Factor Receptor Inhibitor Spectrum.	Lenalidomide	10-22	epidermal growth factor receptor	Homo sapiens	66-98
32898244-0	2020	The immunomodulatory drugs lenalidomide and pomalidomide enhance the potency of AMG 701 in multiple myeloma preclinical models.	Lenalidomide	27-39	amelogenin X-linked	Homo sapiens	80-83
32632752-4	2020	While lenalidomide and pomalidomide induced greater degradation of Ikaros and Aiolos in myeloma cells, BTX306 more potently reduced levels of GSPT1, eRF1, CK1alpha, MCL-1, and c-MYC.	Lenalidomide	6-18	IKAROS family zinc finger 1	Mus musculus	67-73
32632752-4	2020	While lenalidomide and pomalidomide induced greater degradation of Ikaros and Aiolos in myeloma cells, BTX306 more potently reduced levels of GSPT1, eRF1, CK1alpha, MCL-1, and c-MYC.	Lenalidomide	6-18	IKAROS family zinc finger 3	Mus musculus	78-84
32591583-0	2020	Development of Label-Free Impedimetric Immunosensors for IKZF1 and IKZF3 Femtomolar Detection for Monitoring Multiple Myeloma Patients Treated with Lenalidomide.	Lenalidomide	148-160	IKAROS family zinc finger 3	Homo sapiens	67-72
32591583-2	2020	Lenalidomide destroys MM cells by inducing ubiquitination and the consequent degradation of Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	92-134
32591583-2	2020	Lenalidomide destroys MM cells by inducing ubiquitination and the consequent degradation of Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	136-141
32591583-2	2020	Lenalidomide destroys MM cells by inducing ubiquitination and the consequent degradation of Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	146-151
32591583-3	2020	High expression of IKZF1 and IKZF3 in MM results in less sensitivity to lenalidomide treatment and possible cytotoxic effect.	Lenalidomide	72-84	IKAROS family zinc finger 1	Homo sapiens	19-24
32591583-3	2020	High expression of IKZF1 and IKZF3 in MM results in less sensitivity to lenalidomide treatment and possible cytotoxic effect.	Lenalidomide	72-84	IKAROS family zinc finger 3	Homo sapiens	29-34
32317208-0	2020	Discovery and biological evaluation of proteolysis targeting chimeras (PROTACs) as an EGFR degraders based on osimertinib and lenalidomide.	Lenalidomide	126-138	epidermal growth factor receptor	Homo sapiens	86-90
32843459-4	2020	Given how aggressive and difficult to treat ALK+ LBCL is, further research is warranted to more completely elucidate the mechanism of action of lenalidomide in ALK+ LBCL and its role in treatment.	Lenalidomide	144-156	ALK receptor tyrosine kinase	Homo sapiens	160-163
32419317-4	2020	METHODS: An ALF and AKI mouse model was generated using LPS/D-Gal, and a TNF-alpha inhibitor, CC-5013, was used to treat the mice.	Lenalidomide	94-101	tumor necrosis factor	Mus musculus	73-82
32419317-7	2020	RESULTS: Treatment with CC-5013 decreased the activation of TNF-alpha/HMGB1 pathway and pyroptosis in the treated mice and cells compared with the control mice and cells.	Lenalidomide	24-31	tumor necrosis factor	Mus musculus	60-69
32419317-7	2020	RESULTS: Treatment with CC-5013 decreased the activation of TNF-alpha/HMGB1 pathway and pyroptosis in the treated mice and cells compared with the control mice and cells.	Lenalidomide	24-31	high mobility group box 1	Mus musculus	70-75
32437909-1	2020	Our previous study revealed that expression of G protein-coupled receptor 68 (GPR68) was upregulated in MDSL cells, a cell line representing Myelodysplastic Syndromes (MDS), in response to lenalidomide (LEN), and mediated a calcium/calpain proapoptotic pathway.	Lenalidomide	189-201	G protein-coupled receptor 68	Homo sapiens	47-76
32437909-1	2020	Our previous study revealed that expression of G protein-coupled receptor 68 (GPR68) was upregulated in MDSL cells, a cell line representing Myelodysplastic Syndromes (MDS), in response to lenalidomide (LEN), and mediated a calcium/calpain proapoptotic pathway.	Lenalidomide	189-201	G protein-coupled receptor 68	Homo sapiens	78-83
32437909-1	2020	Our previous study revealed that expression of G protein-coupled receptor 68 (GPR68) was upregulated in MDSL cells, a cell line representing Myelodysplastic Syndromes (MDS), in response to lenalidomide (LEN), and mediated a calcium/calpain proapoptotic pathway.	Lenalidomide	203-206	G protein-coupled receptor 68	Homo sapiens	47-76
32437909-1	2020	Our previous study revealed that expression of G protein-coupled receptor 68 (GPR68) was upregulated in MDSL cells, a cell line representing Myelodysplastic Syndromes (MDS), in response to lenalidomide (LEN), and mediated a calcium/calpain proapoptotic pathway.	Lenalidomide	203-206	G protein-coupled receptor 68	Homo sapiens	78-83
32437909-8	2020	Our study suggests a novel mechanism of action of LEN in mediating cytotoxicity in MDS/AML via upregulating RCAN1 thus inhibiting the CaN prosurvival pathway.	Lenalidomide	50-53	regulator of calcineurin 1	Homo sapiens	108-113
32064987-6	2020	This analysis suggests patients with lower EPO levels experience the strongest benefit from lenalidomide.	Lenalidomide	92-104	erythropoietin	Homo sapiens	43-46
32321757-5	2020	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb-mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Lenalidomide	49-61	IKAROS family zinc finger 3	Homo sapiens	29-34
32321757-5	2020	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb-mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Lenalidomide	49-61	IKAROS family zinc finger 3	Homo sapiens	74-79
32321757-5	2020	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb-mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Lenalidomide	49-61	CD28 molecule	Homo sapiens	105-109
32321757-5	2020	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb-mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Lenalidomide	49-61	interleukin 10	Homo sapiens	136-141
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.	Lenalidomide	13-25	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.	Lenalidomide	13-25	IKAROS family zinc finger 3	Homo sapiens	117-123
32251398-8	2020	Megakaryocytic gene-promoter analyses suggested that LEN-induced degradation of IKZF1 enables a RUNX1-GATA2 complex to drive megakaryocytic differentiation.	Lenalidomide	53-56	RUNX family transcription factor 1	Homo sapiens	96-101
32251398-8	2020	Megakaryocytic gene-promoter analyses suggested that LEN-induced degradation of IKZF1 enables a RUNX1-GATA2 complex to drive megakaryocytic differentiation.	Lenalidomide	53-56	GATA binding protein 2	Homo sapiens	102-107
32466489-8	2020	The CRBN-targeting immunomodulatory drug lenalidomide and the cullin E3 ligase inhibitor MLN4924 promotes and attenuates, respectively, proteasomal degradation of ClC-2.	Lenalidomide	41-53	cereblon	Homo sapiens	4-8
32466489-8	2020	The CRBN-targeting immunomodulatory drug lenalidomide and the cullin E3 ligase inhibitor MLN4924 promotes and attenuates, respectively, proteasomal degradation of ClC-2.	Lenalidomide	41-53	chloride voltage-gated channel 2	Homo sapiens	163-168
32397113-3	2020	The computer inferred genomic abnormalities associating with lenalidomide treatment response in non-del(5q) MDS to include trisomy 8, del(20q), or RUNX1 loss of function mutations.	Lenalidomide	61-73	RUNX family transcription factor 1	Homo sapiens	147-152
32397113-4	2020	Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification.	Lenalidomide	39-51	splicing factor 3b subunit 1	Homo sapiens	113-118
32397113-4	2020	Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification.	Lenalidomide	39-51	tet methylcytosine dioxygenase 2	Homo sapiens	120-124
32397113-4	2020	Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification.	Lenalidomide	39-51	Wnt family member 3A	Homo sapiens	126-131
32397113-4	2020	Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification.	Lenalidomide	39-51	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	147-151
32397113-4	2020	Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification.	Lenalidomide	39-51	presenilin 2	Homo sapiens	174-179
32435618-6	2020	Among the novel anti-myeloma IT-based agents, anti-CD38 monoclonal antibodies (mAbs) are now becoming the new backbone of treatment for NTE patients, in association with lenalidomide and dexamethasone.	Lenalidomide	170-182	CD38 molecule	Homo sapiens	51-55
32248251-11	2020	Thus, VMP induction therapy followed by Rd consolidation and lenalidomide maintenance is considered a well-tolerated and effective regimen in transplant-ineligible NDMM.	Lenalidomide	61-73	neurensin 1	Homo sapiens	6-9
32323826-10	2020	Western blot analysis and RT-qPCR revealed that p53 activation and the expression of p21 were increased in glioma cells treated with lenalidomide.	Lenalidomide	133-145	tumor protein p53	Homo sapiens	48-51
32323826-10	2020	Western blot analysis and RT-qPCR revealed that p53 activation and the expression of p21 were increased in glioma cells treated with lenalidomide.	Lenalidomide	133-145	H3 histone pseudogene 16	Homo sapiens	85-88
32373374-5	2020	Lenalidomide, an immunosuppressant, inhibits TNF.	Lenalidomide	0-12	tumor necrosis factor	Homo sapiens	45-48
32411498-2	2020	We have previously found that GPR68 induces a proapoptotic pathway in bone marrow (BM) cells from the patients with myelodysplastic syndromes (MDS) after treated with lenalidomide.	Lenalidomide	167-179	G protein-coupled receptor 68	Homo sapiens	30-35
31702836-0	2020	Lenalidomide maintenance for diffuse large B-cell lymphoma patients responding to R-CHOP: quality of life, dosing, and safety results from the randomised controlled REMARC study.	Lenalidomide	0-12	DNA damage inducible transcript 3	Homo sapiens	84-88
31746254-0	2020	Cereblon (CRBN) gene polymorphisms predict clinical response and progression-free survival in relapsed/refractory multiple myeloma patients treated with lenalidomide: a pharmacogenetic study from the IMMEnSE consortium.	Lenalidomide	153-165	cereblon	Homo sapiens	0-8
32251398-3	2020	TP53 mutations are detected in ~20% of LEN-resistant patients3.	Lenalidomide	39-42	tumor protein p53	Homo sapiens	0-4
32251398-8	2020	Megakaryocytic gene-promoter analyses suggested that LEN-induced degradation of IKZF1 enables a RUNX1-GATA2 complex to drive megakaryocytic differentiation.	Lenalidomide	53-56	IKAROS family zinc finger 1	Homo sapiens	80-85
31804723-5	2020	To test whether LEN-induced mitochondrial priming predicted clinical response to LEN-MEC therapy, we performed DBP on patient myeloblasts.	Lenalidomide	16-19	C-C motif chemokine ligand 28	Homo sapiens	85-88
31289205-10	2020	Three kinases inhibitors (CHK1i, MELKi and PBKi) overcome resistance to Lenalidomide, while CHK1, PBK and DBF4 inhibitors re-sensitized Melphalan resistant cell line to this conventional therapeutic agent.	Lenalidomide	72-84	checkpoint kinase 1	Homo sapiens	26-30
31289205-10	2020	Three kinases inhibitors (CHK1i, MELKi and PBKi) overcome resistance to Lenalidomide, while CHK1, PBK and DBF4 inhibitors re-sensitized Melphalan resistant cell line to this conventional therapeutic agent.	Lenalidomide	72-84	PDZ binding kinase	Homo sapiens	43-46
31746254-0	2020	Cereblon (CRBN) gene polymorphisms predict clinical response and progression-free survival in relapsed/refractory multiple myeloma patients treated with lenalidomide: a pharmacogenetic study from the IMMEnSE consortium.	Lenalidomide	153-165	cereblon	Homo sapiens	10-14
31746254-2	2020	The objective of this study was to verify whether germline single nucleotide polymorphisms (SNPs) in the CRBN gene may influence response to lenalidomide in multiple myeloma (MM).	Lenalidomide	141-153	cereblon	Homo sapiens	105-109
31746254-3	2020	Fourteen tagging SNPs covering the genetic variability in the CRBN gene region were genotyped in 167 Polish patients with refractory/relapsed MM treated with lenalidomide-based regimens.	Lenalidomide	158-170	cereblon	Homo sapiens	62-66
31746254-6	2020	It is suggested that selected germline CRBN allelic variants (rs1714327G > C and rs1705814T > C) affect lenalidomide efficacy in patients with relapsed/refractory MM.	Lenalidomide	104-116	cereblon	Homo sapiens	39-43
31963193-13	2020	IMiDs decreased TLR4-induced mediator release; this effect was stronger for pomalidomide than for lenalidomide and especially thalidomide.	Lenalidomide	98-110	toll like receptor 4	Homo sapiens	16-20
31400013-0	2020	Successful lenalidomide treatment in high risk myelodysplastic syndrome with germline DDX41 mutation.	Lenalidomide	11-23	DEAD-box helicase 41	Homo sapiens	86-91
31672767-10	2020	CONCLUSIONS: This study showed that blockade of the CXCR4-CXCL12 axis by ulocuplumab is safe with acceptable AEs and leads to a high response rate in combination with lenalidomide and dexamethasone in patients with relapsed/refractory myeloma, making CXCR4 inhibitors a promising class of antimyeloma drugs that should be further explored in clinical trials.	Lenalidomide	167-179	C-X-C motif chemokine receptor 4	Homo sapiens	52-57
32759572-8	2020	Administration of lenalidomide prevented the LPS-triggered activation of MM cells by targeting CD180.	Lenalidomide	18-30	CD180 molecule	Homo sapiens	95-100
31672767-10	2020	CONCLUSIONS: This study showed that blockade of the CXCR4-CXCL12 axis by ulocuplumab is safe with acceptable AEs and leads to a high response rate in combination with lenalidomide and dexamethasone in patients with relapsed/refractory myeloma, making CXCR4 inhibitors a promising class of antimyeloma drugs that should be further explored in clinical trials.	Lenalidomide	167-179	C-X-C motif chemokine ligand 12	Homo sapiens	58-64
32984863-2	2020	Lenalidomide interacts with cereblon (CRBN), a component of the CRL4CRBN E3 ubiquitin ligase complex, leading to ubiquitination and subsequent degradation of substrates, such as transcription factor Ikaros (Ikaros family zinc finger 1, IKZF1).	Lenalidomide	0-12	cereblon	Homo sapiens	38-42
32984863-2	2020	Lenalidomide interacts with cereblon (CRBN), a component of the CRL4CRBN E3 ubiquitin ligase complex, leading to ubiquitination and subsequent degradation of substrates, such as transcription factor Ikaros (Ikaros family zinc finger 1, IKZF1).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	199-205
32984863-2	2020	Lenalidomide interacts with cereblon (CRBN), a component of the CRL4CRBN E3 ubiquitin ligase complex, leading to ubiquitination and subsequent degradation of substrates, such as transcription factor Ikaros (Ikaros family zinc finger 1, IKZF1).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	207-234
32984863-2	2020	Lenalidomide interacts with cereblon (CRBN), a component of the CRL4CRBN E3 ubiquitin ligase complex, leading to ubiquitination and subsequent degradation of substrates, such as transcription factor Ikaros (Ikaros family zinc finger 1, IKZF1).	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	236-241
32984863-5	2020	Depletion of G protein-coupled receptor 68 (GPR68) or an endogenous calcineurin (CaN) inhibitor, regulator of calcineurin 1 (RCAN1), reversed the inhibitory effect of lenalidomide on MDSL cells, an MDS cell line.	Lenalidomide	167-179	G protein-coupled receptor 68	Homo sapiens	13-42
32984863-5	2020	Depletion of G protein-coupled receptor 68 (GPR68) or an endogenous calcineurin (CaN) inhibitor, regulator of calcineurin 1 (RCAN1), reversed the inhibitory effect of lenalidomide on MDSL cells, an MDS cell line.	Lenalidomide	167-179	G protein-coupled receptor 68	Homo sapiens	44-49
32984863-5	2020	Depletion of G protein-coupled receptor 68 (GPR68) or an endogenous calcineurin (CaN) inhibitor, regulator of calcineurin 1 (RCAN1), reversed the inhibitory effect of lenalidomide on MDSL cells, an MDS cell line.	Lenalidomide	167-179	regulator of calcineurin 1	Homo sapiens	97-123
32984863-5	2020	Depletion of G protein-coupled receptor 68 (GPR68) or an endogenous calcineurin (CaN) inhibitor, regulator of calcineurin 1 (RCAN1), reversed the inhibitory effect of lenalidomide on MDSL cells, an MDS cell line.	Lenalidomide	167-179	regulator of calcineurin 1	Homo sapiens	125-130
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	G protein-coupled receptor 68	Homo sapiens	19-24
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	regulator of calcineurin 1	Homo sapiens	29-34
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	IKAROS family zinc finger 1	Homo sapiens	156-161
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	IKAROS family zinc finger 1	Homo sapiens	179-184
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	G protein-coupled receptor 68	Homo sapiens	229-234
32984863-6	2020	Intriguingly, both GPR68 and RCAN1 expression levels were upregulated in MDSL cells after treatment with lenalidomide that was dependent on diminishment of IKZF1, indicating that IKZF1 functioned as a transcription repressor for GPR68 and RCAN1.	Lenalidomide	105-117	regulator of calcineurin 1	Homo sapiens	239-244
32984863-10	2020	Our studies suggest that lenalidomide mediates degradation of IKZF1, leading to derepression of GPR68 and RCAN1 that activates the Ca2+/calpain pro- apoptotic pathway and inhibits the CaN pro-survival pathway, respectively.	Lenalidomide	25-37	IKAROS family zinc finger 1	Homo sapiens	62-67
32984863-10	2020	Our studies suggest that lenalidomide mediates degradation of IKZF1, leading to derepression of GPR68 and RCAN1 that activates the Ca2+/calpain pro- apoptotic pathway and inhibits the CaN pro-survival pathway, respectively.	Lenalidomide	25-37	G protein-coupled receptor 68	Homo sapiens	96-101
32984863-10	2020	Our studies suggest that lenalidomide mediates degradation of IKZF1, leading to derepression of GPR68 and RCAN1 that activates the Ca2+/calpain pro- apoptotic pathway and inhibits the CaN pro-survival pathway, respectively.	Lenalidomide	25-37	regulator of calcineurin 1	Homo sapiens	106-111
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	Janus kinase 1	Homo sapiens	0-6
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	tribbles pseudokinase 1	Homo sapiens	117-122
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	mucin 1, cell surface associated	Homo sapiens	124-128
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	CD44 molecule (Indian blood group)	Homo sapiens	130-134
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	C-X-C motif chemokine ligand 12	Homo sapiens	136-142
31423579-0	2020	JAK1/2 pathway inhibition suppresses M2 polarization and overcomes resistance of myeloma to lenalidomide by reducing TRIB1, MUC1, CD44, CXCL12, and CXCR4 expression.	Lenalidomide	92-104	C-X-C motif chemokine receptor 4	Homo sapiens	148-153
32967454-2	2020	Immunomodulator lenalidomide may improve CAR T-cell function.	Lenalidomide	16-28	nuclear receptor subfamily 1 group I member 3	Homo sapiens	41-44
32967454-3	2020	In this study, the effects of lenalidomide on CAR T-cell functions (cytotoxicity, cytokine secretion, and cell proliferation) were investigated.	Lenalidomide	30-42	nuclear receptor subfamily 1 group I member 3	Homo sapiens	46-49
32967454-5	2020	We found that lenalidomide promoted the killing of U251 CD133-OE by CD133-CAR T cells, the cytokine secretion, and the proliferation of CD133-CAR T cells.	Lenalidomide	14-26	prominin 1	Homo sapiens	56-61
32967454-5	2020	We found that lenalidomide promoted the killing of U251 CD133-OE by CD133-CAR T cells, the cytokine secretion, and the proliferation of CD133-CAR T cells.	Lenalidomide	14-26	prominin 1	Homo sapiens	68-73
32967454-5	2020	We found that lenalidomide promoted the killing of U251 CD133-OE by CD133-CAR T cells, the cytokine secretion, and the proliferation of CD133-CAR T cells.	Lenalidomide	14-26	nuclear receptor subfamily 1 group I member 3	Homo sapiens	74-77
32967454-5	2020	We found that lenalidomide promoted the killing of U251 CD133-OE by CD133-CAR T cells, the cytokine secretion, and the proliferation of CD133-CAR T cells.	Lenalidomide	14-26	prominin 1	Homo sapiens	68-73
32967454-5	2020	We found that lenalidomide promoted the killing of U251 CD133-OE by CD133-CAR T cells, the cytokine secretion, and the proliferation of CD133-CAR T cells.	Lenalidomide	14-26	nuclear receptor subfamily 1 group I member 3	Homo sapiens	142-145
32967454-6	2020	Lenalidomide also enhanced the cytotoxicity against MDA-MB-453 and the cytokine secretion of HER2-CAR T cells but did not affect their proliferation significantly.	Lenalidomide	0-12	erb-b2 receptor tyrosine kinase 2	Homo sapiens	93-97
32967454-6	2020	Lenalidomide also enhanced the cytotoxicity against MDA-MB-453 and the cytokine secretion of HER2-CAR T cells but did not affect their proliferation significantly.	Lenalidomide	0-12	nuclear receptor subfamily 1 group I member 3	Homo sapiens	98-101
32967454-7	2020	Furthermore, lenalidomide may regulate the function of CAR T cells by inducing the degradation of transcription factors Ikaros and Aiolos.	Lenalidomide	13-25	nuclear receptor subfamily 1 group I member 3	Homo sapiens	55-58
31358854-7	2020	Pharmacological targeting of Ikaros by lenalidomide and its analog pomalidomide downregulated SLAMF7 expression and ameliorated the response of MM cells to sSLAMF7.	Lenalidomide	39-51	IKAROS family zinc finger 1	Homo sapiens	29-35
31358854-7	2020	Pharmacological targeting of Ikaros by lenalidomide and its analog pomalidomide downregulated SLAMF7 expression and ameliorated the response of MM cells to sSLAMF7.	Lenalidomide	39-51	SLAM family member 7	Homo sapiens	94-100
31287161-3	2019	Activated B-cell-like DLBCL is characterized by NF-kappaB activation and chronic B-cell receptor signaling and may be targeted with lenalidomide or ibrutinib in the relapsed setting.	Lenalidomide	132-144	nuclear factor kappa B subunit 1	Homo sapiens	48-57
31074316-4	2019	The MTD was DL3: lenalidomide 5 mg daily D8-21 of C1, then 10 mg D1-21 of C2-6.	Lenalidomide	17-29	metallothionein 1E	Homo sapiens	4-7
31395689-2	2019	Lenalidomide, an immunomodulatory drug, potentiates T cell functionality, drives antimyeloma activity, and alters the suppressive microenvironment; these properties may effectively combine with anti-BCMA CAR T cells to enhance function.	Lenalidomide	0-12	TNF receptor superfamily member 17	Homo sapiens	199-203
31395689-3	2019	Using an anti-BCMA CAR T, we demonstrated that lenalidomide enhances CAR T cell function in a concentration-dependent manner.	Lenalidomide	47-59	TNF receptor superfamily member 17	Homo sapiens	14-18
31395689-4	2019	Lenalidomide increased CAR T effector cytokine production, particularly under low CAR stimulation or in the presence of inhibitory ligand programmed cell death 1 ligand 1.	Lenalidomide	0-12	CD274 molecule	Homo sapiens	138-170
31395689-8	2019	Finally, study of lenalidomide and anti-BCMA CAR T cells in a murine, disseminated, multiple myeloma model indicated that lenalidomide increased CAR T cell counts in blood and significantly prolonged animal survival.	Lenalidomide	122-134	tumor necrosis factor receptor superfamily, member 17	Mus musculus	40-44
31413179-0	2019	Lenalidomide Augments the Antitumor Activities of Eps8 Peptide-Specific Cytotoxic T Lymphocytes against Multiple Myeloma.	Lenalidomide	0-12	epidermal growth factor receptor pathway substrate 8	Homo sapiens	50-54
31413179-8	2019	Importantly, we revealed that lenalidomide effectively stimulated the antitumor activity of the Eps8cocktail-CTLs, with increasing expression trends for T-cell markers (CD28, CD40L, 41BB, and OX40).	Lenalidomide	30-42	epidermal growth factor receptor pathway substrate 8	Homo sapiens	96-100
31413179-8	2019	Importantly, we revealed that lenalidomide effectively stimulated the antitumor activity of the Eps8cocktail-CTLs, with increasing expression trends for T-cell markers (CD28, CD40L, 41BB, and OX40).	Lenalidomide	30-42	CD40 ligand	Homo sapiens	175-180
31413179-8	2019	Importantly, we revealed that lenalidomide effectively stimulated the antitumor activity of the Eps8cocktail-CTLs, with increasing expression trends for T-cell markers (CD28, CD40L, 41BB, and OX40).	Lenalidomide	30-42	TNF receptor superfamily member 4	Homo sapiens	192-196
31413179-9	2019	Compared with unstimulated CTLs and Eps8cocktail-CTLs, lenalidomide-treated Eps8cocktail-CTLs showed superior anti-multiple myeloma activity in humanized multiple myeloma models, including delaying tumor burden increases due to enhanced immune function.	Lenalidomide	55-67	epidermal growth factor receptor pathway substrate 8	Homo sapiens	36-40
31413179-9	2019	Compared with unstimulated CTLs and Eps8cocktail-CTLs, lenalidomide-treated Eps8cocktail-CTLs showed superior anti-multiple myeloma activity in humanized multiple myeloma models, including delaying tumor burden increases due to enhanced immune function.	Lenalidomide	55-67	epidermal growth factor receptor pathway substrate 8	Homo sapiens	76-80
31493176-3	2019	Lenalidomide is a weak substrate of P-glycoprotein (P-gp), though it is unclear whether P-gp is solely responsible for lenalidomide transport.	Lenalidomide	0-12	phosphoglycolate phosphatase	Mus musculus	36-50
31493176-3	2019	Lenalidomide is a weak substrate of P-glycoprotein (P-gp), though it is unclear whether P-gp is solely responsible for lenalidomide transport.	Lenalidomide	0-12	phosphoglycolate phosphatase	Mus musculus	52-56
31493176-12	2019	CONCLUSION: As P-gp transport at the blood-brain barrier did not explain the observed brain concentrations alone, there may be other transporters involved in lenalidomide disposition.	Lenalidomide	158-170	phosphoglycolate phosphatase	Mus musculus	15-19
30760870-2	2019	The immunomodulatory imide drug (IMiD) lenalidomide promotes myeloma cell death via Cereblon (CRBN)-dependent ubiquitylation and proteasome-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	39-51	cereblon	Homo sapiens	94-98
31151137-0	2019	Suppression of Aiolos and Ikaros expression by lenalidomide reduces human ILC3-ILC1/NK cell transdifferentiation.	Lenalidomide	47-59	IKAROS family zinc finger 3	Homo sapiens	15-21
31151137-0	2019	Suppression of Aiolos and Ikaros expression by lenalidomide reduces human ILC3-ILC1/NK cell transdifferentiation.	Lenalidomide	47-59	IKAROS family zinc finger 1	Homo sapiens	26-32
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	IKAROS family zinc finger 3	Homo sapiens	25-31
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	IKAROS family zinc finger 1	Homo sapiens	36-42
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	lymphoid enhancer binding factor 1	Homo sapiens	159-163
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	perforin 1	Homo sapiens	165-169
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	CD244 molecule	Homo sapiens	177-182
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	natural cytotoxicity triggering receptor 3	Homo sapiens	184-188
31151137-6	2019	Selective degradation of Aiolos and Ikaros by lenalidomide suppressed ILC1 and NK cell differentiation and expression of ILC1 and NK cell-related transcripts (LEF1, PRF1, GRZB, CD244, NCR3, and IRF8).	Lenalidomide	46-58	interferon regulatory factor 8	Homo sapiens	194-198
31371506-4	2019	Genetic disruption of IRE1alpha or XBP1s, or pharmacologic IRE1alpha kinase inhibition, attenuated subcutaneous or orthometastatic growth of MM tumors in mice and augmented efficacy of two established frontline antimyeloma agents, bortezomib and lenalidomide.	Lenalidomide	246-258	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	22-31
30721106-0	2019	Detection of hemophagocytic extremely multinucleated giant plasma cells after rituximab/low-dose lenalidomide treatment in CD20+ multiple myeloma.	Lenalidomide	97-109	keratin 20	Homo sapiens	123-127
31406628-3	2019	Furthermore, we investigated if lenalidomide, a potential sensitizer to anti-CD20 treatment, could prevent an inhibitory effect of ibrutinib.	Lenalidomide	32-44	keratin 20	Homo sapiens	77-81
31268156-3	2019	It was shown that the combination of the HDAC6-selective inhibitor, A452, with either of the IMiDs tested (lenalidomide or pomalidomide) led to the synergistic inhibition of cell growth, a decrease in the viability of MM cells and in an increase in the levels of apoptosis.	Lenalidomide	107-119	histone deacetylase 6	Homo sapiens	41-46
30760870-2	2019	The immunomodulatory imide drug (IMiD) lenalidomide promotes myeloma cell death via Cereblon (CRBN)-dependent ubiquitylation and proteasome-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	39-51	IKAROS family zinc finger 1	Homo sapiens	165-170
30760870-2	2019	The immunomodulatory imide drug (IMiD) lenalidomide promotes myeloma cell death via Cereblon (CRBN)-dependent ubiquitylation and proteasome-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	39-51	IKAROS family zinc finger 3	Homo sapiens	175-180
30760870-5	2019	Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment.	Lenalidomide	122-134	RUNX family transcription factor 1	Homo sapiens	17-22
30760870-5	2019	Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment.	Lenalidomide	122-134	RUNX family transcription factor 3	Homo sapiens	27-32
30760870-5	2019	Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment.	Lenalidomide	122-134	cereblon	Homo sapiens	42-46
30760870-5	2019	Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment.	Lenalidomide	122-134	IKAROS family zinc finger 1	Homo sapiens	101-106
30760870-5	2019	Interaction with RUNX1 and RUNX3 inhibits CRBN-dependent binding, ubiquitylation, and degradation of IKZF1 and IKZF3 upon lenalidomide treatment.	Lenalidomide	122-134	IKAROS family zinc finger 3	Homo sapiens	111-116
31292266-8	2019	The expression of the variant ERFE transcript that was restricted to SF3B1-mutated erythroblasts decreased in lenalidomide-responsive anemic patients, identifying variant ERFE as a specific biomarker of clonal erythropoiesis.	Lenalidomide	110-122	erythroferrone	Homo sapiens	30-34
30650184-1	2019	There is limited data regarding the efficacy and safety of lenalidomide, adriamycin and dexamethasone (RAD) combination on newly diagnosed multiple myeloma (NDMM) patients.	Lenalidomide	59-71	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	103-106
30650184-8	2019	Interestingly, RAD also increased bone formation markers bone-specific alkaline phosphatase (p = 0.036), procollagen type 1 amino-terminal propeptide (p = 0.028) and osteocalcin (p = 0.026), which has not been described before with lenalidomide-containing regimens in the absence of bortezomib coadministration.	Lenalidomide	232-244	RRAD, Ras related glycolysis inhibitor and calcium channel regulator	Homo sapiens	15-18
31255504-8	2019	Factors such as exposure to lenalidomide-based pretreatment regimen, peripheral blood WBC count and CD34 count are associated with the adequate CD34 yield.	Lenalidomide	28-40	CD34 molecule	Homo sapiens	144-148
31292266-8	2019	The expression of the variant ERFE transcript that was restricted to SF3B1-mutated erythroblasts decreased in lenalidomide-responsive anemic patients, identifying variant ERFE as a specific biomarker of clonal erythropoiesis.	Lenalidomide	110-122	splicing factor 3b subunit 1	Homo sapiens	69-74
31292266-8	2019	The expression of the variant ERFE transcript that was restricted to SF3B1-mutated erythroblasts decreased in lenalidomide-responsive anemic patients, identifying variant ERFE as a specific biomarker of clonal erythropoiesis.	Lenalidomide	110-122	erythroferrone	Homo sapiens	171-175
31043801-10	2019	Bortezomib (40 nmol/L, 24 hours) and lenalidomide (3,200 nmol/L, 24 hours) effectively removed CD38+CD138+ cells from peripheral mononuclear cells.	Lenalidomide	37-49	CD38 molecule	Homo sapiens	95-99
30655375-4	2019	Bone marrow B lineage clonality decreased significantly and hypermutated IGH clones normalized upon lenalidomide treatment, well in line with the proliferative effect on healthy antigen-inexperienced B-cell precursors previously described for this drug.	Lenalidomide	100-112	immunoglobulin heavy constant delta	Homo sapiens	73-76
30989487-4	2019	Here, we report the two cases in which hematopoietic stem cells were mobilized using plerixafor plus granulocyte-colony stimulating factor after exposure to lenalidomide and pomalidomide.	Lenalidomide	157-169	colony stimulating factor 3	Homo sapiens	101-138
30707764-0	2019	Phase 1 study of lenalidomide plus dose-adjusted EPOCH-R in patients with aggressive B-cell lymphomas with deregulated MYC and BCL2.	Lenalidomide	17-29	BCL2 apoptosis regulator	Homo sapiens	127-131
31273172-9	2019	Patients with an estimated glomerular filtration rate of less than 50mL/min/1.73m2 received a lower cumulative dose of ixazomib and lenalidomide than those with other rates.	Lenalidomide	132-144	CD59 molecule (CD59 blood group)	Homo sapiens	72-77
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.	Lenalidomide	64-76	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.	Lenalidomide	64-76	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.	Lenalidomide	64-76	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.	Lenalidomide	64-76	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.	Lenalidomide	64-76	mitochondrial E3 ubiquitin protein ligase 1	Homo sapiens	291-310
31089832-0	2019	Influence of ABCB1 polymorphisms on the pharmacokinetics and toxicity of lenalidomide in patients with multiple myeloma.	Lenalidomide	73-85	ATP binding cassette subfamily B member 1	Homo sapiens	13-18
31089832-3	2019	Here, we investigated the association between ABCB1 polymorphisms and pharmacokinetics of lenalidomide in patients with multiple myeloma (MM) treated with lenalidomide and dexamethasone.	Lenalidomide	90-102	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
31089832-3	2019	Here, we investigated the association between ABCB1 polymorphisms and pharmacokinetics of lenalidomide in patients with multiple myeloma (MM) treated with lenalidomide and dexamethasone.	Lenalidomide	155-167	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
31089832-10	2019	We show that lenalidomide pharmacokinetics is influenced by the ABCB1 3435C>T polymorphism, which could be useful to individualize dosage design and reduce unexpected toxicity.	Lenalidomide	13-25	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
31141702-3	2019	Lenalidomide did not affect the viability or expression of costimulatory molecules, but it potently suppressed the production of the key inflammatory cytokines IL-12 and IL-23, and enhanced the production of the anti-inflammatory cytokine IL-10 by CD1c+ DCs.	Lenalidomide	0-12	interleukin 23 subunit alpha	Homo sapiens	170-175
31141702-3	2019	Lenalidomide did not affect the viability or expression of costimulatory molecules, but it potently suppressed the production of the key inflammatory cytokines IL-12 and IL-23, and enhanced the production of the anti-inflammatory cytokine IL-10 by CD1c+ DCs.	Lenalidomide	0-12	interleukin 10	Homo sapiens	239-244
31141702-3	2019	Lenalidomide did not affect the viability or expression of costimulatory molecules, but it potently suppressed the production of the key inflammatory cytokines IL-12 and IL-23, and enhanced the production of the anti-inflammatory cytokine IL-10 by CD1c+ DCs.	Lenalidomide	0-12	CD1c molecule	Homo sapiens	248-252
31141702-4	2019	Lenalidomide also suppressed the production of IFN-alpha by CD141+ DCs but not that by plasmacytoid DCs.	Lenalidomide	0-12	interferon alpha 1	Homo sapiens	47-56
31141702-4	2019	Lenalidomide also suppressed the production of IFN-alpha by CD141+ DCs but not that by plasmacytoid DCs.	Lenalidomide	0-12	thrombomodulin	Homo sapiens	60-65
31141702-5	2019	Lenalidomide likely targets pathways downstream of the nuclear translocation of the transcription factors nuclear factor kappaB (NF-kappaB) and IFN regulatory 5 (IRF5) in CD1c+ DCs.	Lenalidomide	0-12	nuclear factor kappa B subunit 1	Homo sapiens	129-138
31141702-5	2019	Lenalidomide likely targets pathways downstream of the nuclear translocation of the transcription factors nuclear factor kappaB (NF-kappaB) and IFN regulatory 5 (IRF5) in CD1c+ DCs.	Lenalidomide	0-12	interferon regulatory factor 5	Homo sapiens	162-166
31141702-5	2019	Lenalidomide likely targets pathways downstream of the nuclear translocation of the transcription factors nuclear factor kappaB (NF-kappaB) and IFN regulatory 5 (IRF5) in CD1c+ DCs.	Lenalidomide	0-12	CD1c molecule	Homo sapiens	171-175
31141702-6	2019	Consistent with the direct immunomodulatory effects on DCs, lenalidomide decreased the capacity of CD1c+ DCs to induce differentiation of naive CD4+ T cells into effector cells producing immune activating and myeloma-promoting cytokines.	Lenalidomide	60-72	CD1c molecule	Homo sapiens	99-103
31141702-6	2019	Consistent with the direct immunomodulatory effects on DCs, lenalidomide decreased the capacity of CD1c+ DCs to induce differentiation of naive CD4+ T cells into effector cells producing immune activating and myeloma-promoting cytokines.	Lenalidomide	60-72	CD4 molecule	Homo sapiens	144-147
30926391-2	2019	Retrospective series and 1 prospective study suggest that clinically significant responses were predominantly limited to patients with activated B cell (ABC) lymphoma, a finding in agreement with lenalidomide"s potent inhibition of nuclear factor kappaB, the key driver of ABC lymphomas.	Lenalidomide	196-208	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	153-156
30608891-8	2019	However, the potential synergistic anti-neoplastic effects of lenalidomide in combination with other biological agents, i.e. ibrutinib and venetoclax, especially in the management of p53-mutated cases, still remain an open issue.	Lenalidomide	62-74	tumor protein p53	Homo sapiens	183-186
30949411-8	2019	Lenalidomide and low dose of bortezomib had synergistic effect with chidamide, and similarly this effect was attenuated by SDHA siRNA.	Lenalidomide	0-12	succinate dehydrogenase complex flavoprotein subunit A	Homo sapiens	123-127
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.	Lenalidomide	116-128	vascular endothelial growth factor A	Homo sapiens	233-237
30423172-3	2019	Agents like the Bruton tyrosine kinase (BTK) inhibitor ibrutinib or immunomodulatory drugs (IMiDs) like pomalidomide and lenalidomide have shown promising high response rates in the salvage setting.	Lenalidomide	121-133	Bruton tyrosine kinase	Homo sapiens	16-38
30741931-0	2019	Identification of lenalidomide resistance pathways in myeloma and targeted resensitization using cereblon replacement, inhibition of STAT3 or targeting of IRF4.	Lenalidomide	18-30	signal transducer and activator of transcription 3	Homo sapiens	133-138
30741931-0	2019	Identification of lenalidomide resistance pathways in myeloma and targeted resensitization using cereblon replacement, inhibition of STAT3 or targeting of IRF4.	Lenalidomide	18-30	interferon regulatory factor 4	Homo sapiens	155-159
30741931-7	2019	Inhibition of STAT3 with a selective compound (PB-1-102) re-sensitized XG1LenRes to lenalidomide.	Lenalidomide	84-96	signal transducer and activator of transcription 3	Homo sapiens	14-19
30741931-9	2019	This strategy also appeared to be more broadly applicable as SGC-CBP30 could re-sensitize two resistant HMCLs with low but detectable CRBN expression to lenalidomide, suggesting that targeting CBP/E300 is a promising approach to restore IMiD sensitivity in MM with detectable CRBN expression.	Lenalidomide	153-165	CREB binding protein	Homo sapiens	65-68
30550941-6	2019	The immunomodulatory drug lenalidomide had direct anti-proliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated spheroids.	Lenalidomide	26-38	C-C motif chemokine ligand 2	Homo sapiens	172-176
30550941-6	2019	The immunomodulatory drug lenalidomide had direct anti-proliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated spheroids.	Lenalidomide	26-38	C-C motif chemokine ligand 3	Homo sapiens	178-182
30550941-6	2019	The immunomodulatory drug lenalidomide had direct anti-proliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated spheroids.	Lenalidomide	26-38	C-C motif chemokine ligand 4	Homo sapiens	184-188
30550941-6	2019	The immunomodulatory drug lenalidomide had direct anti-proliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated spheroids.	Lenalidomide	26-38	TNF receptor superfamily member 9	Homo sapiens	190-195
30550941-6	2019	The immunomodulatory drug lenalidomide had direct anti-proliferative effect on activated B-cell like DLBCL spheroids and reduced several cytokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated spheroids.	Lenalidomide	26-38	angiopoietin 1	Homo sapiens	200-205
30423172-3	2019	Agents like the Bruton tyrosine kinase (BTK) inhibitor ibrutinib or immunomodulatory drugs (IMiDs) like pomalidomide and lenalidomide have shown promising high response rates in the salvage setting.	Lenalidomide	121-133	Bruton tyrosine kinase	Homo sapiens	40-43
29788898-9	2019	This E3 ubiquitin ligase in the absence of lenalidomide ubiquitinates CRBN itself and the other components of CRL4CRBN complex.	Lenalidomide	43-55	cereblon	Homo sapiens	70-74
30598450-12	2019	Combining MDM2 inhibitors with lenalidomide targeting CK1alpha or an MDM4 inhibitor caused synergistic activation of p53, leading to an apoptotic response in MCV-positive MCC cells and MCC-derived xenografts in mice.	Lenalidomide	31-43	tumor protein p53	Homo sapiens	117-120
29788898-10	2019	Presence of lenalidomide changes specificity of CRL4CRBN which ubiquitinates two transcription factors, IKZF1 (Ikaros) and IKZF3 (Aiolos), and casein kinase 1alpha (CK1alpha) and marks them for degradation in proteasomes.	Lenalidomide	12-24	IKAROS family zinc finger 1	Homo sapiens	104-109
29788898-10	2019	Presence of lenalidomide changes specificity of CRL4CRBN which ubiquitinates two transcription factors, IKZF1 (Ikaros) and IKZF3 (Aiolos), and casein kinase 1alpha (CK1alpha) and marks them for degradation in proteasomes.	Lenalidomide	12-24	IKAROS family zinc finger 1	Homo sapiens	111-117
29788898-10	2019	Presence of lenalidomide changes specificity of CRL4CRBN which ubiquitinates two transcription factors, IKZF1 (Ikaros) and IKZF3 (Aiolos), and casein kinase 1alpha (CK1alpha) and marks them for degradation in proteasomes.	Lenalidomide	12-24	IKAROS family zinc finger 3	Homo sapiens	123-128
29788898-10	2019	Presence of lenalidomide changes specificity of CRL4CRBN which ubiquitinates two transcription factors, IKZF1 (Ikaros) and IKZF3 (Aiolos), and casein kinase 1alpha (CK1alpha) and marks them for degradation in proteasomes.	Lenalidomide	12-24	IKAROS family zinc finger 3	Homo sapiens	130-136
29788898-12	2019	Low CRBN level was connected with insensitivity of MM cells to lenalidomide.	Lenalidomide	63-75	cereblon	Homo sapiens	4-8
29788898-13	2019	Lenalidomide decreases expression of protein argonaute-2, which binds to cereblon.	Lenalidomide	0-12	argonaute RISC catalytic component 2	Homo sapiens	37-56
29788898-15	2019	Lenalidomide decreases also basigin and monocarboxylate transporter 1 in MM cells.	Lenalidomide	0-12	basigin (Ok blood group)	Homo sapiens	28-35
29788898-15	2019	Lenalidomide decreases also basigin and monocarboxylate transporter 1 in MM cells.	Lenalidomide	0-12	solute carrier family 16 member 1	Homo sapiens	40-69
29788898-16	2019	MM cells with low expression of Ikaros, Aiolos and basigin are more sensitive to lenalidomide treatment.	Lenalidomide	81-93	IKAROS family zinc finger 1	Homo sapiens	32-38
29788898-16	2019	MM cells with low expression of Ikaros, Aiolos and basigin are more sensitive to lenalidomide treatment.	Lenalidomide	81-93	IKAROS family zinc finger 3	Homo sapiens	40-46
29788898-16	2019	MM cells with low expression of Ikaros, Aiolos and basigin are more sensitive to lenalidomide treatment.	Lenalidomide	81-93	basigin (Ok blood group)	Homo sapiens	51-58
29788898-21	2019	High level of full length CRBN mRNA in mononuclear cells of bone marrow and of peripheral blood seems to be necessary for successful therapy of del(5q) MDS with lenalidomide.	Lenalidomide	161-173	cereblon	Homo sapiens	26-30
30026574-1	2019	Immunomodulatory drugs (IMiDs) including lenalidomide and pomalidomide bind cereblon (CRBN) and activate the CRL4CRBN ubiquitin ligase to trigger proteasomal degradation of the essential transcription factors IKZF1 and IKZF3 and multiple myeloma (MM) cytotoxicity.	Lenalidomide	41-53	cereblon	Homo sapiens	86-90
30826127-8	2019	Preclinical and clinical studies have demonstrated that CD38-targeting antibodies have synergistic activity with several other anti-cancer drugs, including various agents with immune stimulating activity, such as lenalidomide and pomalidomide, as well as PD1/PD-L1 inhibitors.	Lenalidomide	213-225	CD38 molecule	Homo sapiens	56-60
29718735-3	2019	Using standard immunohistochemistry in formalin-fixed paraffin embedded (FFPE) bone marrow samples of 23 patients treated with a lenalidomide-containing regimen, we found that the malignant plasma cells of all the patients stained positive for CRBN, IKZF1, and IKZF3, regardless of sensitivity to IMiDs.	Lenalidomide	129-141	cereblon	Homo sapiens	244-248
30608448-0	2019	Novel EZH2 mutation in a patient with secondary B-cell acute lymphocytic leukemia after deletion 5q myelodysplastic syndrome treated with lenalidomide: A case report.	Lenalidomide	138-150	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	6-10
30608448-4	2019	He was administered lenalidomide for 27 months, then developed acute B-cell lymphocytic leukemia and acquired a previously unreported mutation in the gene enhancer of zeste homolog 2 (EZH2).	Lenalidomide	20-32	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	155-182
30608448-4	2019	He was administered lenalidomide for 27 months, then developed acute B-cell lymphocytic leukemia and acquired a previously unreported mutation in the gene enhancer of zeste homolog 2 (EZH2).	Lenalidomide	20-32	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	184-188
31068561-2	2019	All of them had markedly elevated serum vascular endothelial growth factor (VEGF) levels treated with lenalidomide and dexamethasone for severe peripheral neuropathy, which normalized serum VEGF levels and improved peripheral neuropathy.	Lenalidomide	102-114	vascular endothelial growth factor A	Homo sapiens	40-74
31068561-2	2019	All of them had markedly elevated serum vascular endothelial growth factor (VEGF) levels treated with lenalidomide and dexamethasone for severe peripheral neuropathy, which normalized serum VEGF levels and improved peripheral neuropathy.	Lenalidomide	102-114	vascular endothelial growth factor A	Homo sapiens	76-80
31068561-2	2019	All of them had markedly elevated serum vascular endothelial growth factor (VEGF) levels treated with lenalidomide and dexamethasone for severe peripheral neuropathy, which normalized serum VEGF levels and improved peripheral neuropathy.	Lenalidomide	102-114	vascular endothelial growth factor A	Homo sapiens	190-194
30026574-1	2019	Immunomodulatory drugs (IMiDs) including lenalidomide and pomalidomide bind cereblon (CRBN) and activate the CRL4CRBN ubiquitin ligase to trigger proteasomal degradation of the essential transcription factors IKZF1 and IKZF3 and multiple myeloma (MM) cytotoxicity.	Lenalidomide	41-53	interleukin 17 receptor B	Homo sapiens	109-113
30026574-1	2019	Immunomodulatory drugs (IMiDs) including lenalidomide and pomalidomide bind cereblon (CRBN) and activate the CRL4CRBN ubiquitin ligase to trigger proteasomal degradation of the essential transcription factors IKZF1 and IKZF3 and multiple myeloma (MM) cytotoxicity.	Lenalidomide	41-53	IKAROS family zinc finger 1	Homo sapiens	209-214
30026574-1	2019	Immunomodulatory drugs (IMiDs) including lenalidomide and pomalidomide bind cereblon (CRBN) and activate the CRL4CRBN ubiquitin ligase to trigger proteasomal degradation of the essential transcription factors IKZF1 and IKZF3 and multiple myeloma (MM) cytotoxicity.	Lenalidomide	41-53	IKAROS family zinc finger 3	Homo sapiens	219-224
30619281-5	2018	The immunomodulatory drug lenalidomide may regulate the expression of ILT2 and its ligands in CLL since it significantly increased the expression of ILT2 and partially reestablished the expression of its ligands on leukemic cells.	Lenalidomide	26-38	leukocyte immunoglobulin like receptor B1	Homo sapiens	70-74
30619281-5	2018	The immunomodulatory drug lenalidomide may regulate the expression of ILT2 and its ligands in CLL since it significantly increased the expression of ILT2 and partially reestablished the expression of its ligands on leukemic cells.	Lenalidomide	26-38	leukocyte immunoglobulin like receptor B1	Homo sapiens	149-153
30619281-6	2018	Furthermore, lenalidomide significantly increased the activation and proliferation of NK cells, which was strongly enhanced by ILT2 blockade.	Lenalidomide	13-25	leukocyte immunoglobulin like receptor B1	Homo sapiens	127-131
30128502-15	2018	Of note, PVX-410 was immunogenic as monotherapy (10 of 11 patients) and in combination with lenalidomide (9 of 9 patients), as demonstrated by an increase in percentage of tetramer-positive cells and IFN-gamma cells in the CD3+CD8+ cell population.	Lenalidomide	92-104	interferon gamma	Homo sapiens	200-209
30312729-0	2019	Pan-PIM kinase inhibitors enhance Lenalidomide"s anti-myeloma activity via cereblon-IKZF1/3 cascade.	Lenalidomide	34-46	IKAROS family zinc finger 1	Mus musculus	84-91
30312729-4	2019	Combining a pan-PIM kinase inhibitor with lenalidomide led to more effective degradation of IKZF1 and IKZF3 in multiple myeloma cell lines as well as xenografts of myeloma tumors.	Lenalidomide	42-54	IKAROS family zinc finger 1	Mus musculus	92-97
30312729-4	2019	Combining a pan-PIM kinase inhibitor with lenalidomide led to more effective degradation of IKZF1 and IKZF3 in multiple myeloma cell lines as well as xenografts of myeloma tumors.	Lenalidomide	42-54	IKAROS family zinc finger 3	Mus musculus	102-107
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.	Lenalidomide	207-219	complement C1q like 1	Homo sapiens	0-22
30064974-6	2018	We use the Crbn I391V model to demonstrate that the in vivo therapeutic activity of lenalidomide in del(5q) myelodysplastic syndrome can be explained by heterozygous expression of Ck1alpha in del(5q) cells.	Lenalidomide	84-96	cereblon	Mus musculus	11-15
30455698-3	2018	Elotuzumab is a humanized IgG1 monoclonal antibody targeting SLAMF7, which is highly expressed on myeloma cells, and the antibody is approved for the treatment of relapsed and/or refractory (RR) MM in combination with lenalidomide and dexamethasone.	Lenalidomide	218-230	SLAM family member 7	Homo sapiens	61-67
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.	Lenalidomide	33-45	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.	Lenalidomide	33-45	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.	Lenalidomide	33-45	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.	Lenalidomide	33-45	cereblon	Homo sapiens	246-250
29938309-0	2018	Low frequency of CD3+CD4+CD161+ T cells correlates with the occurrence of infections in refractory/relapsed multiple myeloma patients receiving lenalidomide plus low-dose dexamethasone treatment.	Lenalidomide	144-156	CD4 molecule	Homo sapiens	21-24
30349293-8	2018	For this purpose, several drugs may have a role: specific COX-2 inhibitors such as celecoxib or other anti-inflammatory drugs such as lenalidomide may further inhibit lipopolysaccharide-mediated induction of COX-2.	Lenalidomide	134-146	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	58-63
30349293-8	2018	For this purpose, several drugs may have a role: specific COX-2 inhibitors such as celecoxib or other anti-inflammatory drugs such as lenalidomide may further inhibit lipopolysaccharide-mediated induction of COX-2.	Lenalidomide	134-146	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	208-213
30285865-7	2018	We also demonstrate a synergistic effect of EPZ-6438 and lenalidomide, a conventional drug used for MM treatment, activating B cell transcription factors and tumor suppressor gene expression in concert with MYC repression.	Lenalidomide	57-69	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	207-210
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.	Lenalidomide	48-60	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.	Lenalidomide	48-60	cereblon	Homo sapiens	234-238
30338042-0	2018	Lenalidomide combined with low-dose cyclophosphamide and prednisone modulates Ikaros and Aiolos in lymphocytes, resulting in immunostimulatory effects in lenalidomide-refractory multiple myeloma patients.	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	89-95
29870139-5	2018	Binding studies with the IMiD target protein cereblon (CRBN) reveals a narrow structure-activity relationship with only a few compounds showing sub-micromolar binding affinity in the range of pomalidomide and lenalidomide.	Lenalidomide	209-221	cereblon	Homo sapiens	55-59
30154887-7	2018	Results: Mobilization increased blood CD34+ frequency in lenalidomide-treated subjects and controls similarly (0.25% (95% confidence interval (CI): 0.03-1.39% vs. 0.32%, 0.04-1.47%), p = 0.472).	Lenalidomide	57-69	CD34 molecule	Homo sapiens	38-42
30154887-10	2018	In contrast, mean CXCR4 intensity on bone marrow cells in lenalidomide-treated subjects increased from 55 +-43 to 89 +-40 (p = 0.017, comparing the deviation between two groups).	Lenalidomide	58-70	C-X-C motif chemokine receptor 4	Homo sapiens	18-23
30154887-11	2018	Median numbers of CD34+ cells collected in lenalidomide-treated subjects and controls were 2.3 x 106/kg (0.6-6.8 x 106/kg) and 2.8106/kg (1.0-8.9 x 106/kg; p = 0.521).	Lenalidomide	43-55	CD34 molecule	Homo sapiens	18-22
30154887-12	2018	Conclusions: Brief lenalidomide treatment for POEMS did not reduce numbers of CD34+ blood cells collected but increased CXCR4 expression on bone marrow CD34+ cells.	Lenalidomide	19-31	C-X-C motif chemokine receptor 4	Homo sapiens	120-125
30154887-12	2018	Conclusions: Brief lenalidomide treatment for POEMS did not reduce numbers of CD34+ blood cells collected but increased CXCR4 expression on bone marrow CD34+ cells.	Lenalidomide	19-31	CD34 molecule	Homo sapiens	152-156
30097406-2	2018	Lenalidomide resistance, including primary resistance, occurs by clonal evolution, which is frequently attributable to the presence of somatic mutations in the DNA-binding domain of the TP53 gene.	Lenalidomide	0-12	tumor protein p53	Homo sapiens	186-190
30104242-0	2018	Activation of Th1 Immunity within the Tumor Microenvironment Is Associated with Clinical Response to Lenalidomide in Chronic Lymphocytic Leukemia.	Lenalidomide	101-113	negative elongation factor complex member C/D	Homo sapiens	14-17
30104242-6	2018	Within days of starting lenalidomide, T cells increased in the tumor microenvironment and showed Th1-type polarization.	Lenalidomide	24-36	negative elongation factor complex member C/D	Homo sapiens	97-100
30104242-7	2018	Gene expression profiling of pretreatment and on-treatment lymph node biopsy specimens revealed upregulation of IFN-gamma and many of its target genes in response to lenalidomide.	Lenalidomide	166-178	interferon gamma	Homo sapiens	112-121
30104242-11	2018	Taken together, our data demonstrate that lenalidomide induced Th1 immunity in the lymph node that is associated with clinical response.	Lenalidomide	42-54	negative elongation factor complex member C/D	Homo sapiens	63-66
30146162-1	2018	CKIalpha ablation induces p53 activation, and CKIalpha degradation underlies the therapeutic effect of lenalidomide in a pre-leukemia syndrome.	Lenalidomide	103-115	casein kinase 1 alpha 1	Homo sapiens	0-8
30146162-1	2018	CKIalpha ablation induces p53 activation, and CKIalpha degradation underlies the therapeutic effect of lenalidomide in a pre-leukemia syndrome.	Lenalidomide	103-115	casein kinase 1 alpha 1	Homo sapiens	46-54
30234487-1	2018	The cereblon modulating agents (CMs) including lenalidomide, pomalidomide and CC-220 repurpose the Cul4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase complex to induce the degradation of specific neomorphic substrates via polyubiquitination in conjunction with E2 ubiquitin-conjugating enzymes, which have until now remained elusive.	Lenalidomide	47-59	ring-box 1	Homo sapiens	104-108
30234487-1	2018	The cereblon modulating agents (CMs) including lenalidomide, pomalidomide and CC-220 repurpose the Cul4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase complex to induce the degradation of specific neomorphic substrates via polyubiquitination in conjunction with E2 ubiquitin-conjugating enzymes, which have until now remained elusive.	Lenalidomide	47-59	damage specific DNA binding protein 1	Homo sapiens	109-113
30234487-1	2018	The cereblon modulating agents (CMs) including lenalidomide, pomalidomide and CC-220 repurpose the Cul4-RBX1-DDB1-CRBN (CRL4CRBN) E3 ubiquitin ligase complex to induce the degradation of specific neomorphic substrates via polyubiquitination in conjunction with E2 ubiquitin-conjugating enzymes, which have until now remained elusive.	Lenalidomide	47-59	cereblon	Homo sapiens	114-118
30234487-4	2018	For example, UBE2G1 inactivation significantly attenuated the degradation of myeloma survival factors IKZF1 and IKZF3 induced by lenalidomide and pomalidomide, hence conferring drug resistance.	Lenalidomide	129-141	ubiquitin conjugating enzyme E2 G1	Homo sapiens	13-19
30234487-4	2018	For example, UBE2G1 inactivation significantly attenuated the degradation of myeloma survival factors IKZF1 and IKZF3 induced by lenalidomide and pomalidomide, hence conferring drug resistance.	Lenalidomide	129-141	IKAROS family zinc finger 1	Homo sapiens	102-107
30234487-4	2018	For example, UBE2G1 inactivation significantly attenuated the degradation of myeloma survival factors IKZF1 and IKZF3 induced by lenalidomide and pomalidomide, hence conferring drug resistance.	Lenalidomide	129-141	IKAROS family zinc finger 3	Homo sapiens	112-117
30190454-9	2018	Lenalidomide can be given at full dose 25 mg daily 21/28 in patients with a CrCl > 30, and can be given daily to those with CrCl < 30, even when on dialysis, at doses of at least 15 mg daily.	Lenalidomide	0-12	CRCL	Homo sapiens	76-80
30190454-9	2018	Lenalidomide can be given at full dose 25 mg daily 21/28 in patients with a CrCl > 30, and can be given daily to those with CrCl < 30, even when on dialysis, at doses of at least 15 mg daily.	Lenalidomide	0-12	CRCL	Homo sapiens	127-131
29545338-0	2018	Cereblon loss and up-regulation of c-Myc are associated with lenalidomide resistance in multiple myeloma patients.	Lenalidomide	61-73	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	35-40
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.	Lenalidomide	48-60	IKAROS family zinc finger 1	Homo sapiens	190-195
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.	Lenalidomide	48-60	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.	Lenalidomide	48-60	IKAROS family zinc finger 3	Homo sapiens	209-214
29611764-0	2018	Lenalidomide combined with R-GDP in a patient with refractory CD5-positive diffuse large B-cell lymphoma: A promising response and review.	Lenalidomide	0-12	CD5 molecule	Homo sapiens	62-65
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).	Lenalidomide	182-194	IKAROS family zinc finger 3	Homo sapiens	28-33
30111438-3	2018	The combination of lenalidomide and CRBN recruited a new substrate that binds to the CRBN-CRL4 complex, leading to increased ubiquitination and proteasome-dependent degradation, thus resulting in anti-myeloma activity.	Lenalidomide	19-31	cereblon	Homo sapiens	85-89
30111438-3	2018	The combination of lenalidomide and CRBN recruited a new substrate that binds to the CRBN-CRL4 complex, leading to increased ubiquitination and proteasome-dependent degradation, thus resulting in anti-myeloma activity.	Lenalidomide	19-31	interleukin 17 receptor B	Homo sapiens	90-94
30111438-5	2018	The CRBN-dependent degradation of IKZF1 and IKZF3 after lenalidomide treatment is also the result of H2O2-mediated oxidative stress.	Lenalidomide	56-68	cereblon	Homo sapiens	4-8
30111438-5	2018	The CRBN-dependent degradation of IKZF1 and IKZF3 after lenalidomide treatment is also the result of H2O2-mediated oxidative stress.	Lenalidomide	56-68	IKAROS family zinc finger 1	Homo sapiens	34-39
30111438-5	2018	The CRBN-dependent degradation of IKZF1 and IKZF3 after lenalidomide treatment is also the result of H2O2-mediated oxidative stress.	Lenalidomide	56-68	IKAROS family zinc finger 3	Homo sapiens	44-49
30111438-6	2018	In addition to ubiquitination, lenalidomide also mediates ubiquitin-independent pathways that prevent CRBN from binding to CD147-MCT1 in a competitive manner to regulate its antitumor activity.	Lenalidomide	31-43	cereblon	Homo sapiens	102-106
30111438-6	2018	In addition to ubiquitination, lenalidomide also mediates ubiquitin-independent pathways that prevent CRBN from binding to CD147-MCT1 in a competitive manner to regulate its antitumor activity.	Lenalidomide	31-43	basigin (Ok blood group)	Homo sapiens	123-128
30111438-6	2018	In addition to ubiquitination, lenalidomide also mediates ubiquitin-independent pathways that prevent CRBN from binding to CD147-MCT1 in a competitive manner to regulate its antitumor activity.	Lenalidomide	31-43	solute carrier family 16 member 1	Homo sapiens	129-133
30111438-7	2018	Lenalidomide can also play a role in multiple myeloma(MM) cells by modulating miRNA levels and CRBN binding to downstream protein AGO2 expression.	Lenalidomide	0-12	cereblon	Homo sapiens	95-99
30111438-7	2018	Lenalidomide can also play a role in multiple myeloma(MM) cells by modulating miRNA levels and CRBN binding to downstream protein AGO2 expression.	Lenalidomide	0-12	argonaute RISC catalytic component 2	Homo sapiens	130-134
30111438-9	2018	This review summarizes the molecular mechanisms of CRBN in lenalidomide against myeloma activity in terms of ubiquitin-dependent and ubiquitin-independent pathways.	Lenalidomide	59-71	cereblon	Homo sapiens	51-55
30228947-8	2018	When administered as a single agent, lenalidomide specifically mobilizes non-del5q/5q- AML cells, but not healthy CD34+ cells, to peripheral blood (PB) through specific downregulation of CXCR4 in AML blasts.	Lenalidomide	37-49	C-X-C motif chemokine receptor 4	Homo sapiens	187-192
30079070-1	2018	Monoclonal antibodies against the cell surface antigen CD38, e.g., isatuximab, daratumumab, or Mor202, have entered the therapeutic armamentarium in multiple myeloma due to single agent overall response rates of 29 vs. 36 vs. 31%, effectivity in combination regimen, e.g., with lenalidomide or bortezomib plus dexamethasone, and tolerable side effects.	Lenalidomide	278-290	CD38 molecule	Homo sapiens	55-59
29986852-10	2018	Change in CSF interleukin-10 at 1 month correlated with clinical response and response duration to lenalidomide.	Lenalidomide	99-111	interleukin 10	Homo sapiens	14-28
29611764-11	2018	The clinical features, pathogenesis, and possible mechanism of action of lenalidomide in CD5+ DLBCL have been described in the literature.	Lenalidomide	73-85	CD5 molecule	Homo sapiens	89-92
29611764-13	2018	Lenalidomide is expected to induce favorable responses in patients with CD5+ DLBCL.	Lenalidomide	0-12	CD5 molecule	Homo sapiens	72-75
29707981-3	2018	METHODS: In MM cell lines and primary cells derived by patients affected by MGUS and MM, we investigated sensitivity to bortezomib and lenalidomide in presence of Arg-1 and PMN-MDSC.	Lenalidomide	135-147	arginase 1	Homo sapiens	163-168
29707981-9	2018	PMN-MDSC and Arg-1 are reduced in vivo after lenalidomide but not bortezomib treatment.	Lenalidomide	45-57	arginase 1	Homo sapiens	13-18
29702148-8	2018	Preclinical and clinical studies have demonstrated that CD38-targeting antibodies have synergistic activity with several other anti-cancer drugs, including various agents with immune stimulating activity, such as lenalidomide and pomalidomide, as well as PD1/PD-L1 inhibitors.	Lenalidomide	213-225	CD38 molecule	Homo sapiens	56-60
29958267-10	2018	RESULTS: Lenalidomide in combination with dexamethasone treatment provided 1.41 incremental life years and 0.83 incremental quality-adjusted life years in comparison with bortezomib in combination with dexamethasone, with an incremental cost of 11 864 597.86 CLP (19 589.86 US$).	Lenalidomide	9-21	calmodulin like 3	Homo sapiens	259-262
29946110-2	2018	We hypothesized that adding lenalidomide to R-CHOP (R2CHOP) may decrease the risk of CNS relapse.	Lenalidomide	28-40	DNA damage inducible transcript 3	Homo sapiens	46-50
29746861-0	2018	Lenalidomide regulates osteocytes fate and related osteoclastogenesis via IL-1beta/NF-kappaB/RANKL signaling.	Lenalidomide	0-12	interleukin 1 beta	Mus musculus	74-82
29746861-0	2018	Lenalidomide regulates osteocytes fate and related osteoclastogenesis via IL-1beta/NF-kappaB/RANKL signaling.	Lenalidomide	0-12	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	93-98
29746861-3	2018	Our data revealed that lenalidomide treatment notably rescued IL-1beta induced loss of osteocyte viability by inhibiting osteocyte apoptosis with decreased osteoclast-related factors, RANKL and Sclerostin, as demonstrated by the restricted osteoclast formation and reduced bone resorption.	Lenalidomide	23-35	interleukin 1 beta	Mus musculus	62-70
29746861-3	2018	Our data revealed that lenalidomide treatment notably rescued IL-1beta induced loss of osteocyte viability by inhibiting osteocyte apoptosis with decreased osteoclast-related factors, RANKL and Sclerostin, as demonstrated by the restricted osteoclast formation and reduced bone resorption.	Lenalidomide	23-35	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	184-189
29746861-4	2018	Additionally, iTRAQ assay revealed that IL-1beta induced activation of NF-kappaB inhibitor alpha/beta were remarkably downregulated by lenalidomide, showing that lenalidomide impaired NF-kappaB signaling in osteocytes for inhibiting the expression of osteoclast specific genes in osteoclasts, which was further confirmed by KEGG pathway analysis and Western blot.	Lenalidomide	135-147	interleukin 1 beta	Mus musculus	40-48
29746861-4	2018	Additionally, iTRAQ assay revealed that IL-1beta induced activation of NF-kappaB inhibitor alpha/beta were remarkably downregulated by lenalidomide, showing that lenalidomide impaired NF-kappaB signaling in osteocytes for inhibiting the expression of osteoclast specific genes in osteoclasts, which was further confirmed by KEGG pathway analysis and Western blot.	Lenalidomide	135-147	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	71-96
29746861-4	2018	Additionally, iTRAQ assay revealed that IL-1beta induced activation of NF-kappaB inhibitor alpha/beta were remarkably downregulated by lenalidomide, showing that lenalidomide impaired NF-kappaB signaling in osteocytes for inhibiting the expression of osteoclast specific genes in osteoclasts, which was further confirmed by KEGG pathway analysis and Western blot.	Lenalidomide	162-174	interleukin 1 beta	Mus musculus	40-48
29746861-4	2018	Additionally, iTRAQ assay revealed that IL-1beta induced activation of NF-kappaB inhibitor alpha/beta were remarkably downregulated by lenalidomide, showing that lenalidomide impaired NF-kappaB signaling in osteocytes for inhibiting the expression of osteoclast specific genes in osteoclasts, which was further confirmed by KEGG pathway analysis and Western blot.	Lenalidomide	162-174	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	71-96
29746861-5	2018	More interestingly, the in vivo analysis of osteocyte apoptosis and osteoclastogenesis in osteoarthritis mice model indicated a role of lenalidomide in the regulation of osteocyte fate and the consequent inhibition of RANKL-induced osteoclastogenesis.	Lenalidomide	136-148	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	218-223
29746861-6	2018	Together, these results suggest that lenalidomide regulates osteocyte fate by attenuating IL-1beta/NF-kappaB signaling, thereby inhibiting RANKL expression for the attenuated osteoclastogenesis both in vitro and vivo, indicating a more efficient remedy among future anti-osteoclastogenesis approaches.	Lenalidomide	37-49	interleukin 1 beta	Mus musculus	90-98
29746861-6	2018	Together, these results suggest that lenalidomide regulates osteocyte fate by attenuating IL-1beta/NF-kappaB signaling, thereby inhibiting RANKL expression for the attenuated osteoclastogenesis both in vitro and vivo, indicating a more efficient remedy among future anti-osteoclastogenesis approaches.	Lenalidomide	37-49	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	139-144
30701929-4	2018	Lenalidomide have shown activity in the ABC-DLBCL in combination with R-CHOP.	Lenalidomide	0-12	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	40-43
29967612-8	2018	These findings suggest that the combination of DCs plus lenalidomide and PD-1 blockade synergistically establishes a robust anti-myeloma immunity through a two-way mechanism, which inhibits immunosuppressive cells while activating effector cells with superior polarization of the Th1/Th2 balance in favor of the tumor immune response.	Lenalidomide	56-68	negative elongation factor complex member C/D, Th1l	Mus musculus	280-283
29951065-12	2018	In summary, DCs derived from monocytes in the presence of lenalidomide present a semi-mature phenotype, increased phagocytic capacity, reduced production of proinflammatory cytokines, and the ability to polarize T-cells toward predominant Th1-type responses; these are qualities that might be useful in the development of new immunotherapeutic treatments.	Lenalidomide	58-70	negative elongation factor complex member C/D	Homo sapiens	239-242
29967612-8	2018	These findings suggest that the combination of DCs plus lenalidomide and PD-1 blockade synergistically establishes a robust anti-myeloma immunity through a two-way mechanism, which inhibits immunosuppressive cells while activating effector cells with superior polarization of the Th1/Th2 balance in favor of the tumor immune response.	Lenalidomide	56-68	heart and neural crest derivatives expressed 2	Mus musculus	284-287
29380550-7	2018	On the other hand, patients with del(13q14) and del(9p21) were less likely to benefit from lenalidomide.	Lenalidomide	91-103	DEL13Q14	Homo sapiens	33-42
29755672-9	2018	PP242 exhibited a synergistic effect with lenalidomide and bortezomib, suggesting that mTOR inhibition can enhance the anti-angiogenic effect of these drugs.	Lenalidomide	42-54	mechanistic target of rapamycin kinase	Homo sapiens	87-91
29363546-8	2018	Pharmacological targeting of Ikaros by the immunomodulatory drug lenalidomide ameliorated the response of MM cells to LPS in a CD180-dependent manner in vitro and in vivo Thus, the CD180/MD-1 pathway may represent a novel mechanism of growth regulation of MM cells in a BM milieu and may be a therapeutic target of preventing the regrowth of dormant MM cells.Significance: This study describes a novel mechanism by which myeloma cells are regulated in the bone marrow, where drug resistance and dormancy can evolve after treatment, with potential therapeutic implications for treating this often untreatable blood cancer.	Lenalidomide	65-77	IKAROS family zinc finger 1	Homo sapiens	29-35
29363546-8	2018	Pharmacological targeting of Ikaros by the immunomodulatory drug lenalidomide ameliorated the response of MM cells to LPS in a CD180-dependent manner in vitro and in vivo Thus, the CD180/MD-1 pathway may represent a novel mechanism of growth regulation of MM cells in a BM milieu and may be a therapeutic target of preventing the regrowth of dormant MM cells.Significance: This study describes a novel mechanism by which myeloma cells are regulated in the bone marrow, where drug resistance and dormancy can evolve after treatment, with potential therapeutic implications for treating this often untreatable blood cancer.	Lenalidomide	65-77	CD180 molecule	Homo sapiens	127-132
29363546-8	2018	Pharmacological targeting of Ikaros by the immunomodulatory drug lenalidomide ameliorated the response of MM cells to LPS in a CD180-dependent manner in vitro and in vivo Thus, the CD180/MD-1 pathway may represent a novel mechanism of growth regulation of MM cells in a BM milieu and may be a therapeutic target of preventing the regrowth of dormant MM cells.Significance: This study describes a novel mechanism by which myeloma cells are regulated in the bone marrow, where drug resistance and dormancy can evolve after treatment, with potential therapeutic implications for treating this often untreatable blood cancer.	Lenalidomide	65-77	CD180 molecule	Homo sapiens	181-186
29269520-0	2018	Emergence and evolution of TP53 mutations are key features of disease progression in myelodysplastic patients with lower-risk del(5q) treated with lenalidomide.	Lenalidomide	147-159	tumor protein p53	Homo sapiens	27-31
29363149-7	2018	Finally, lenalidomide maintenance after ASCT2 was associated with longer PFS (41.0 vs 21.6 mo; P = .0034) and better OS (not yet reached vs 129.6 mo; P = .0434) compared with patients without maintenance.	Lenalidomide	9-21	solute carrier family 1 member 5	Homo sapiens	40-45
29363149-8	2018	Our data suggest that a second ASCT and lenalidomide maintenance given at first relapse in MM after prior ASCT are associated with better survival rates.	Lenalidomide	40-52	solute carrier family 1 member 5	Homo sapiens	106-110
29588478-4	2018	Lenalidomide, a drug that induces proteosomal degradation of IKZF1, also decreases pDC numbers in vivo, and reduces the ratio of pDC/cDC1 differentiated from progenitor cells in vitro in a dose-dependent manner.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	61-66
29588478-6	2018	DC and monocytes from patients with IKZF1 deficiency or lenalidomide-treated cultures secrete less IFN-alpha, TNF and IL-12.	Lenalidomide	56-68	interferon alpha 1	Homo sapiens	99-108
29693175-13	2018	The expression levels of vascular endothelial growth factor (VEGF), interleukin 6 (IL-6) and basic fibroblast growth factor (bFGF) were reduced in the MVs from the RPMI-8226 cells exposed to bortezomib and lenalidomide.	Lenalidomide	206-218	vascular endothelial growth factor A	Homo sapiens	25-59
29693175-13	2018	The expression levels of vascular endothelial growth factor (VEGF), interleukin 6 (IL-6) and basic fibroblast growth factor (bFGF) were reduced in the MVs from the RPMI-8226 cells exposed to bortezomib and lenalidomide.	Lenalidomide	206-218	fibroblast growth factor 2	Homo sapiens	125-129
29616116-7	2018	Lenalidomide treatment alone significantly reduced the p-ERK level compared with the control (P<0.05) and cisplatin treatment alone significantly increased it (P<0.01), however treatment with them in combination significantly reduced the p-ERK level in MDA-MB-231 cells compared with cisplatin treatment alone (P<0.05).	Lenalidomide	0-12	mitogen-activated protein kinase 1	Homo sapiens	57-60
29616116-7	2018	Lenalidomide treatment alone significantly reduced the p-ERK level compared with the control (P<0.05) and cisplatin treatment alone significantly increased it (P<0.01), however treatment with them in combination significantly reduced the p-ERK level in MDA-MB-231 cells compared with cisplatin treatment alone (P<0.05).	Lenalidomide	0-12	mitogen-activated protein kinase 1	Homo sapiens	246-249
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.	Lenalidomide	29-41	platelet derived growth factor, B polypeptide	Mus musculus	154-159
29380550-9	2018	Predictive values of del(17p13) and t(14;16) to bortezomib and autoSCT are seemingly universal, but predictive marker del(13q14) and del(9p21) for lenalidomide response appears ethnicity-specific.	Lenalidomide	147-159	DEL13Q14	Homo sapiens	118-127
29246938-10	2018	The groups had similar immune responses, including a two- to threefold increase in inducible ICOS+CD4+FoxP3- T-cell number.Conclusions: Our early-phase data suggested that ipilimumab plus lenalidomide is well tolerated after HSCT.	Lenalidomide	188-200	inducible T cell costimulator	Homo sapiens	93-97
29246938-10	2018	The groups had similar immune responses, including a two- to threefold increase in inducible ICOS+CD4+FoxP3- T-cell number.Conclusions: Our early-phase data suggested that ipilimumab plus lenalidomide is well tolerated after HSCT.	Lenalidomide	188-200	forkhead box P3	Homo sapiens	102-107
29237802-0	2018	Phase I Dose-Escalation Study of Anti-CTLA-4 Antibody Ipilimumab and Lenalidomide in Patients with Advanced Cancers.	Lenalidomide	69-81	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	38-44
29317217-8	2018	Adding Z-DEVD-FMK, a caspase-3 inhibitor, abolished the HO-1/IRF4 reduction by panobinostat alone or in combination with lenalidomide, suggesting that caspase-3-mediated HO-1/IRF4/MYC degradation occurred.	Lenalidomide	121-133	interferon regulatory factor 4	Homo sapiens	61-65
29588478-6	2018	DC and monocytes from patients with IKZF1 deficiency or lenalidomide-treated cultures secrete less IFN-alpha, TNF and IL-12.	Lenalidomide	56-68	tumor necrosis factor	Homo sapiens	110-113
29588478-7	2018	These results indicate that human DC development and function are regulated by IKZF1, providing further insights into the consequences of IKZF1 mutation on immune function and the mechanism of immunomodulation by lenalidomide.	Lenalidomide	213-225	IKAROS family zinc finger 1	Homo sapiens	79-84
29317217-0	2018	Crucial role of HO-1/IRF4-dependent apoptosis induced by panobinostat and lenalidomide in multiple myeloma.	Lenalidomide	74-86	heme oxygenase 1	Homo sapiens	16-20
29317217-0	2018	Crucial role of HO-1/IRF4-dependent apoptosis induced by panobinostat and lenalidomide in multiple myeloma.	Lenalidomide	74-86	interferon regulatory factor 4	Homo sapiens	21-25
29317217-8	2018	Adding Z-DEVD-FMK, a caspase-3 inhibitor, abolished the HO-1/IRF4 reduction by panobinostat alone or in combination with lenalidomide, suggesting that caspase-3-mediated HO-1/IRF4/MYC degradation occurred.	Lenalidomide	121-133	caspase 3	Homo sapiens	21-30
29317217-8	2018	Adding Z-DEVD-FMK, a caspase-3 inhibitor, abolished the HO-1/IRF4 reduction by panobinostat alone or in combination with lenalidomide, suggesting that caspase-3-mediated HO-1/IRF4/MYC degradation occurred.	Lenalidomide	121-133	heme oxygenase 1	Homo sapiens	56-60
29445144-3	2018	Here, we identify that lenalidomide alone could promote macrophages M2 polarization to prevent the progression of EAE, which is associated with subsequent inhibition of proinflammatory Th1 and Th17 cells both in peripheral lymph system and CNS.	Lenalidomide	23-35	negative elongation factor complex member C/D, Th1l	Mus musculus	185-188
29445144-5	2018	The macrophages-derived IL10 was upregulated both in vivo and in vitro after lenalidomide treatment.	Lenalidomide	77-89	interleukin 10	Mus musculus	24-28
29445144-6	2018	Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.	Lenalidomide	10-22	interleukin 10	Mus musculus	31-35
29445144-6	2018	Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.	Lenalidomide	139-151	interleukin 10	Mus musculus	160-164
29445144-6	2018	Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.	Lenalidomide	139-151	interleukin 10	Mus musculus	160-164
29445144-6	2018	Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.	Lenalidomide	139-151	interleukin 10	Mus musculus	160-164
29445144-6	2018	Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE.	Lenalidomide	139-151	interleukin 10	Mus musculus	160-164
29445144-7	2018	Mechanistically, lenalidomide significantly increased expression and autocrine secretion of IL10, subsequently activated STAT3-mediated expression of Ym1.	Lenalidomide	17-29	interleukin 10	Mus musculus	92-96
29445144-7	2018	Mechanistically, lenalidomide significantly increased expression and autocrine secretion of IL10, subsequently activated STAT3-mediated expression of Ym1.	Lenalidomide	17-29	signal transducer and activator of transcription 3	Mus musculus	121-126
29445144-7	2018	Mechanistically, lenalidomide significantly increased expression and autocrine secretion of IL10, subsequently activated STAT3-mediated expression of Ym1.	Lenalidomide	17-29	chitinase-like 3	Mus musculus	150-153
29440639-8	2018	Furthermore, we found that even though lenalidomide positively regulated RhoU expression leading to higher cell migration rates, it actually led to cell cycle arrest probably through a p21 dependent mechanism.	Lenalidomide	39-51	ras homolog family member U	Homo sapiens	73-77
28833354-0	2018	Immunohistochemical expression of cereblon and MUM1 as potential predictive markers of response to lenalidomide in extranodal marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT lymphoma).	Lenalidomide	99-111	cereblon	Homo sapiens	34-42
28833354-2	2018	Recently, high expression levels of cereblon (CRBN) and MUM1 have been associated with better response rates in multiple myeloma treated with lenalidomide.	Lenalidomide	142-154	cereblon	Homo sapiens	36-44
28833354-2	2018	Recently, high expression levels of cereblon (CRBN) and MUM1 have been associated with better response rates in multiple myeloma treated with lenalidomide.	Lenalidomide	142-154	cereblon	Homo sapiens	46-50
28833354-2	2018	Recently, high expression levels of cereblon (CRBN) and MUM1 have been associated with better response rates in multiple myeloma treated with lenalidomide.	Lenalidomide	142-154	PWWP domain containing 3A, DNA repair factor	Homo sapiens	56-60
28833354-4	2018	In the current study, we have systematically investigated a potential correlation of CRBN/MUM1 immunohistochemical expression and response to lenalidomide-based therapy in a series of 46 patients with MALT lymphoma treated at the Medical University Vienna 2009 to 2014.	Lenalidomide	142-154	cereblon	Homo sapiens	85-89
28833354-4	2018	In the current study, we have systematically investigated a potential correlation of CRBN/MUM1 immunohistochemical expression and response to lenalidomide-based therapy in a series of 46 patients with MALT lymphoma treated at the Medical University Vienna 2009 to 2014.	Lenalidomide	142-154	PWWP domain containing 3A, DNA repair factor	Homo sapiens	90-94
28639485-0	2018	Increased SHISA3 expression characterizes chronic lymphocytic leukemia patients sensitive to lenalidomide.	Lenalidomide	93-105	shisa family member 3	Homo sapiens	10-16
28639485-9	2018	SHISA3highCLL are characterized by a restrained activation of Wnt signaling and sensibility to lenalidomide-induced apoptosis.	Lenalidomide	95-107	shisa family member 3	Homo sapiens	0-6
28639485-10	2018	In conclusion, SHISA3 is a candidate gene for the identification of CLL patients who will benefit of lenalidomide treatment as single agent.	Lenalidomide	101-113	shisa family member 3	Homo sapiens	15-21
28425720-1	2018	The drugs lenalidomide and pomalidomide bind to the protein cereblon, directing the CRL4-CRBN E3 ligase toward the transcription factors Ikaros and Aiolos to cause their ubiquitination and degradation.	Lenalidomide	10-22	interleukin 17 receptor B	Homo sapiens	84-88
28425720-1	2018	The drugs lenalidomide and pomalidomide bind to the protein cereblon, directing the CRL4-CRBN E3 ligase toward the transcription factors Ikaros and Aiolos to cause their ubiquitination and degradation.	Lenalidomide	10-22	cereblon	Homo sapiens	89-93
28425720-1	2018	The drugs lenalidomide and pomalidomide bind to the protein cereblon, directing the CRL4-CRBN E3 ligase toward the transcription factors Ikaros and Aiolos to cause their ubiquitination and degradation.	Lenalidomide	10-22	IKAROS family zinc finger 3	Homo sapiens	148-154
29180353-5	2018	Inhibition of the Clec16a pathway by the chemotherapeutic lenalidomide, a selective ubiquitin ligase inhibitor associated with new-onset diabetes, impairs beta-cell mitophagy, oxygen consumption, and insulin secretion.	Lenalidomide	58-70	C-type lectin domain containing 16A	Homo sapiens	18-25
29180353-7	2018	Moreover, the beta-cell Clec16a-Nrdp1-USP8 mitophagy complex is destabilized and dysfunctional after lenalidomide treatment as well as after glucolipotoxic stress.	Lenalidomide	101-113	C-type lectin domain containing 16A	Homo sapiens	24-31
29180353-7	2018	Moreover, the beta-cell Clec16a-Nrdp1-USP8 mitophagy complex is destabilized and dysfunctional after lenalidomide treatment as well as after glucolipotoxic stress.	Lenalidomide	101-113	ring finger protein 41	Homo sapiens	32-37
29180353-7	2018	Moreover, the beta-cell Clec16a-Nrdp1-USP8 mitophagy complex is destabilized and dysfunctional after lenalidomide treatment as well as after glucolipotoxic stress.	Lenalidomide	101-113	ubiquitin specific peptidase 8	Homo sapiens	38-42
29295936-7	2018	In addition, STAT3 negatively regulates the lethal type I IFN signaling pathway by inhibiting expression of IRF7, IRF9, STAT1, and STAT2 Inhibition of STAT3 activity by ruxolitinib synergizes with the type I IFN inducer lenalidomide in growth inhibition of ABC DLBCL cells in vitro and in a xenograft mouse model.	Lenalidomide	220-232	signal transducer and activator of transcription 3	Mus musculus	13-18
29295936-7	2018	In addition, STAT3 negatively regulates the lethal type I IFN signaling pathway by inhibiting expression of IRF7, IRF9, STAT1, and STAT2 Inhibition of STAT3 activity by ruxolitinib synergizes with the type I IFN inducer lenalidomide in growth inhibition of ABC DLBCL cells in vitro and in a xenograft mouse model.	Lenalidomide	220-232	interferon regulatory factor 7	Mus musculus	108-112
29295936-7	2018	In addition, STAT3 negatively regulates the lethal type I IFN signaling pathway by inhibiting expression of IRF7, IRF9, STAT1, and STAT2 Inhibition of STAT3 activity by ruxolitinib synergizes with the type I IFN inducer lenalidomide in growth inhibition of ABC DLBCL cells in vitro and in a xenograft mouse model.	Lenalidomide	220-232	interferon regulatory factor 9	Mus musculus	114-118
29295936-7	2018	In addition, STAT3 negatively regulates the lethal type I IFN signaling pathway by inhibiting expression of IRF7, IRF9, STAT1, and STAT2 Inhibition of STAT3 activity by ruxolitinib synergizes with the type I IFN inducer lenalidomide in growth inhibition of ABC DLBCL cells in vitro and in a xenograft mouse model.	Lenalidomide	220-232	signal transducer and activator of transcription 3	Mus musculus	151-156
29317217-8	2018	Adding Z-DEVD-FMK, a caspase-3 inhibitor, abolished the HO-1/IRF4 reduction by panobinostat alone or in combination with lenalidomide, suggesting that caspase-3-mediated HO-1/IRF4/MYC degradation occurred.	Lenalidomide	121-133	caspase 3	Homo sapiens	151-160
29317217-8	2018	Adding Z-DEVD-FMK, a caspase-3 inhibitor, abolished the HO-1/IRF4 reduction by panobinostat alone or in combination with lenalidomide, suggesting that caspase-3-mediated HO-1/IRF4/MYC degradation occurred.	Lenalidomide	121-133	heme oxygenase 1	Homo sapiens	170-174
29317217-9	2018	Given that lenalidomide stabilized cereblon and facilitated IRF4 degradation in MM cells, we combined it with LBH589, an HDAC inhibitor.	Lenalidomide	11-23	interferon regulatory factor 4	Homo sapiens	60-64
29317217-10	2018	LBH589 and lenalidomide exerted synergistic effects, and LBH589 reversed the efficacy of lenalidomide on the resistance of CD138+ primary MM cells, in part due to simultaneous suppression of HO-1, IRF4 and MYC.	Lenalidomide	89-101	heme oxygenase 1	Homo sapiens	191-195
29379494-0	2017	The CXCR4-STAT3-IL-10 Pathway Controls the Immunoregulatory Function of Chronic Lymphocytic Leukemia and Is Modulated by Lenalidomide.	Lenalidomide	121-133	C-X-C motif chemokine receptor 4	Homo sapiens	4-9
29317217-10	2018	LBH589 and lenalidomide exerted synergistic effects, and LBH589 reversed the efficacy of lenalidomide on the resistance of CD138+ primary MM cells, in part due to simultaneous suppression of HO-1, IRF4 and MYC.	Lenalidomide	89-101	interferon regulatory factor 4	Homo sapiens	197-201
29379494-0	2017	The CXCR4-STAT3-IL-10 Pathway Controls the Immunoregulatory Function of Chronic Lymphocytic Leukemia and Is Modulated by Lenalidomide.	Lenalidomide	121-133	signal transducer and activator of transcription 3	Homo sapiens	10-15
29317217-10	2018	LBH589 and lenalidomide exerted synergistic effects, and LBH589 reversed the efficacy of lenalidomide on the resistance of CD138+ primary MM cells, in part due to simultaneous suppression of HO-1, IRF4 and MYC.	Lenalidomide	89-101	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	206-209
29379494-0	2017	The CXCR4-STAT3-IL-10 Pathway Controls the Immunoregulatory Function of Chronic Lymphocytic Leukemia and Is Modulated by Lenalidomide.	Lenalidomide	121-133	interleukin 10	Homo sapiens	16-21
29177954-0	2018	Pharmacogenetic study of the impact of ABCB1 single-nucleotide polymorphisms on lenalidomide treatment outcomes in patients with multiple myeloma: results from a phase IV observational study and subsequent phase II clinical trial.	Lenalidomide	80-92	ATP binding cassette subfamily B member 1	Homo sapiens	39-44
29379494-5	2017	Furthermore, experiments to assess the role of lenalidomide, an immunomodulatory agent with direct antitumor effect as well as pleiotropic activity on the immune system, showed that this agent prevents a CXCL12-induced increase in p-S727-STAT3 and the IL-10 response by CLL cells.	Lenalidomide	47-59	C-X-C motif chemokine ligand 12	Homo sapiens	204-210
29379494-5	2017	Furthermore, experiments to assess the role of lenalidomide, an immunomodulatory agent with direct antitumor effect as well as pleiotropic activity on the immune system, showed that this agent prevents a CXCL12-induced increase in p-S727-STAT3 and the IL-10 response by CLL cells.	Lenalidomide	47-59	signal transducer and activator of transcription 3	Homo sapiens	238-243
29379494-5	2017	Furthermore, experiments to assess the role of lenalidomide, an immunomodulatory agent with direct antitumor effect as well as pleiotropic activity on the immune system, showed that this agent prevents a CXCL12-induced increase in p-S727-STAT3 and the IL-10 response by CLL cells.	Lenalidomide	47-59	interleukin 10	Homo sapiens	252-257
29379494-6	2017	Lenalidomide also suppressed IL-10-induced Y705-STAT3 phosphorylation in healthy T cells, thus reversing CLL-induced T-cell dysfunction.	Lenalidomide	0-12	interleukin 10	Homo sapiens	29-34
29379494-6	2017	Lenalidomide also suppressed IL-10-induced Y705-STAT3 phosphorylation in healthy T cells, thus reversing CLL-induced T-cell dysfunction.	Lenalidomide	0-12	signal transducer and activator of transcription 3	Homo sapiens	48-53
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	C-X-C motif chemokine ligand 12	Homo sapiens	109-115
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	C-X-C motif chemokine receptor 4	Homo sapiens	116-121
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	signal transducer and activator of transcription 3	Homo sapiens	127-132
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	interleukin 10	Homo sapiens	142-147
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	interleukin 10	Homo sapiens	188-193
29379494-8	2017	Lenalidomide appears to be able to reverse CLL-induced immunosuppression through including abrogation of the CXCL12-CXCR4-S727-STAT3-mediated IL-10 response by CLL cells and prevention of IL-10-induced phosphorylation of Y705-STAT3 in T cells.	Lenalidomide	0-12	signal transducer and activator of transcription 3	Homo sapiens	226-231
29445483-0	2018	Lenalidomide decreased the PSA level for castration-resistant prostate cancer: a case report.	Lenalidomide	0-12	aminopeptidase puromycin sensitive	Homo sapiens	27-30
29177954-3	2018	Lenalidomide (Len) is excreted mainly via the kidneys, and, given the expression of P-gp in the renal tubuli, single-nucleotide polymorphisms (SNPs) in the ABCB1 gene may influence Len plasma concentrations and, subsequently, the outcome of treatment.	Lenalidomide	0-12	phosphoglycolate phosphatase	Homo sapiens	84-88
29177954-3	2018	Lenalidomide (Len) is excreted mainly via the kidneys, and, given the expression of P-gp in the renal tubuli, single-nucleotide polymorphisms (SNPs) in the ABCB1 gene may influence Len plasma concentrations and, subsequently, the outcome of treatment.	Lenalidomide	0-12	ATP binding cassette subfamily B member 1	Homo sapiens	156-161
29177954-3	2018	Lenalidomide (Len) is excreted mainly via the kidneys, and, given the expression of P-gp in the renal tubuli, single-nucleotide polymorphisms (SNPs) in the ABCB1 gene may influence Len plasma concentrations and, subsequently, the outcome of treatment.	Lenalidomide	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	156-161
29177954-8	2018	CONCLUSIONS: Our findings show a limited influence of ABCB1 genotype on lenalidomide treatment efficacy and safety.	Lenalidomide	72-84	ATP binding cassette subfamily B member 1	Homo sapiens	54-59
29348877-9	2017	IRF4 was identified as the potential mechanism of resistance to lenalidomide and pomalidomide in WM.	Lenalidomide	64-76	interferon regulatory factor 4	Homo sapiens	0-4
29061640-0	2018	Lenalidomide Enhances the Function of CS1 Chimeric Antigen Receptor-Redirected T Cells Against Multiple Myeloma.	Lenalidomide	0-12	ITPR interacting domain containing 2	Mus musculus	38-41
29061640-3	2018	CS1 CAR T cells were transduced and expanded in the presence of lenalidomide in vitro The phenotype and effector function of CS1 CAR T cells treated with and without lenalidomide were compared.	Lenalidomide	64-76	ITPR interacting domain containing 2	Mus musculus	0-3
29061640-4	2018	Finally, CS1 CAR T cells and lenalidomide were administered to treat multiple myeloma-bearing mice as combinatorial therapy.Results: CS1 CAR T cells exhibited efficient antitumor activity when adoptively transferred into mice.	Lenalidomide	29-41	ITPR interacting domain containing 2	Mus musculus	133-136
29061640-5	2018	Mechanistic studies indicated that the addition of lenalidomide during CS1 CAR T-cell expansion in vitro enhanced the immune functions of CS1 CAR T cells, including cytotoxicity, memory maintenance, Th1 cytokine production, and immune synapse formation.	Lenalidomide	51-63	ITPR interacting domain containing 2	Mus musculus	71-74
29061640-5	2018	Mechanistic studies indicated that the addition of lenalidomide during CS1 CAR T-cell expansion in vitro enhanced the immune functions of CS1 CAR T cells, including cytotoxicity, memory maintenance, Th1 cytokine production, and immune synapse formation.	Lenalidomide	51-63	recoverin	Mus musculus	75-78
29061640-5	2018	Mechanistic studies indicated that the addition of lenalidomide during CS1 CAR T-cell expansion in vitro enhanced the immune functions of CS1 CAR T cells, including cytotoxicity, memory maintenance, Th1 cytokine production, and immune synapse formation.	Lenalidomide	51-63	ITPR interacting domain containing 2	Mus musculus	138-141
29061640-5	2018	Mechanistic studies indicated that the addition of lenalidomide during CS1 CAR T-cell expansion in vitro enhanced the immune functions of CS1 CAR T cells, including cytotoxicity, memory maintenance, Th1 cytokine production, and immune synapse formation.	Lenalidomide	51-63	recoverin	Mus musculus	142-145
29061640-5	2018	Mechanistic studies indicated that the addition of lenalidomide during CS1 CAR T-cell expansion in vitro enhanced the immune functions of CS1 CAR T cells, including cytotoxicity, memory maintenance, Th1 cytokine production, and immune synapse formation.	Lenalidomide	51-63	negative elongation factor complex member C/D, Th1l	Mus musculus	199-202
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	13-25	ITPR interacting domain containing 2	Mus musculus	100-103
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	13-25	recoverin	Mus musculus	104-107
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	13-25	ITPR interacting domain containing 2	Mus musculus	226-229
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	13-25	recoverin	Mus musculus	239-242
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	13-25	ITPR interacting domain containing 2	Mus musculus	226-229
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	100-103
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	recoverin	Mus musculus	104-107
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	226-229
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	recoverin	Mus musculus	239-242
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	226-229
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	100-103
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	recoverin	Mus musculus	104-107
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	226-229
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	recoverin	Mus musculus	239-242
29061640-6	2018	Furthermore, lenalidomide enhanced the antitumor activity and persistence of adoptively transferred CS1 CAR T cells in vivoConclusions: The study demonstrates that lenalidomide improves the anti-multiple myeloma properties of CS1-directed CAR T cells and provides a basis for a planned clinical trial using the combination of lenalidomide with engineered T cells against CS1 in relapsed myeloma.	Lenalidomide	164-176	ITPR interacting domain containing 2	Mus musculus	226-229
29578180-0	2018	Effect of lenalidomide on the human gastric cancer cell line SGC7901/vincristine Notch signaling.	Lenalidomide	10-22	notch receptor 2	Homo sapiens	81-86
29578180-1	2018	Aim of Study: To examine the function of lenalidomide (LEN) on the human multidrug resistance (MDR)-type gastric cancer line SGC7901/vincristine (VCR) via regulating Notch signaling.	Lenalidomide	41-53	notch receptor 2	Homo sapiens	166-171
30185705-7	2018	Pharmacological targeting of Ikaros with lenalidomide ameliorated the response of MM cells to LPS in a CD180-dependent manner in vitro and in vivo.	Lenalidomide	41-53	IKAROS family zinc finger 1	Mus musculus	29-35
30185705-7	2018	Pharmacological targeting of Ikaros with lenalidomide ameliorated the response of MM cells to LPS in a CD180-dependent manner in vitro and in vivo.	Lenalidomide	41-53	CD180 antigen	Mus musculus	103-108
27301994-0	2017	Durable remission in a patient with leptomeningeal relapse of a MYC/BCL6-positive double-hit DLBCL treated with lenalidomide monotherapy.	Lenalidomide	112-124	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-67
28893618-0	2017	Lenalidomide modulates gene expression in human ABC-DLBCL cells by regulating IKAROS interaction with an intronic control region of SPIB.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	78-84
28893618-0	2017	Lenalidomide modulates gene expression in human ABC-DLBCL cells by regulating IKAROS interaction with an intronic control region of SPIB.	Lenalidomide	0-12	Spi-B transcription factor	Homo sapiens	132-136
28893618-2	2017	Lenalidomide, an immunomodulatory drug in trials for treatment of ABC-DLBCL, targets the transcription factor IKAROS for degradation by the cereblon E3 ubiquitin ligase complex.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	110-116
28893618-4	2017	Using cultured ABC-DLBCL cell lines, we found that high levels of SPI-B expression conferred resistance to lenalidomide.	Lenalidomide	107-119	Spi-B transcription factor	Homo sapiens	66-71
28893618-5	2017	Lenalidomide treatment of ABC-DLBCL cells resulted in downregulation of SPIB at the level of transcription.	Lenalidomide	0-12	Spi-B transcription factor	Homo sapiens	72-76
28893618-9	2017	These results show that the mechanism of action of lenalidomide in ABC-DLBCL cells involves downregulation of SPIB transcription by cereblon-induced degradation of IKAROS.	Lenalidomide	51-63	Spi-B transcription factor	Homo sapiens	110-114
28893618-9	2017	These results show that the mechanism of action of lenalidomide in ABC-DLBCL cells involves downregulation of SPIB transcription by cereblon-induced degradation of IKAROS.	Lenalidomide	51-63	IKAROS family zinc finger 1	Homo sapiens	164-170
28983059-8	2017	Pre-incubation with lenalidomide significantly diminished suppression of erythropoietin production by S100A9 or tumor necrosis factor-alpha.	Lenalidomide	20-32	erythropoietin	Homo sapiens	73-87
28983059-8	2017	Pre-incubation with lenalidomide significantly diminished suppression of erythropoietin production by S100A9 or tumor necrosis factor-alpha.	Lenalidomide	20-32	S100 calcium binding protein A9	Homo sapiens	102-139
28983059-9	2017	Moreover, in peripheral blood mononuclear cells from patients with myelodysplastic syndromes, lenalidomide significantly reduced steady-state S100A9 generation (P=0.01) and lipopolysaccharide-induced tumor necrosis factor-alpha elaboration (P=0.002).	Lenalidomide	94-106	S100 calcium binding protein A9	Homo sapiens	142-148
28983059-9	2017	Moreover, in peripheral blood mononuclear cells from patients with myelodysplastic syndromes, lenalidomide significantly reduced steady-state S100A9 generation (P=0.01) and lipopolysaccharide-induced tumor necrosis factor-alpha elaboration (P=0.002).	Lenalidomide	94-106	tumor necrosis factor	Homo sapiens	200-227
28983059-11	2017	Moreover, baseline serum tumor necrosis factor-alpha concentration was significantly higher in responders to erythroid-stimulating agents (P=0.03), whereas lenalidomide responders had significantly lower tumor necrosis factor-alpha and higher S100A9 serum concentrations (P=0.03).	Lenalidomide	156-168	tumor necrosis factor	Homo sapiens	204-231
28983059-11	2017	Moreover, baseline serum tumor necrosis factor-alpha concentration was significantly higher in responders to erythroid-stimulating agents (P=0.03), whereas lenalidomide responders had significantly lower tumor necrosis factor-alpha and higher S100A9 serum concentrations (P=0.03).	Lenalidomide	156-168	S100 calcium binding protein A9	Homo sapiens	243-249
27301994-0	2017	Durable remission in a patient with leptomeningeal relapse of a MYC/BCL6-positive double-hit DLBCL treated with lenalidomide monotherapy.	Lenalidomide	112-124	BCL6 transcription repressor	Homo sapiens	68-72
27301994-4	2017	Here we present the first case, to our knowledge, of a MYC/BCL6-positive double-hit diffuse large B-cell lymphoma relapsing in the leptomeninges that achieved an outstanding durable remission with single-agent lenalidomide following salvage chemotherapy.	Lenalidomide	210-222	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	55-58
27301994-4	2017	Here we present the first case, to our knowledge, of a MYC/BCL6-positive double-hit diffuse large B-cell lymphoma relapsing in the leptomeninges that achieved an outstanding durable remission with single-agent lenalidomide following salvage chemotherapy.	Lenalidomide	210-222	BCL6 transcription repressor	Homo sapiens	59-63
28828689-3	2017	METHODS: In the previously completed phase 1 study RBP with a dose of 75 mg/m2 bendamustine days 1-2, prednisolone 100 mg days 1-4 and 25 mg lenalidomide days 1-21 was well tolerated.	Lenalidomide	141-153	SURP and G-patch domain containing 1	Homo sapiens	51-54
29290933-0	2017	Prognostic impact of Ikaros expression in lenalidomide-treated multiple myeloma.	Lenalidomide	42-54	IKAROS family zinc finger 1	Homo sapiens	21-27
28815645-2	2017	advanced hepatocellular carcinoma (HCC) AIM: To explore potential biomarkers of lenalidomide efficacy as second-line therapy for HCC.	Lenalidomide	80-92	HCC	Homo sapiens	35-38
28581522-10	2017	Finally, blockade of Rpn11 increases the cytotoxic activity of anti-MM agents lenalidomide, pomalidomide or dexamethasone.	Lenalidomide	78-90	proteasome 26S subunit, non-ATPase 14	Homo sapiens	21-26
28958469-18	2017	PFS2 was significantly longer in the lenalidomide group than in the placebo group (median 57 5 months [47 7-NE] vs 32 7 months [26 4-49 0]; HR 0 46, 95% CI 0 29-0 70; p<0 01).	Lenalidomide	37-49	GINS complex subunit 2	Homo sapiens	0-4
28815645-2	2017	advanced hepatocellular carcinoma (HCC) AIM: To explore potential biomarkers of lenalidomide efficacy as second-line therapy for HCC.	Lenalidomide	80-92	HCC	Homo sapiens	129-132
28815645-16	2017	CONCLUSIONS: Lenalidomide exhibited moderate activity as second-line therapy for advanced HCC.	Lenalidomide	13-25	HCC	Homo sapiens	90-93
28751557-2	2017	Clinical activity of lenalidomide relies on degradation of Ikaros and the consequent reduction in IRF4 expression, both required for myeloma cell survival and involved in the regulation of MYC transcription.	Lenalidomide	21-33	IKAROS family zinc finger 1	Homo sapiens	59-65
28751557-2	2017	Clinical activity of lenalidomide relies on degradation of Ikaros and the consequent reduction in IRF4 expression, both required for myeloma cell survival and involved in the regulation of MYC transcription.	Lenalidomide	21-33	interferon regulatory factor 4	Homo sapiens	98-102
28751557-2	2017	Clinical activity of lenalidomide relies on degradation of Ikaros and the consequent reduction in IRF4 expression, both required for myeloma cell survival and involved in the regulation of MYC transcription.	Lenalidomide	21-33	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	189-192
28278708-0	2017	Myelodysplastic syndrome with concomitant del(5q) and JAK2 V617F mutation transformed to acute myeloid leukemia with an additional chromosomal abnormality after a long-term treatment with lenalidomide.	Lenalidomide	188-200	Janus kinase 2	Homo sapiens	54-58
28681435-0	2017	Impact of lenalidomide-based induction therapy on the mobilization of CD34+ cells, blood graft cellular composition, and post-transplant recovery in myeloma patients: a prospective multicenter study.	Lenalidomide	10-22	CD34 molecule	Homo sapiens	70-74
28681435-2	2017	Previous studies have suggested a negative impact of lenalidomide on the mobilization of CD34+ cells.	Lenalidomide	53-65	CD34 molecule	Homo sapiens	89-93
28681435-8	2017	RESULTS: Patients in the lenalidomide arm had lower median peak CD34+ counts and approximately 40% lower CD34+ cell yields from the first apheresis session, but these differences were not significant.	Lenalidomide	25-37	CD34 molecule	Homo sapiens	64-68
28681435-8	2017	RESULTS: Patients in the lenalidomide arm had lower median peak CD34+ counts and approximately 40% lower CD34+ cell yields from the first apheresis session, but these differences were not significant.	Lenalidomide	25-37	CD34 molecule	Homo sapiens	105-109
28785100-0	2017	JAM-A overexpression is related to disease progression in diffuse large B-cell lymphoma and downregulated by lenalidomide.	Lenalidomide	109-121	F11 receptor	Homo sapiens	0-5
29228683-2	2017	While CD8+CD28- regulatory T-cells in patients with hematologic disorders display a known immune-escape mechanism, we show that lenalidomide can overcome the immunosuppressive impact of CD8+CD28- T-cells.	Lenalidomide	128-140	CD28 molecule	Homo sapiens	190-194
29228683-4	2017	We found that lenalidomide enhances the antigen-specific secretion of IFN-gamma and Granzyme B despite the addition of CD8+CD28- T-cells.	Lenalidomide	14-26	interferon gamma	Homo sapiens	70-79
29228683-4	2017	We found that lenalidomide enhances the antigen-specific secretion of IFN-gamma and Granzyme B despite the addition of CD8+CD28- T-cells.	Lenalidomide	14-26	granzyme B	Homo sapiens	84-94
29228683-5	2017	Furthermore, we showed that lenalidomide inhibits the IL-6 secretion of mononuclear cells, triggered by CD8+CD28- T-cells.	Lenalidomide	28-40	interleukin 6	Homo sapiens	54-58
29228683-5	2017	Furthermore, we showed that lenalidomide inhibits the IL-6 secretion of mononuclear cells, triggered by CD8+CD28- T-cells.	Lenalidomide	28-40	CD8a molecule	Homo sapiens	104-107
29228683-5	2017	Furthermore, we showed that lenalidomide inhibits the IL-6 secretion of mononuclear cells, triggered by CD8+CD28- T-cells.	Lenalidomide	28-40	CD28 molecule	Homo sapiens	108-112
29228683-6	2017	The addition of IL-6 counteracts the action of lenalidomide based stimulation of IFN-gamma secretion and induction of T-cell maturation but not the secretion of Granzyme B.	Lenalidomide	47-59	interleukin 6	Homo sapiens	16-20
29228683-6	2017	The addition of IL-6 counteracts the action of lenalidomide based stimulation of IFN-gamma secretion and induction of T-cell maturation but not the secretion of Granzyme B.	Lenalidomide	47-59	interferon gamma	Homo sapiens	81-90
29228683-8	2017	Analysis of the IL-6 modulating cereblon-binding protein KPNA2 showed the similar degradation capacity of lenalidomide and pomalidomide without explaining the divergent effects.	Lenalidomide	106-118	interleukin 6	Homo sapiens	16-20
29228683-8	2017	Analysis of the IL-6 modulating cereblon-binding protein KPNA2 showed the similar degradation capacity of lenalidomide and pomalidomide without explaining the divergent effects.	Lenalidomide	106-118	karyopherin subunit alpha 2	Homo sapiens	57-62
28709135-4	2017	Sustained inhibition of lymphatic vessels regeneration induced by lenalidomide or the soluble form of vascular endothelial growth factor receptor 3 (sVEGFR3) that neutralises lymphangiogenic vascular endothelial growth factor C (VEGF-C), significantly impaired antitumour efficacy of PDT.	Lenalidomide	66-78	vascular endothelial growth factor C	Mus musculus	191-227
28709135-6	2017	Lenalidomide also abrogated antitumour effects of the combination immunotherapy with PDT and anti-programmed death-ligand 1 (PD-L1) antibodies.	Lenalidomide	0-12	CD274 antigen	Mus musculus	125-130
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	70-82	cereblon	Homo sapiens	151-155
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	70-82	IKAROS family zinc finger 1	Homo sapiens	227-269
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	70-82	IKAROS family zinc finger 1	Homo sapiens	271-276
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	70-82	IKAROS family zinc finger 3	Homo sapiens	281-286
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	110-122	cereblon	Homo sapiens	151-155
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	110-122	IKAROS family zinc finger 1	Homo sapiens	227-269
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	110-122	IKAROS family zinc finger 1	Homo sapiens	271-276
28927072-1	2017	The mechanism of the anti-myeloma effect of the immunomodulatory drug lenalidomide relies upon the binding of lenalidomide or an analogue to cereblon (CRBN) ubiquitin ligase, which inhibits it and results in the degradation of Ikaros-family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	110-122	IKAROS family zinc finger 3	Homo sapiens	281-286
28927072-3	2017	The present study revealed that arsenic trioxide upregulates the transcription and protein levels of CRBN, the anti-myeloma target of lenalidomide, thus potentiating the sensitivity of multiple myeloma cells to lenalidomide and enhancing the lenalidomide-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	134-146	cereblon	Homo sapiens	101-105
28927072-3	2017	The present study revealed that arsenic trioxide upregulates the transcription and protein levels of CRBN, the anti-myeloma target of lenalidomide, thus potentiating the sensitivity of multiple myeloma cells to lenalidomide and enhancing the lenalidomide-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	134-146	IKAROS family zinc finger 1	Homo sapiens	280-285
28927072-3	2017	The present study revealed that arsenic trioxide upregulates the transcription and protein levels of CRBN, the anti-myeloma target of lenalidomide, thus potentiating the sensitivity of multiple myeloma cells to lenalidomide and enhancing the lenalidomide-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	134-146	IKAROS family zinc finger 3	Homo sapiens	290-295
28927072-3	2017	The present study revealed that arsenic trioxide upregulates the transcription and protein levels of CRBN, the anti-myeloma target of lenalidomide, thus potentiating the sensitivity of multiple myeloma cells to lenalidomide and enhancing the lenalidomide-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	211-223	cereblon	Homo sapiens	101-105
28927072-3	2017	The present study revealed that arsenic trioxide upregulates the transcription and protein levels of CRBN, the anti-myeloma target of lenalidomide, thus potentiating the sensitivity of multiple myeloma cells to lenalidomide and enhancing the lenalidomide-dependent degradation of IKZF1 and IKZF3.	Lenalidomide	211-223	cereblon	Homo sapiens	101-105
28619709-5	2017	CRISPR-mediated depletion of endogenous FAM46C enhanced multiple myeloma cell growth, decreased Ig light chain and HSPA5/BIP expression, activated ERK and antiapoptotic signaling, and conferred relative resistance to dexamethasone and lenalidomide treatments.	Lenalidomide	235-247	terminal nucleotidyltransferase 5C	Mus musculus	40-46
28801515-0	2017	Lenalidomide-associated arterial thrombosis in a patient with JAK2 positive atypical myeloproliferative neoplasm.	Lenalidomide	0-12	Janus kinase 2	Homo sapiens	62-66
29228683-0	2017	Lenalidomide overcomes the immunosuppression of regulatory CD8+CD28- T-cells.	Lenalidomide	0-12	CD8a molecule	Homo sapiens	59-62
29228683-0	2017	Lenalidomide overcomes the immunosuppression of regulatory CD8+CD28- T-cells.	Lenalidomide	0-12	CD28 molecule	Homo sapiens	63-67
29228683-2	2017	While CD8+CD28- regulatory T-cells in patients with hematologic disorders display a known immune-escape mechanism, we show that lenalidomide can overcome the immunosuppressive impact of CD8+CD28- T-cells.	Lenalidomide	128-140	CD8a molecule	Homo sapiens	186-189
28643330-0	2017	MUC1-C is a target in lenalidomide resistant multiple myeloma.	Lenalidomide	22-34	mucin 1, cell surface associated	Homo sapiens	0-4
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	0-12	interferon regulatory factor 4	Homo sapiens	109-139
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	141-147
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	149-155
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	160-165
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	14-17	interferon regulatory factor 4	Homo sapiens	109-139
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	14-17	IKAROS family zinc finger 1	Homo sapiens	141-147
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	14-17	IKAROS family zinc finger 1	Homo sapiens	149-155
28643330-1	2017	Lenalidomide (LEN) acts directly on multiple myeloma (MM) cells by inducing cereblon-mediated degradation of interferon regulatory factor 4, Ikaros (IKZF)1 and IKZF3, transcription factors that are essential for MM cell survival.	Lenalidomide	14-17	IKAROS family zinc finger 3	Homo sapiens	160-165
28643330-4	2017	We show that the GO-203/LEN combination acts by synergistically increasing ROS and, in turn, suppressing beta-catenin.	Lenalidomide	24-27	catenin beta 1	Homo sapiens	105-117
28643330-5	2017	LEN resistance has been linked to activation of the WNT/beta-catenin CD44 pathway.	Lenalidomide	0-3	catenin beta 1	Homo sapiens	56-68
28643330-5	2017	LEN resistance has been linked to activation of the WNT/beta-catenin CD44 pathway.	Lenalidomide	0-3	CD44 molecule (Indian blood group)	Homo sapiens	69-73
28785100-6	2017	Lenalidomide downregulated JAM-A and downstream NODAL expression, resulting in inhibition of B-lymphoma cell invasion and epithelial-to-mesenchymal transition.	Lenalidomide	0-12	F11 receptor	Homo sapiens	27-32
28785100-6	2017	Lenalidomide downregulated JAM-A and downstream NODAL expression, resulting in inhibition of B-lymphoma cell invasion and epithelial-to-mesenchymal transition.	Lenalidomide	0-12	nodal growth differentiation factor	Homo sapiens	48-53
28785100-7	2017	In a murine xenograft model established with subcutaneous injection of JAM-A-overexpressing B-lymphoma cells, lenalidomide retarded tumor growth and prevented cell invasion to mesoendoderm-derived organs, consistent with the downregulation of JAM-A and NODAL expression.	Lenalidomide	110-122	F11 receptor	Mus musculus	71-76
28785100-7	2017	In a murine xenograft model established with subcutaneous injection of JAM-A-overexpressing B-lymphoma cells, lenalidomide retarded tumor growth and prevented cell invasion to mesoendoderm-derived organs, consistent with the downregulation of JAM-A and NODAL expression.	Lenalidomide	110-122	F11 receptor	Mus musculus	243-248
28785100-7	2017	In a murine xenograft model established with subcutaneous injection of JAM-A-overexpressing B-lymphoma cells, lenalidomide retarded tumor growth and prevented cell invasion to mesoendoderm-derived organs, consistent with the downregulation of JAM-A and NODAL expression.	Lenalidomide	110-122	nodal	Mus musculus	253-258
28785100-9	2017	Identified as a biomarker of stem cell property, JAM-A indicated the sensitivity of B-lymphoma cells to lenalidomide.	Lenalidomide	104-116	F11 receptor	Homo sapiens	49-54
28017969-9	2017	Our data suggest a prognostic role of IKZF1, IKZF3 and BSG expression levels in lenalidomide-treated multiple myeloma.	Lenalidomide	80-92	IKAROS family zinc finger 1	Homo sapiens	38-43
28270494-11	2017	Combination of SJB and HDACi ACY-1215, bortezomib, lenalidomide, or pomalidomide triggers synergistic cytotoxicity.Conclusions: Our preclinical studies provide the framework for clinical evaluation of USP1 inhibitors, alone or in combination, as a potential novel multiple myeloma therapy.	Lenalidomide	51-63	ubiquitin specific peptidase 1	Homo sapiens	201-205
28426350-11	2017	Conclusion Lenalidomide maintenance for 24 months after obtaining a CR or PR to R-CHOP significantly prolonged PFS in elderly patients with DLBCL.	Lenalidomide	11-23	DNA damage inducible transcript 3	Homo sapiens	82-86
27967292-5	2017	P53 antagonism by lenalidomide or other therapeutics such as antisense oligonucleotides, repopulates erythroid precursors and enhances effective erythropoiesis.	Lenalidomide	18-30	tumor protein p53	Homo sapiens	0-3
28903429-0	2017	Lenalidomide restores the osteogenic differentiation of bone marrow mesenchymal stem cells from multiple myeloma patients via deactivating Notch signaling pathway.	Lenalidomide	0-12	notch receptor 1	Homo sapiens	139-144
28903429-7	2017	Furthermore, it is shown that the gene expression of Notch signaling molecules, including receptors, ligands and downstream factors are significantly decreased in MM-MSCs following lenalidomide treatment, compared with non-treated MM-MSCs.	Lenalidomide	181-193	notch receptor 1	Homo sapiens	53-58
28903429-8	2017	Taken together, treatment with lenalidomide restores the osteogenic differentiation of MM-MSCs via deactivating Notch signaling pathway.	Lenalidomide	31-43	notch receptor 1	Homo sapiens	112-117
28488026-0	2017	Carfilzomib and lenalidomide response related to VEGF and VEGFR2 germline polymorphisms.	Lenalidomide	16-28	vascular endothelial growth factor A	Homo sapiens	49-53
28488026-0	2017	Carfilzomib and lenalidomide response related to VEGF and VEGFR2 germline polymorphisms.	Lenalidomide	16-28	kinase insert domain receptor	Homo sapiens	58-64
28552667-9	2017	Also, results of the therapeutic mice model, in which SP2/0 cells- challenged mice were treated with 5mg/kg lenalidomide in combination with pcDNA3.1+NS3, reasonably agreed with those of the prophylactic model.	Lenalidomide	108-120	Sp2 transcription factor	Mus musculus	54-57
28017969-0	2017	IKZF1 expression is a prognostic marker in newly diagnosed standard-risk multiple myeloma treated with lenalidomide and intensive chemotherapy: a study of the German Myeloma Study Group (DSMM).	Lenalidomide	103-115	IKAROS family zinc finger 1	Homo sapiens	0-5
28017969-2	2017	Lenalidomide binding to the Cereblon (CRBN) E3 ubiquitin ligase results in targeted ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) leading to growth inhibition of multiple myeloma cells.	Lenalidomide	0-12	cereblon	Homo sapiens	28-36
28017969-2	2017	Lenalidomide binding to the Cereblon (CRBN) E3 ubiquitin ligase results in targeted ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) leading to growth inhibition of multiple myeloma cells.	Lenalidomide	0-12	cereblon	Homo sapiens	38-42
28017969-2	2017	Lenalidomide binding to the Cereblon (CRBN) E3 ubiquitin ligase results in targeted ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) leading to growth inhibition of multiple myeloma cells.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	161-166
28017969-2	2017	Lenalidomide binding to the Cereblon (CRBN) E3 ubiquitin ligase results in targeted ubiquitination and degradation of the lymphoid transcription factors Ikaros (IKZF1) and Aiolos (IKZF3) leading to growth inhibition of multiple myeloma cells.	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	180-185
28017969-3	2017	Recently, Basigin (BSG) was identified as another protein regulated by CRBN that is involved in the activity of lenalidomide.	Lenalidomide	112-124	basigin (Ok blood group)	Homo sapiens	10-17
28017969-3	2017	Recently, Basigin (BSG) was identified as another protein regulated by CRBN that is involved in the activity of lenalidomide.	Lenalidomide	112-124	basigin (Ok blood group)	Homo sapiens	19-22
28249894-4	2017	CD38 levels and the percentages of CD38high Tregs are increased by lenalidomide and pomalidomide.	Lenalidomide	67-79	CD38 molecule	Homo sapiens	0-4
28249894-4	2017	CD38 levels and the percentages of CD38high Tregs are increased by lenalidomide and pomalidomide.	Lenalidomide	67-79	CD38 molecule	Homo sapiens	35-39
28693194-9	2017	Therefore, the combination of warfarin and lenalidomide may cause a pharmacodynamic interaction, more likely by inhibiting the production of interleukin-6.	Lenalidomide	43-55	interleukin 6	Homo sapiens	141-154
28958290-4	2017	In contrast, in non-del(5q) MDS, lenalidomide restores effective erythropoiesis via enhancement of erythropoietin (EPO) receptor-initiated transcriptional response arising from the assembly of signaling-competent receptor complexes within membrane lipid raft domains.	Lenalidomide	33-45	erythropoietin	Homo sapiens	99-113
28958290-4	2017	In contrast, in non-del(5q) MDS, lenalidomide restores effective erythropoiesis via enhancement of erythropoietin (EPO) receptor-initiated transcriptional response arising from the assembly of signaling-competent receptor complexes within membrane lipid raft domains.	Lenalidomide	33-45	erythropoietin	Homo sapiens	115-118
29296763-1	2017	A man with cytopenias, dysplasia, excess blasts, P53 and RUNX1 mutations, and ring chromosome 7 recovered after stopping lenalidomide.	Lenalidomide	121-133	tumor protein p53	Homo sapiens	49-52
29296763-1	2017	A man with cytopenias, dysplasia, excess blasts, P53 and RUNX1 mutations, and ring chromosome 7 recovered after stopping lenalidomide.	Lenalidomide	121-133	RUNX family transcription factor 1	Homo sapiens	57-62
28529032-0	2017	Synergistic Cytotoxicity of Lenalidomide and Dexamethasone in Mantle Cell Lymphoma via Cereblon-dependent Targeting of the IL-6/STAT3/PI3K Axis.	Lenalidomide	28-40	interleukin 6	Homo sapiens	123-127
28529032-0	2017	Synergistic Cytotoxicity of Lenalidomide and Dexamethasone in Mantle Cell Lymphoma via Cereblon-dependent Targeting of the IL-6/STAT3/PI3K Axis.	Lenalidomide	28-40	signal transducer and activator of transcription 3	Homo sapiens	128-133
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	interleukin 6	Homo sapiens	201-205
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	signal transducer and activator of transcription 3	Homo sapiens	206-211
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	214-243
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	AKT serine/threonine kinase 1	Homo sapiens	251-254
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	AKT serine/threonine kinase 2	Homo sapiens	259-263
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	forkhead box O3	Homo sapiens	264-279
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	forkhead box O3	Homo sapiens	281-287
28529032-2	2017	Cereblon is probably targeted by both lenalidomide and dexamethasone, which leads to synergistic cytotoxicity in MCL by inhibiting the interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3), phosphatidylinositol 3-kinase (PI3K)/AKT and AKT2/Forkhead box O3 (FOXO3A)/BCL2-like 11 (BIM) pathways.	Lenalidomide	38-50	BCL2 like 11	Homo sapiens	289-301
28630385-10	2017	CONCLUSION: Treatment by lenalidomide and pcDNA3.1(+)/NS3 improves NK cytotoxicity up to 66.80% suggesting that lenalidomide can be used in parallel with such therapeutic vaccines as cancer vaccine or virus vaccines.	Lenalidomide	112-124	KRAS proto-oncogene, GTPase	Homo sapiens	54-57
28017969-3	2017	Recently, Basigin (BSG) was identified as another protein regulated by CRBN that is involved in the activity of lenalidomide.	Lenalidomide	112-124	cereblon	Homo sapiens	71-75
28017969-9	2017	Our data suggest a prognostic role of IKZF1, IKZF3 and BSG expression levels in lenalidomide-treated multiple myeloma.	Lenalidomide	80-92	IKAROS family zinc finger 3	Homo sapiens	45-50
28017969-9	2017	Our data suggest a prognostic role of IKZF1, IKZF3 and BSG expression levels in lenalidomide-treated multiple myeloma.	Lenalidomide	80-92	basigin (Ok blood group)	Homo sapiens	55-58
28437394-2	2017	In particular, the substrate-receptor proteins of the cullin-ubiquitin ligase system play a key role in selective protein degradation, which is an essential component of the anti-myeloma activity of immunomodulatory drugs (IMiDs), such as lenalidomide.	Lenalidomide	239-251	CDK2 associated cullin domain 1	Homo sapiens	54-60
28530236-4	2017	Using a pulse-chase SILAC mass spectrometry-based proteomics approach, we demonstrate that lenalidomide induces the ubiquitination and degradation of ZFP91.	Lenalidomide	91-103	ZFP91 zinc finger protein, atypical E3 ubiquitin ligase	Homo sapiens	150-155
28881567-5	2017	We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells.	Lenalidomide	18-30	intercellular adhesion molecule 1	Homo sapiens	130-136
28881567-5	2017	We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells.	Lenalidomide	18-30	CD86 molecule	Homo sapiens	141-145
28881567-5	2017	We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells.	Lenalidomide	32-35	intercellular adhesion molecule 1	Homo sapiens	130-136
28881567-5	2017	We show here that lenalidomide (Len) and pomalidomide (Pom) prevent down-regulation of MHC-I during lytic activation, and restore ICAM-1 and B7-2 surface expression in latently infected PEL cells.	Lenalidomide	32-35	CD86 molecule	Homo sapiens	141-145
26961690-0	2017	Lenalidomide potentiates CD4+CD25+Treg-related suppression of lymphoma B-cell proliferation.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	25-28
26961690-2	2017	Here we demonstrate that the immunomodulatory drug lenalidomide potentiates suppression of lymphoma B-cell proliferation by freshly isolated CD4+CD25+Tregs, as well as suppression by Tregs expanded polyclonally in the presence of rapamycin from CD4+CD25+T cells or CD4+CD25+CD127loT cells.	Lenalidomide	51-63	CD4 molecule	Homo sapiens	141-144
26961690-2	2017	Here we demonstrate that the immunomodulatory drug lenalidomide potentiates suppression of lymphoma B-cell proliferation by freshly isolated CD4+CD25+Tregs, as well as suppression by Tregs expanded polyclonally in the presence of rapamycin from CD4+CD25+T cells or CD4+CD25+CD127loT cells.	Lenalidomide	51-63	CD4 molecule	Homo sapiens	245-248
26961690-2	2017	Here we demonstrate that the immunomodulatory drug lenalidomide potentiates suppression of lymphoma B-cell proliferation by freshly isolated CD4+CD25+Tregs, as well as suppression by Tregs expanded polyclonally in the presence of rapamycin from CD4+CD25+T cells or CD4+CD25+CD127loT cells.	Lenalidomide	51-63	CD4 molecule	Homo sapiens	245-248
26961690-8	2017	Freshly isolated lymphoma cells activated with multimeric CD40L and IL-4 to support their survival in vitro varied in their sensitivity to lenalidomide, and the regulatory effect of Tregs on such lymphoma cells ranged from suppression to help in individual patients.	Lenalidomide	139-151	interleukin 4	Homo sapiens	68-72
28199990-9	2017	Given the importance of an effective immune response to counteract the MM progression and the promising approaches using anti-PD-1/PD-L1 strategies, we will discuss in this review how Lenalidomide could represent an adequate approach to re-establish the recognition against MM by exhausted NK cell.	Lenalidomide	184-196	programmed cell death 1	Homo sapiens	126-130
28628013-12	2017	DC were treated with lenalidomide and the expression of surface markers MHC Class I, MHC Class II, CD80, CD86, CD 205, and CD40 was increased.	Lenalidomide	21-33	CD80 antigen	Mus musculus	99-103
28628013-12	2017	DC were treated with lenalidomide and the expression of surface markers MHC Class I, MHC Class II, CD80, CD86, CD 205, and CD40 was increased.	Lenalidomide	21-33	CD86 antigen	Mus musculus	105-109
28628013-12	2017	DC were treated with lenalidomide and the expression of surface markers MHC Class I, MHC Class II, CD80, CD86, CD 205, and CD40 was increased.	Lenalidomide	21-33	CD40 antigen	Mus musculus	123-127
28460478-6	2017	This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response.	Lenalidomide	82-94	negative elongation factor complex member C/D, Th1l	Mus musculus	311-314
28460478-6	2017	This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response.	Lenalidomide	82-94	heart and neural crest derivatives expressed 2	Mus musculus	315-318
28460478-6	2017	This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response.	Lenalidomide	82-94	negative elongation factor complex member C/D, Th1l	Mus musculus	339-342
28199990-0	2017	Activation of NK cells and disruption of PD-L1/PD-1 axis: two different ways for lenalidomide to block myeloma progression.	Lenalidomide	81-93	CD274 molecule	Homo sapiens	41-46
28199990-0	2017	Activation of NK cells and disruption of PD-L1/PD-1 axis: two different ways for lenalidomide to block myeloma progression.	Lenalidomide	81-93	programmed cell death 1	Homo sapiens	47-51
28199990-7	2017	This occurs since Lenalidomide acts on several critical points: stimulates T cell proliferation and cytokine secretion; decreases the expression of the immune check-point inhibitor Programmed Death-1 (PD-1) on both T and NK cells in MM patients; decreases the expression of both PD-1 and PD-L1 on MM cells; promotes MM cell death and abrogates MM/stromal microenvironment cross-talk, a process known to promote the MM cell survival and proliferation.	Lenalidomide	18-30	programmed cell death 1	Homo sapiens	201-205
28199990-7	2017	This occurs since Lenalidomide acts on several critical points: stimulates T cell proliferation and cytokine secretion; decreases the expression of the immune check-point inhibitor Programmed Death-1 (PD-1) on both T and NK cells in MM patients; decreases the expression of both PD-1 and PD-L1 on MM cells; promotes MM cell death and abrogates MM/stromal microenvironment cross-talk, a process known to promote the MM cell survival and proliferation.	Lenalidomide	18-30	programmed cell death 1	Homo sapiens	279-283
28199990-7	2017	This occurs since Lenalidomide acts on several critical points: stimulates T cell proliferation and cytokine secretion; decreases the expression of the immune check-point inhibitor Programmed Death-1 (PD-1) on both T and NK cells in MM patients; decreases the expression of both PD-1 and PD-L1 on MM cells; promotes MM cell death and abrogates MM/stromal microenvironment cross-talk, a process known to promote the MM cell survival and proliferation.	Lenalidomide	18-30	CD274 molecule	Sus scrofa	288-293
27686868-8	2017	Concomitant pan-Raf/PI3K inhibition was also effective in carfilzomib- and lenalidomide-resistant MM models underscoring that this attractive therapeutic anti-MM strategy is suitable for immediate clinical translation.	Lenalidomide	75-87	zinc fingers and homeoboxes 2	Homo sapiens	16-19
28199990-9	2017	Given the importance of an effective immune response to counteract the MM progression and the promising approaches using anti-PD-1/PD-L1 strategies, we will discuss in this review how Lenalidomide could represent an adequate approach to re-establish the recognition against MM by exhausted NK cell.	Lenalidomide	184-196	CD274 molecule	Homo sapiens	131-136
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	54-57
28358372-7	2017	Notably, inhibition of TNF-alpha and LRG1 activity by Lenalidomide, an inhibitor of TNF-alpha production, in ACLT mice attenuated degeneration of osteoarthritis articular cartilage.	Lenalidomide	54-66	tumor necrosis factor	Mus musculus	23-32
28358372-7	2017	Notably, inhibition of TNF-alpha and LRG1 activity by Lenalidomide, an inhibitor of TNF-alpha production, in ACLT mice attenuated degeneration of osteoarthritis articular cartilage.	Lenalidomide	54-66	leucine-rich alpha-2-glycoprotein 1	Mus musculus	37-41
28358372-7	2017	Notably, inhibition of TNF-alpha and LRG1 activity by Lenalidomide, an inhibitor of TNF-alpha production, in ACLT mice attenuated degeneration of osteoarthritis articular cartilage.	Lenalidomide	54-66	tumor necrosis factor	Mus musculus	84-93
28358372-10	2017	Inhibition of TNF-alpha and LRG1 by Lenalidomide could be a potential therapeutic approach.	Lenalidomide	36-48	tumor necrosis factor	Mus musculus	14-23
28358372-10	2017	Inhibition of TNF-alpha and LRG1 by Lenalidomide could be a potential therapeutic approach.	Lenalidomide	36-48	leucine-rich alpha-2-glycoprotein 1	Mus musculus	28-32
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	damage specific DNA binding protein 1	Homo sapiens	58-62
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	DET1 and DDB1 associated 1	Homo sapiens	63-67
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	IKAROS family zinc finger 1	Homo sapiens	132-137
28087699-4	2017	Pharmacological inhibition or genetic ablation of the Abl-DDB1-DDA1 axis decreases the ubiquitination of CRL4 substrates, including IKZF1 and IKZF3, in lenalidomide-treated multiple myeloma cells.	Lenalidomide	152-164	IKAROS family zinc finger 3	Homo sapiens	142-147
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Lenalidomide	92-104	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28087699-5	2017	Importantly, panobinostat, a recently approved anti-myeloma drug, and dexamethasone enhance lenalidomide-induced substrate degradation and cytotoxicity by activating c-Abl, therefore providing a mechanism underlying their combination with lenalidomide to treat multiple myeloma.	Lenalidomide	239-251	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
28052520-0	2017	IKAROS expression in distinct bone marrow cell populations as a candidate biomarker for outcome with lenalidomide-dexamethasone therapy in multiple myeloma.	Lenalidomide	101-113	IKAROS family zinc finger 1	Homo sapiens	0-6
27893171-4	2017	RESULTS: Bortezomib-based regimens upfront followed by lenalidomide-based regimens at first relapse resulted in significantly better second progression-free survival (2ndPFS), PFS2, and overall survival (OS) compared to the opposite sequence.	Lenalidomide	55-67	GINS complex subunit 2	Homo sapiens	176-180
27884971-6	2017	TP53 mutations were found in seven of nine patients who developed acute leukemia, and were documented to be present in the earliest sample (n=1) and acquired during lenalidomide treatment (n=6).	Lenalidomide	165-177	tumor protein p53	Homo sapiens	0-4
28028022-6	2017	Lenalidomide increased intracellular H2O2 levels by inhibiting thioredoxin reductase (TrxR) in cells expressing CRBN, causing accumulation of immunoglobulin light-chain dimers, significantly increasing endoplasmic reticulum stress and inducing cytotoxicity by activation of BH3-only protein Bim in MM.	Lenalidomide	0-12	peroxiredoxin 5	Homo sapiens	63-84
27862100-10	2017	DC were treated with 5-AzaC and lenalidomide and the expression of surface markers MHC Class I, MHC Class II, CD80, CD86, CD 205, and CD40 was increased.	Lenalidomide	32-44	CD40 antigen	Mus musculus	134-138
27862100-12	2017	Secretion of IL-12 and IL-15 by DC increased significantly with addition of 5-AzaC or 5-AzaC and lenalidomide.	Lenalidomide	97-109	interleukin 15	Mus musculus	23-28
28028022-6	2017	Lenalidomide increased intracellular H2O2 levels by inhibiting thioredoxin reductase (TrxR) in cells expressing CRBN, causing accumulation of immunoglobulin light-chain dimers, significantly increasing endoplasmic reticulum stress and inducing cytotoxicity by activation of BH3-only protein Bim in MM.	Lenalidomide	0-12	peroxiredoxin 5	Homo sapiens	86-90
28028022-6	2017	Lenalidomide increased intracellular H2O2 levels by inhibiting thioredoxin reductase (TrxR) in cells expressing CRBN, causing accumulation of immunoglobulin light-chain dimers, significantly increasing endoplasmic reticulum stress and inducing cytotoxicity by activation of BH3-only protein Bim in MM.	Lenalidomide	0-12	cereblon	Homo sapiens	112-116
26956578-6	2016	A linear relationship with good correlation coefficient (r = 0.997, n = 9) was found between the peak area and lenalidomide concentrations in the range of 100 to 950 ng   mL-1 The limits of detection and quantitation were 28 and 100 ng   mL-1, respectively.	Lenalidomide	111-123	L1 cell adhesion molecule	Mus musculus	171-175
28057080-4	2017	To test this hypothesis, we combined the use of a single-chain antibody targeting alpha-syn modified for improved central nervous system penetration (CD5-D5) with an unconventional anti-inflammatory treatment (lenalidomide) in the myelin basic protein (MBP)-alpha-syn transgenic mouse model of MSA.	Lenalidomide	210-222	myelin basic protein	Mus musculus	231-251
28057080-4	2017	To test this hypothesis, we combined the use of a single-chain antibody targeting alpha-syn modified for improved central nervous system penetration (CD5-D5) with an unconventional anti-inflammatory treatment (lenalidomide) in the myelin basic protein (MBP)-alpha-syn transgenic mouse model of MSA.	Lenalidomide	210-222	myelin basic protein	Mus musculus	253-256
28057080-5	2017	While the use of either CD5-D5 or lenalidomide alone had positive effects on neuroinflammation and/or alpha-syn accumulation in this mouse model of MSA, the combination of both approaches yielded better results than each single treatment.	Lenalidomide	34-46	synuclein, alpha	Mus musculus	102-111
28484169-5	2017	Moreover, the CSNK1A1 gene is known to play a role in the mechanism of action of lenalidomide.	Lenalidomide	81-93	casein kinase 1 alpha 1	Homo sapiens	14-21
28592763-4	2017	Ibrutinib or lenalidomide was shown to be more effective in activated B-cell (ABC) -type-DLBCL than in germinal center B-cell type-DLBCL.	Lenalidomide	13-25	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	78-81
27889516-7	2017	These results suggest that LEN enhanced the function of DCs generated from patients with multiple myeloma by stimulating the capacity of allogeneic T cells, inhibiting the generation of immunosuppressive cells, inducing naive T cells toward Th1 polarization, and generating potent myeloma-specific cytotoxic T lymphocytes.	Lenalidomide	27-30	negative elongation factor complex member C/D	Homo sapiens	241-244
29212067-0	2017	Lenalidomide Maintenance after R-CHOP Therapy in Diffuse Large B-Cell Lymphoma: Can It Be a Standard of Care.	Lenalidomide	0-12	DNA damage inducible transcript 3	Homo sapiens	33-37
27698446-0	2017	Expansion of Th1-like Vgamma9Vdelta2T cells by new-generation IMiDs, lenalidomide and pomalidomide, in combination with zoledronic acid.	Lenalidomide	69-81	negative elongation factor complex member C/D	Homo sapiens	13-16
26956578-8	2016	In conclusion, the proposed method is suitable for the accurate quantification of lenalidomide in human plasma with a wide linear range, from 100 to 950 ng   mL-1 This is a valuable method for pharmacokinetic studies of lenalidomide in human subjects.	Lenalidomide	82-94	L1 cell adhesion molecule	Mus musculus	158-162
27677742-8	2016	Lenalidomide and trabectedin prevent TAM recruitment mainly through CCL2 blockade.	Lenalidomide	0-12	C-C motif chemokine ligand 2	Homo sapiens	68-72
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).	Lenalidomide	26-38	cereblon	Homo sapiens	65-69
27776107-10	2016	Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes.	Lenalidomide	15-27	ras homolog family member A	Homo sapiens	38-42
27776107-10	2016	Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes.	Lenalidomide	15-27	RAS guanyl releasing protein 1	Homo sapiens	105-112
27881177-0	2016	High IKZF1/3 protein expression is a favorable prognostic factor for survival of relapsed/refractory multiple myeloma patients treated with lenalidomide.	Lenalidomide	140-152	IKAROS family zinc finger 1	Homo sapiens	5-12
27855285-8	2017	This computational biology network approach identified GGH overexpression as a potential resistance factor to HMA treatment and paradoxical activation of beta-catenin (through Csnk1a1 inhibition) as a resistance factor to lenalidomide treatment.	Lenalidomide	222-234	catenin beta 1	Homo sapiens	154-166
27881177-1	2016	The aim of this study is to assess nucleoprotein expression of IKZF1/3 in patients with relapsed/refractory multiple myeloma (MM) who received lenalidomide-based therapy and correlated them with their clinical outcomes.	Lenalidomide	143-155	IKAROS family zinc finger 1	Homo sapiens	63-68
27881177-5	2016	IKZF3 expression also appears predicted a favorable response to the lenalidomide-based therapy.	Lenalidomide	68-80	IKAROS family zinc finger 3	Homo sapiens	0-5
27389073-5	2016	We found that after six months of lenalidomide therapy, the number of CD34(+) HSPCs decreased.	Lenalidomide	34-46	CD34 molecule	Homo sapiens	70-74
27657380-8	2016	Apoptosis was associated with increased hallmarks of ER stress and activation of UPR sensors and was mediated by dephosphorylation of the AKT, MAPK/ERK, and STAT3 pathways.The combination of romidepsin and lenalidomide shows promise as a possible treatment for T-cell lymphoma.	Lenalidomide	206-218	AKT serine/threonine kinase 1	Homo sapiens	138-141
27748917-0	2016	Lenalidomide induces apoptosis and inhibits angiogenesis via caspase-3 and VEGF in hepatocellular carcinoma cells.	Lenalidomide	0-12	caspase 3	Homo sapiens	61-70
27748917-0	2016	Lenalidomide induces apoptosis and inhibits angiogenesis via caspase-3 and VEGF in hepatocellular carcinoma cells.	Lenalidomide	0-12	vascular endothelial growth factor A	Homo sapiens	75-79
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.	Lenalidomide	47-59	vascular endothelial growth factor A	Homo sapiens	200-204
27748917-9	2016	In conclusion, the results indicated that lenalidomide induces apoptosis and inhibits angiogenesis in HCC cells via caspase-3 and VEGF pathway, and these may provide a potential perspective for lenalidomide"s application in clinical.	Lenalidomide	42-54	caspase 3	Homo sapiens	116-125
27748917-9	2016	In conclusion, the results indicated that lenalidomide induces apoptosis and inhibits angiogenesis in HCC cells via caspase-3 and VEGF pathway, and these may provide a potential perspective for lenalidomide"s application in clinical.	Lenalidomide	42-54	vascular endothelial growth factor A	Homo sapiens	130-134
27748917-9	2016	In conclusion, the results indicated that lenalidomide induces apoptosis and inhibits angiogenesis in HCC cells via caspase-3 and VEGF pathway, and these may provide a potential perspective for lenalidomide"s application in clinical.	Lenalidomide	194-206	caspase 3	Homo sapiens	116-125
27748917-9	2016	In conclusion, the results indicated that lenalidomide induces apoptosis and inhibits angiogenesis in HCC cells via caspase-3 and VEGF pathway, and these may provide a potential perspective for lenalidomide"s application in clinical.	Lenalidomide	194-206	vascular endothelial growth factor A	Homo sapiens	130-134
26186254-1	2016	Clinical interest in the measurement of Cereblon (CRBN), the primary target of the IMiDs immunomodulatory drugs lenalidomide and pomalidomide, has been fueled by its essential requirement for antitumor or immunomodulatory activity of both drugs in multiple myeloma (MM).	Lenalidomide	112-124	cereblon	Homo sapiens	40-48
26186254-1	2016	Clinical interest in the measurement of Cereblon (CRBN), the primary target of the IMiDs immunomodulatory drugs lenalidomide and pomalidomide, has been fueled by its essential requirement for antitumor or immunomodulatory activity of both drugs in multiple myeloma (MM).	Lenalidomide	112-124	cereblon	Homo sapiens	50-54
27657380-8	2016	Apoptosis was associated with increased hallmarks of ER stress and activation of UPR sensors and was mediated by dephosphorylation of the AKT, MAPK/ERK, and STAT3 pathways.The combination of romidepsin and lenalidomide shows promise as a possible treatment for T-cell lymphoma.	Lenalidomide	206-218	mitogen-activated protein kinase 1	Homo sapiens	148-151
27657380-8	2016	Apoptosis was associated with increased hallmarks of ER stress and activation of UPR sensors and was mediated by dephosphorylation of the AKT, MAPK/ERK, and STAT3 pathways.The combination of romidepsin and lenalidomide shows promise as a possible treatment for T-cell lymphoma.	Lenalidomide	206-218	signal transducer and activator of transcription 3	Homo sapiens	157-162
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.	Lenalidomide	165-177	cereblon	Homo sapiens	10-14
27465366-8	2016	Finally, using lenalidomide (an inhibitor of TNF-alpha), a lower viral load was found in animals with lenalidomide.	Lenalidomide	15-27	tumor necrosis factor	Homo sapiens	45-54
27601648-0	2016	Rabex-5 is a lenalidomide target molecule that negatively regulates TLR-induced type 1 IFN production.	Lenalidomide	13-25	RAB guanine nucleotide exchange factor 1	Homo sapiens	0-7
27601648-4	2016	Treatment with lenalidomide prevented the association of Cereblon with Rabex-5.	Lenalidomide	15-27	RAB guanine nucleotide exchange factor 1	Homo sapiens	71-78
27611189-7	2016	Furthermore, anti-CD38-IFNalpha(attenuated) is more efficacious than standard MM treatments (lenalidomide, bortezomib, dexamethasone) and exhibits strong synergy with lenalidomide and with bortezomib in xenograft models.	Lenalidomide	93-105	CD38 molecule	Homo sapiens	18-22
27611189-7	2016	Furthermore, anti-CD38-IFNalpha(attenuated) is more efficacious than standard MM treatments (lenalidomide, bortezomib, dexamethasone) and exhibits strong synergy with lenalidomide and with bortezomib in xenograft models.	Lenalidomide	93-105	interferon alpha 1	Homo sapiens	23-31
27611189-7	2016	Furthermore, anti-CD38-IFNalpha(attenuated) is more efficacious than standard MM treatments (lenalidomide, bortezomib, dexamethasone) and exhibits strong synergy with lenalidomide and with bortezomib in xenograft models.	Lenalidomide	167-179	CD38 molecule	Homo sapiens	18-22
27611189-7	2016	Furthermore, anti-CD38-IFNalpha(attenuated) is more efficacious than standard MM treatments (lenalidomide, bortezomib, dexamethasone) and exhibits strong synergy with lenalidomide and with bortezomib in xenograft models.	Lenalidomide	167-179	interferon alpha 1	Homo sapiens	23-31
27465366-8	2016	Finally, using lenalidomide (an inhibitor of TNF-alpha), a lower viral load was found in animals with lenalidomide.	Lenalidomide	102-114	tumor necrosis factor	Homo sapiens	45-54
27479651-6	2016	The expression of P-gp was induced in SKM-1 cells by selective pressure using vincristine (VCR), mitoxantrone (MTX), azacytidine (AzaC) and lenalidomide (LEN).	Lenalidomide	140-152	ATP binding cassette subfamily B member 1	Homo sapiens	18-22
27133825-0	2016	Prevalence, clonal dynamics and clinical impact of TP53 mutations in patients with myelodysplastic syndrome with isolated deletion (5q) treated with lenalidomide: results from a prospective multicenter study of the german MDS study group (GMDS).	Lenalidomide	149-161	tumor protein p53	Homo sapiens	51-55
27479651-6	2016	The expression of P-gp was induced in SKM-1 cells by selective pressure using vincristine (VCR), mitoxantrone (MTX), azacytidine (AzaC) and lenalidomide (LEN).	Lenalidomide	140-152	sodium voltage-gated channel alpha subunit 4	Homo sapiens	38-43
27479651-6	2016	The expression of P-gp was induced in SKM-1 cells by selective pressure using vincristine (VCR), mitoxantrone (MTX), azacytidine (AzaC) and lenalidomide (LEN).	Lenalidomide	154-157	ATP binding cassette subfamily B member 1	Homo sapiens	18-22
27479651-6	2016	The expression of P-gp was induced in SKM-1 cells by selective pressure using vincristine (VCR), mitoxantrone (MTX), azacytidine (AzaC) and lenalidomide (LEN).	Lenalidomide	154-157	sodium voltage-gated channel alpha subunit 4	Homo sapiens	38-43
27089170-0	2016	ROBUST: Lenalidomide-R-CHOP versus placebo-R-CHOP in previously untreated ABC-type diffuse large B-cell lymphoma.	Lenalidomide	8-20	DNA damage inducible transcript 3	Homo sapiens	23-27
27538006-0	2016	Erythema Nodosum-like Septal Panniculitis Secondary to Lenalidomide Therapy in a Patient With Janus Kinase 2-Positive Myelofibrosis.	Lenalidomide	55-67	Janus kinase 2	Homo sapiens	94-108
27538006-2	2016	We present a case of a 66-year-old gentleman with JAK2-positive myelofibrosis who developed transient EN-like lesions on his trunk and upper and lower extremities approximately three weeks after starting lenalidomide therapy.	Lenalidomide	204-216	Janus kinase 2	Homo sapiens	50-54
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.	Lenalidomide	221-233	cereblon	Homo sapiens	46-50
27286995-7	2016	Lenalidomide clearance declined with decreased CrCl.	Lenalidomide	0-12	CRCL	Homo sapiens	47-51
26823144-8	2016	Furthermore, treatment with an anti-MM agent, lenalidomide, caused ubiquitination and proteasomal degradation of Blimp-1, leading to the de-repression of a new Blimp-1 direct target, CULLIN 4A (CUL4A), and reduced Aiolos levels.	Lenalidomide	46-58	PR/SET domain 1	Homo sapiens	113-120
26823144-8	2016	Furthermore, treatment with an anti-MM agent, lenalidomide, caused ubiquitination and proteasomal degradation of Blimp-1, leading to the de-repression of a new Blimp-1 direct target, CULLIN 4A (CUL4A), and reduced Aiolos levels.	Lenalidomide	46-58	PR/SET domain 1	Homo sapiens	160-167
26823144-8	2016	Furthermore, treatment with an anti-MM agent, lenalidomide, caused ubiquitination and proteasomal degradation of Blimp-1, leading to the de-repression of a new Blimp-1 direct target, CULLIN 4A (CUL4A), and reduced Aiolos levels.	Lenalidomide	46-58	cullin 4A	Homo sapiens	183-192
26823144-8	2016	Furthermore, treatment with an anti-MM agent, lenalidomide, caused ubiquitination and proteasomal degradation of Blimp-1, leading to the de-repression of a new Blimp-1 direct target, CULLIN 4A (CUL4A), and reduced Aiolos levels.	Lenalidomide	46-58	cullin 4A	Homo sapiens	194-199
26823144-8	2016	Furthermore, treatment with an anti-MM agent, lenalidomide, caused ubiquitination and proteasomal degradation of Blimp-1, leading to the de-repression of a new Blimp-1 direct target, CULLIN 4A (CUL4A), and reduced Aiolos levels.	Lenalidomide	46-58	IKAROS family zinc finger 3	Homo sapiens	214-220
26823144-9	2016	Accordingly, lenalidomide-induced cell death was partially rescued by reintroduction of Blimp-1 or knockdown of CUL4A.	Lenalidomide	13-25	PR/SET domain 1	Homo sapiens	88-95
26823144-9	2016	Accordingly, lenalidomide-induced cell death was partially rescued by reintroduction of Blimp-1 or knockdown of CUL4A.	Lenalidomide	13-25	cullin 4A	Homo sapiens	112-117
26823144-11	2016	We also showed that interruption of Blimp-1/Aiolos regulatory pathways contributes to lenalidomide-mediated anti-MM activity.	Lenalidomide	86-98	PR/SET domain 1	Homo sapiens	36-43
26823144-11	2016	We also showed that interruption of Blimp-1/Aiolos regulatory pathways contributes to lenalidomide-mediated anti-MM activity.	Lenalidomide	86-98	IKAROS family zinc finger 3	Homo sapiens	44-50
27089170-2	2016	In Phase II studies, lenalidomide combined with R-CHOP (R(2)-CHOP) improved outcomes relative to historical R-CHOP in newly diagnosed DLBCL, particularly in non-GCB cases.	Lenalidomide	21-33	DNA damage inducible transcript 3	Homo sapiens	61-65
27089170-2	2016	In Phase II studies, lenalidomide combined with R-CHOP (R(2)-CHOP) improved outcomes relative to historical R-CHOP in newly diagnosed DLBCL, particularly in non-GCB cases.	Lenalidomide	21-33	DNA damage inducible transcript 3	Homo sapiens	61-65
27330758-0	2016	Durable response to lenalidomide in a patient with myelodysplastic syndrome associated with isolated 5q deletion and JAK2 V617F mutation despite discontinuation of treatment.	Lenalidomide	20-32	Janus kinase 2	Homo sapiens	117-121
27330758-10	2016	The present case highlights the coexistence of the JAK2 V617F mutation in del(5q) MDS and suggests that lenalidomide treatment is beneficial and effective for these patients, leading to complete hematological, cytogenetic and molecular response.	Lenalidomide	104-116	Janus kinase 2	Homo sapiens	51-55
27294874-5	2016	In contrast, deletion of GPR68 or inhibition of calcium and calpain activation suppressed LEN-induced cytotoxicity.	Lenalidomide	90-93	G protein-coupled receptor 68	Homo sapiens	25-30
27294874-7	2016	Depletion of CAST restored responsiveness of LEN-resistant non-del(5q) MDS cells and AML cells, providing an explanation for the superior responses of patients with del(5q) MDS to LEN treatment.	Lenalidomide	45-48	calpastatin	Homo sapiens	13-17
27287425-0	2016	Lenalidomide Induces Interleukin-21 Production by T Cells and Enhances IL21-Mediated Cytotoxicity in Chronic Lymphocytic Leukemia B Cells.	Lenalidomide	0-12	interleukin 21	Homo sapiens	21-35
27287425-0	2016	Lenalidomide Induces Interleukin-21 Production by T Cells and Enhances IL21-Mediated Cytotoxicity in Chronic Lymphocytic Leukemia B Cells.	Lenalidomide	0-12	interleukin 21	Homo sapiens	71-75
27287425-3	2016	Lenalidomide also induced production of interleukin-21 (IL21) and its mRNA in T cells from patients with CLL.	Lenalidomide	0-12	interleukin 21	Homo sapiens	40-54
27287425-3	2016	Lenalidomide also induced production of interleukin-21 (IL21) and its mRNA in T cells from patients with CLL.	Lenalidomide	0-12	interleukin 21	Homo sapiens	56-60
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	13-25	interleukin 21 receptor	Homo sapiens	62-75
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	13-25	interleukin 21 receptor	Homo sapiens	77-82
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	13-25	interleukin 21	Homo sapiens	62-66
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	13-25	interleukin 21	Homo sapiens	77-81
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	178-190	interleukin 21 receptor	Homo sapiens	62-75
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	178-190	interleukin 21 receptor	Homo sapiens	77-82
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	178-190	interleukin 21	Homo sapiens	62-66
27287425-4	2016	In addition, lenalidomide enhanced upregulation of functional IL21 receptor (IL21R) on the cell surface and increased receptor mRNA in vitro The in vitro combination of IL21 and lenalidomide enhanced IL21-mediated cytotoxicity toward CLL cells through a variety of mechanisms.	Lenalidomide	178-190	interleukin 21	Homo sapiens	77-81
27287425-6	2016	Collectively, we demonstrated an immune cell-tumor cell interaction through lenalidomide-mediated induction of IL21 and IL21R, with enhanced IL21-mediated cytotoxicity, which provides justification for this combination in clinical trials for patients with CLL.	Lenalidomide	76-88	interleukin 21	Homo sapiens	111-115
27287425-6	2016	Collectively, we demonstrated an immune cell-tumor cell interaction through lenalidomide-mediated induction of IL21 and IL21R, with enhanced IL21-mediated cytotoxicity, which provides justification for this combination in clinical trials for patients with CLL.	Lenalidomide	76-88	interleukin 21 receptor	Homo sapiens	120-125
27287425-6	2016	Collectively, we demonstrated an immune cell-tumor cell interaction through lenalidomide-mediated induction of IL21 and IL21R, with enhanced IL21-mediated cytotoxicity, which provides justification for this combination in clinical trials for patients with CLL.	Lenalidomide	76-88	interleukin 21	Homo sapiens	120-124
27089170-0	2016	ROBUST: Lenalidomide-R-CHOP versus placebo-R-CHOP in previously untreated ABC-type diffuse large B-cell lymphoma.	Lenalidomide	8-20	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	74-77
26991062-3	2016	Lenalidomide increased von Willebrand factor (VWF), lowered VWF clearance and resolved bleeding.	Lenalidomide	0-12	von Willebrand factor	Homo sapiens	23-44
27224912-5	2016	Based on in vitro cell line-based experiments, overexpression of CARD11 mutants were demonstrated to confer resistance to the BCR-inhibitor ibrutinib and NF-kappaB-inhibitor lenalidomide.	Lenalidomide	174-186	caspase recruitment domain family member 11	Homo sapiens	65-71
27197154-0	2016	Lenalidomide Stabilizes the Erythropoietin Receptor by Inhibiting the E3 Ubiquitin Ligase RNF41.	Lenalidomide	0-12	ring finger protein 41	Homo sapiens	90-95
27197154-2	2016	To determine the mechanism by which lenalidomide promotes erythropoiesis, we investigated its action on erythropoietin receptor (EpoR) cellular dynamics.	Lenalidomide	36-48	erythropoietin receptor	Homo sapiens	129-133
27197154-3	2016	Lenalidomide upregulated expression and stability of JAK2-associated EpoR in UT7 erythroid cells and primary CD71+ erythroid progenitors.	Lenalidomide	0-12	erythropoietin receptor	Homo sapiens	69-73
27197154-5	2016	To elucidate this mechanism, we investigated the effects of lenalidomide on the E3 ubiquitin ligase RNF41.	Lenalidomide	60-72	ring finger protein 41	Homo sapiens	100-105
27197154-6	2016	Lenalidomide promoted EpoR/RNF41 association and inhibited RNF41 auto-ubiquitination, accompanied by a reduction in EpoR ubiquitination.	Lenalidomide	0-12	erythropoietin receptor	Homo sapiens	22-26
27197154-6	2016	Lenalidomide promoted EpoR/RNF41 association and inhibited RNF41 auto-ubiquitination, accompanied by a reduction in EpoR ubiquitination.	Lenalidomide	0-12	ring finger protein 41	Homo sapiens	27-32
27197154-6	2016	Lenalidomide promoted EpoR/RNF41 association and inhibited RNF41 auto-ubiquitination, accompanied by a reduction in EpoR ubiquitination.	Lenalidomide	0-12	ring finger protein 41	Homo sapiens	59-64
27197154-6	2016	Lenalidomide promoted EpoR/RNF41 association and inhibited RNF41 auto-ubiquitination, accompanied by a reduction in EpoR ubiquitination.	Lenalidomide	0-12	erythropoietin receptor	Homo sapiens	116-120
27197154-10	2016	Immunohistochemical staining showed that RNF41 expression decreased in primary erythroid cells of lenalidomide-responding patients, suggesting that cellular RNF41 expression merits investigation as a biomarker for lenalidomide response.	Lenalidomide	98-110	ring finger protein 41	Homo sapiens	41-46
27197154-10	2016	Immunohistochemical staining showed that RNF41 expression decreased in primary erythroid cells of lenalidomide-responding patients, suggesting that cellular RNF41 expression merits investigation as a biomarker for lenalidomide response.	Lenalidomide	98-110	ring finger protein 41	Homo sapiens	157-162
27197154-10	2016	Immunohistochemical staining showed that RNF41 expression decreased in primary erythroid cells of lenalidomide-responding patients, suggesting that cellular RNF41 expression merits investigation as a biomarker for lenalidomide response.	Lenalidomide	214-226	ring finger protein 41	Homo sapiens	41-46
27197154-11	2016	Our findings indicate that lenalidomide has E3 ubiquitin ligase inhibitory effects that extend to RNF41 and that inhibition of RNF41 auto-ubiquitination promotes membrane accumulation of signaling competent JAK2/EpoR complexes that augment Epo responsiveness.	Lenalidomide	27-39	ring finger protein 41	Homo sapiens	98-103
27197154-11	2016	Our findings indicate that lenalidomide has E3 ubiquitin ligase inhibitory effects that extend to RNF41 and that inhibition of RNF41 auto-ubiquitination promotes membrane accumulation of signaling competent JAK2/EpoR complexes that augment Epo responsiveness.	Lenalidomide	27-39	erythropoietin receptor	Homo sapiens	212-216
26991062-16	2016	The biological mechanism(s) through which lenalidomide causes a sustained increase in plasma VWF levels in AVWS independently of paraprotein level requires further study, but is in part modulated through inhibition of enhanced VWF clearance.	Lenalidomide	42-54	von Willebrand factor	Homo sapiens	93-96
26991062-16	2016	The biological mechanism(s) through which lenalidomide causes a sustained increase in plasma VWF levels in AVWS independently of paraprotein level requires further study, but is in part modulated through inhibition of enhanced VWF clearance.	Lenalidomide	42-54	von Willebrand factor	Homo sapiens	227-230
27342494-0	2016	[Clinical Curative Efficacy of Lenalidomide Combined with Chemotherapy for Acute Leukemia and Its Impact on VEGF].	Lenalidomide	31-43	vascular endothelial growth factor A	Homo sapiens	108-112
27342494-1	2016	OBJECTIVE: To investigate the clinical efficacy of regimen consisting of lenalidomide combined with chemotherapy for acute leukemia and its impact on vascular endothilial growth factor (vEGF) and basic fibroblast growth factor (bFGF), and to analyze the relationship lenalidomide with therapeutic efficacy of leukemia.	Lenalidomide	73-85	vascular endothelial growth factor A	Homo sapiens	150-184
27342494-1	2016	OBJECTIVE: To investigate the clinical efficacy of regimen consisting of lenalidomide combined with chemotherapy for acute leukemia and its impact on vascular endothilial growth factor (vEGF) and basic fibroblast growth factor (bFGF), and to analyze the relationship lenalidomide with therapeutic efficacy of leukemia.	Lenalidomide	73-85	vascular endothelial growth factor A	Homo sapiens	186-190
27342494-1	2016	OBJECTIVE: To investigate the clinical efficacy of regimen consisting of lenalidomide combined with chemotherapy for acute leukemia and its impact on vascular endothilial growth factor (vEGF) and basic fibroblast growth factor (bFGF), and to analyze the relationship lenalidomide with therapeutic efficacy of leukemia.	Lenalidomide	73-85	fibroblast growth factor 2	Homo sapiens	196-226
27342494-1	2016	OBJECTIVE: To investigate the clinical efficacy of regimen consisting of lenalidomide combined with chemotherapy for acute leukemia and its impact on vascular endothilial growth factor (vEGF) and basic fibroblast growth factor (bFGF), and to analyze the relationship lenalidomide with therapeutic efficacy of leukemia.	Lenalidomide	73-85	fibroblast growth factor 2	Homo sapiens	228-232
27342494-8	2016	CONCLUSION: The lenalidomide combined with chemotherapy can significantly decrease the expression level of VEGF and bFGF, and enhance the remission rate of patients with AML.	Lenalidomide	16-28	vascular endothelial growth factor A	Homo sapiens	107-111
27342494-8	2016	CONCLUSION: The lenalidomide combined with chemotherapy can significantly decrease the expression level of VEGF and bFGF, and enhance the remission rate of patients with AML.	Lenalidomide	16-28	fibroblast growth factor 2	Homo sapiens	116-120
27142104-1	2016	BACKGROUND: Immunomodulatory drugs (IMiDs), such as lenalidomide, are therapeutically active compounds that bind and modulate the E3 ubiquitin ligase substrate recruiter cereblon, thereby affect steady-state levels of cereblon and cereblon binding partners, such as ikaros and aiolos, and induce many cellular responses, including cytotoxicity to multiple myeloma (MM) cells.	Lenalidomide	52-64	Cbl proto-oncogene like 2	Homo sapiens	130-149
27142104-6	2016	Upon treatment of IMiD-sensitive MM cells with lenalidomide, the steady-state levels of cereblon were significantly increased, whereas levels of AGO2 were significantly decreased.	Lenalidomide	47-59	argonaute RISC catalytic component 2	Homo sapiens	145-149
27232930-0	2016	Increased circulating VCAM-1 correlates with advanced disease and poor survival in patients with multiple myeloma: reduction by post-bortezomib and lenalidomide treatment.	Lenalidomide	148-160	vascular cell adhesion molecule 1	Homo sapiens	22-28
26991062-3	2016	Lenalidomide increased von Willebrand factor (VWF), lowered VWF clearance and resolved bleeding.	Lenalidomide	0-12	von Willebrand factor	Homo sapiens	46-49
26991062-3	2016	Lenalidomide increased von Willebrand factor (VWF), lowered VWF clearance and resolved bleeding.	Lenalidomide	0-12	von Willebrand factor	Homo sapiens	60-63
26991062-7	2016	Results In both patients, lenalidomide treatment resulted in significant clinical improvement, and marked increases in plasma VWF antigen (VWF:Ag) and VWF ristocetin cofactor levels.	Lenalidomide	26-38	von Willebrand factor	Homo sapiens	126-129
26991062-7	2016	Results In both patients, lenalidomide treatment resulted in significant clinical improvement, and marked increases in plasma VWF antigen (VWF:Ag) and VWF ristocetin cofactor levels.	Lenalidomide	26-38	von Willebrand factor	Homo sapiens	139-142
26991062-7	2016	Results In both patients, lenalidomide treatment resulted in significant clinical improvement, and marked increases in plasma VWF antigen (VWF:Ag) and VWF ristocetin cofactor levels.	Lenalidomide	26-38	von Willebrand factor	Homo sapiens	139-142
26991062-9	2016	Furthermore, in one patient, plasma VWF levels remain normal for at least 14 months following discontinuation of lenalidomide treatment.	Lenalidomide	113-125	von Willebrand factor	Homo sapiens	36-39
26991062-12	2016	Importantly, lenalidomide treatment resulted in normalization of VWFpp/VWF:Ag ratios in both patients.	Lenalidomide	13-25	von Willebrand factor	Homo sapiens	65-68
26991062-13	2016	These novel data suggest that lenalidomide functions to attenuate enhanced VWF clearance in AVWS.	Lenalidomide	30-42	von Willebrand factor	Homo sapiens	75-78
26991062-14	2016	Interestingly, in a patient with MGUS, lenalidomide treatment was associated with a significant increase in plasma VWF levels, despite no major change in paraprotein level.	Lenalidomide	39-51	von Willebrand factor	Homo sapiens	115-118
27009084-7	2016	NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL.	Lenalidomide	25-37	BCL2-associated X protein	Mus musculus	116-119
26119939-6	2016	Although microarray examination of PEL cells treated with lenalidomide revealed activation of interferon (IFN) signaling, blocking the IFN pathway did not block the anti-PEL activity of IMiDs.	Lenalidomide	58-70	interferon alpha 1	Homo sapiens	94-104
26119939-6	2016	Although microarray examination of PEL cells treated with lenalidomide revealed activation of interferon (IFN) signaling, blocking the IFN pathway did not block the anti-PEL activity of IMiDs.	Lenalidomide	58-70	interferon alpha 1	Homo sapiens	106-109
26119939-12	2016	Lenalidomide displayed synergistic cytotoxicity with several structurally distinct BRD4 inhibitors (JQ-1, IBET151 and PFI-1).	Lenalidomide	0-12	bromodomain containing 4	Homo sapiens	83-87
27009084-7	2016	NVP-Bez235 combined with lenalidomide remarkably increased apoptosis through intrinsic pathway by upregulating Bim, Bax and downregulating Bcl-xL.	Lenalidomide	25-37	BCL2-like 1	Mus musculus	139-145
27009084-11	2016	CONCLUSIONS: Our findings demonstrated the synergistic effect of low dose of NVP-Bez235 and lenalidomide in ABC-DLBCL, the underlying mechanism may be multifunctional, involving apoptosis, Akt and NF-kappaB inactivation and cell cycle arrest.	Lenalidomide	92-104	thymoma viral proto-oncogene 1	Mus musculus	189-192
26437056-8	2016	Although CY-based mobilization was more effective, G-CSF alone was successful in a great majority of patients to reach the defined collection target after three cycles of lenalidomide-based induction.	Lenalidomide	171-183	colony stimulating factor 3	Homo sapiens	51-56
26967821-7	2016	This analysis indicates that lenalidomide is active in patients with relapsed/refractory CLL with unfavorable genetic profiles, including TP53 inactivation or unmutated IGHV.	Lenalidomide	29-41	tumor protein p53	Homo sapiens	138-142
26967821-7	2016	This analysis indicates that lenalidomide is active in patients with relapsed/refractory CLL with unfavorable genetic profiles, including TP53 inactivation or unmutated IGHV.	Lenalidomide	29-41	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	169-173
26914976-4	2016	Typical hallmarks of IMiD compound activity, including IKZF3 (Aiolos) degradation, and the downregulation of interferon regulatory factor (IRF) 4 and MYC, seen in lenalidomide-sensitive H929 MM cell lines, were also observed in PomDex-treated lenalidomide-resistant H929 MM cells.	Lenalidomide	163-175	interferon regulatory factor 4	Homo sapiens	109-145
26914976-4	2016	Typical hallmarks of IMiD compound activity, including IKZF3 (Aiolos) degradation, and the downregulation of interferon regulatory factor (IRF) 4 and MYC, seen in lenalidomide-sensitive H929 MM cell lines, were also observed in PomDex-treated lenalidomide-resistant H929 MM cells.	Lenalidomide	163-175	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	150-153
26700310-0	2016	Potential crosstalk of the interleukin-6-heme oxygenase-1-dependent mechanism involved in resistance to lenalidomide in multiple myeloma cells.	Lenalidomide	104-116	heme oxygenase 1	Homo sapiens	41-57
26700310-5	2016	Culture of U266, RPMI8226 and CD138(+) cells with exogenous IL-6 in vitro induced high HO-1 expression levels and allowed them to resist lenalidomide.	Lenalidomide	137-149	interleukin 6	Homo sapiens	60-64
26700310-9	2016	Reduced HO-1 expression sensitized MM cells to lenalidomide.	Lenalidomide	47-59	heme oxygenase 1	Homo sapiens	8-12
26700310-10	2016	Therefore, we postulated that IL-6 in the bone marrow microenvironment of MM patients stimulated high HO-1 expression in MM cells and their resistance to lenalidomide.	Lenalidomide	154-166	interleukin 6	Homo sapiens	30-34
26659917-0	2016	The anti-tumoral effect of lenalidomide is increased in vivo by hypoxia-inducible factor (HIF)-1alpha inhibition in myeloma cells.	Lenalidomide	27-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-101
26657848-10	2016	In this study, we found that low-dose lenalidomide and pomalidomide up-regulate PU.1 expression through inducing demethylation of the PU.1 promoter.	Lenalidomide	38-50	Spi-1 proto-oncogene	Homo sapiens	80-84
27358895-13	2016	Lenalidomide is approved for treatment of anemia in low and intermediate risk MDS with del (5q), however based on a search of literature it seems that RUNX1 mutations are also more prominent in patients who have responded to Lenalidomide therapy.	Lenalidomide	0-12	RUNX family transcription factor 1	Homo sapiens	151-156
27358895-13	2016	Lenalidomide is approved for treatment of anemia in low and intermediate risk MDS with del (5q), however based on a search of literature it seems that RUNX1 mutations are also more prominent in patients who have responded to Lenalidomide therapy.	Lenalidomide	225-237	RUNX family transcription factor 1	Homo sapiens	151-156
27467960-7	2016	Furthermore, we found on T-cells from patients treated with lenalidomide a decreased CD45RA expression, indicating a maturated immunophenotype and a decreased expression of CD57, indicating functional T cells.	Lenalidomide	60-72	beta-1,3-glucuronyltransferase 1	Homo sapiens	173-177
27467960-9	2016	Complementary to the results in vivo, lenalidomide decreased CD45RA expression on T cells in vitro.	Lenalidomide	38-50	protein tyrosine phosphatase receptor type C	Homo sapiens	61-65
26657848-10	2016	In this study, we found that low-dose lenalidomide and pomalidomide up-regulate PU.1 expression through inducing demethylation of the PU.1 promoter.	Lenalidomide	38-50	Spi-1 proto-oncogene	Homo sapiens	134-138
26504152-4	2016	Data discussed here from the pivotal phase 2 (MDS-003) and phase 3 (MDS-004) studies of lenalidomide demonstrate that lenalidomide treatment was associated with both short- and long-term benefits.	Lenalidomide	88-100	proteasome assembly chaperone 2	Homo sapiens	46-53
26504152-4	2016	Data discussed here from the pivotal phase 2 (MDS-003) and phase 3 (MDS-004) studies of lenalidomide demonstrate that lenalidomide treatment was associated with both short- and long-term benefits.	Lenalidomide	118-130	proteasome assembly chaperone 2	Homo sapiens	46-53
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.	Lenalidomide	121-133	latexin	Homo sapiens	138-141
27980307-4	2016	Furthermore, some targeting drugs, such as lenalidomide, bortezomib and ibrutinib, directly or indirectly affect CD20 protein expression.	Lenalidomide	43-55	keratin 20	Homo sapiens	113-117
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.	Lenalidomide	121-133	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.	Lenalidomide	121-133	cereblon	Homo sapiens	193-197
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.	Lenalidomide	158-170	cereblon	Homo sapiens	45-49
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.	Lenalidomide	257-269	cereblon	Homo sapiens	45-49
26521987-8	2015	However, the occurrence of neutropenia during lenalidomide therapy was more frequent among the CTNNB1 (rs4135385) AA carriers (p=0.019), while the CTNNB1 (rs4533622) AA homozygosity characterized patients with high grade (3-4) neutropenia (p=0.044).	Lenalidomide	46-58	catenin beta 1	Homo sapiens	95-101
26438514-1	2015	Lenalidomide acts by a novel drug mechanism-modulation of the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase.	Lenalidomide	0-12	interleukin 17 receptor B	Homo sapiens	91-95
26438514-1	2015	Lenalidomide acts by a novel drug mechanism-modulation of the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase.	Lenalidomide	0-12	cereblon	Homo sapiens	96-100
26438514-1	2015	Lenalidomide acts by a novel drug mechanism-modulation of the substrate specificity of the CRL4(CRBN) E3 ubiquitin ligase.	Lenalidomide	0-12	Cbl proto-oncogene like 2	Homo sapiens	102-121
26438514-2	2015	In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4(CRBN).	Lenalidomide	21-33	IKAROS family zinc finger 1	Homo sapiens	64-69
26438514-2	2015	In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4(CRBN).	Lenalidomide	21-33	IKAROS family zinc finger 3	Homo sapiens	74-79
26438514-2	2015	In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4(CRBN).	Lenalidomide	21-33	interleukin 17 receptor B	Homo sapiens	83-87
26438514-2	2015	In multiple myeloma, lenalidomide induces the ubiquitination of IKZF1 and IKZF3 by CRL4(CRBN).	Lenalidomide	21-33	cereblon	Homo sapiens	88-92
26447613-0	2015	CD4+ T cells play a crucial role for lenalidomide in vivo anti-tumor activity in murine multiple myeloma.	Lenalidomide	37-49	CD4 antigen	Mus musculus	0-3
26447613-4	2015	Depletion of CD4+ T cells, but not NK cells, B cells, or CD8+ T cells, deprived lenalidomide of its therapeutic effects on 5TGM1-bearing immunocompetent mice.	Lenalidomide	80-92	CD4 antigen	Mus musculus	13-16
26447613-5	2015	Lenalidomide significantly increased the numbers of IFN-gamma-secreting CD4+ and CD8+ T cells but had no effects on NK cells and B cells in this mouse model.	Lenalidomide	0-12	interferon gamma	Mus musculus	52-61
26447613-5	2015	Lenalidomide significantly increased the numbers of IFN-gamma-secreting CD4+ and CD8+ T cells but had no effects on NK cells and B cells in this mouse model.	Lenalidomide	0-12	CD4 antigen	Mus musculus	72-75
26447613-6	2015	Lenalidomide slightly decreased the number of CD25+Foxp3+ T cells but increased perforin expression in CD8+ T cells in vivo.	Lenalidomide	0-12	interleukin 2 receptor, alpha chain	Mus musculus	46-50
26447613-8	2015	The CD4+ T cell subset may play a critical role in the lenalidomide-mediated anti-myeloma immune response in vivo.	Lenalidomide	55-67	CD4 antigen	Mus musculus	4-7
26535672-5	2015	We confirmed that CRBN may be a target of lenalidomide.	Lenalidomide	42-54	cereblon	Homo sapiens	18-22
26341959-3	2015	8226/AMY1 showed a survival advantage over mock control when treated with dexamethasone, bortezomib, and lenalidomide in vitro partly through inhibition of apoptosis induced by these reagents.	Lenalidomide	105-117	amylase alpha 1A	Homo sapiens	5-9
25979485-10	2015	Finally, lenalidomide with PD-1/PD-L1 blockade inhibits MDSC-mediated immune suppression.	Lenalidomide	9-21	programmed cell death 1	Homo sapiens	27-31
25979485-10	2015	Finally, lenalidomide with PD-1/PD-L1 blockade inhibits MDSC-mediated immune suppression.	Lenalidomide	9-21	CD274 molecule	Homo sapiens	32-37
25979485-11	2015	CONCLUSIONS: Our data therefore demonstrate that checkpoint signaling plays an important role in providing the tumor-promoting, immune-suppressive microenvironment in multiple myeloma, and that PD-1/PD-L1 blockade induces anti-multiple myeloma immune response that can be enhanced by lenalidomide, providing the framework for clinical evaluation of combination therapy.	Lenalidomide	284-296	programmed cell death 1	Homo sapiens	194-198
26429859-6	2015	Here, we show that a novel pan-HDACi AR-42 downregulates CD44, a glycoprotein that has been associated with lenalidomide and dexamethasone resistance in myeloma both in vitro and in vivo.	Lenalidomide	108-120	CD44 molecule (Indian blood group)	Homo sapiens	57-61
25979485-11	2015	CONCLUSIONS: Our data therefore demonstrate that checkpoint signaling plays an important role in providing the tumor-promoting, immune-suppressive microenvironment in multiple myeloma, and that PD-1/PD-L1 blockade induces anti-multiple myeloma immune response that can be enhanced by lenalidomide, providing the framework for clinical evaluation of combination therapy.	Lenalidomide	284-296	CD274 molecule	Homo sapiens	199-204
26429859-9	2015	Thus, our findings shed light on potential novel combinatorial therapeutic approaches modulating CD44 expression, which may help overcome lenalidomide resistance in myeloma patients.	Lenalidomide	138-150	CD44 molecule (Indian blood group)	Homo sapiens	97-101
26255966-4	2015	Lenalidomide inhibits retinal endothelial cell viability in normal and pathological condition, and inhibits VEGF-induced endothelial cell migration and tube formation in vitro.	Lenalidomide	0-12	vascular endothelial growth factor A	Homo sapiens	108-112
26131937-2	2015	Here, we demonstrate that lenalidomide induces the ubiquitination of casein kinase 1A1 (CK1alpha) by the E3 ubiquitin ligase CUL4-RBX1-DDB1-CRBN (known as CRL4(CRBN)), resulting in CK1alpha degradation.	Lenalidomide	26-38	cereblon	Mus musculus	140-144
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	interleukin 17 receptor B	Homo sapiens	8-12
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	cereblon	Homo sapiens	13-17
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	IKAROS family zinc finger 1	Homo sapiens	29-35
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	IKAROS family zinc finger 3	Homo sapiens	40-46
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	167-172
26430725-0	2015	Rate of CRL4(CRBN) substrate Ikaros and Aiolos degradation underlies differential activity of lenalidomide and pomalidomide in multiple myeloma cells by regulation of c-Myc and IRF4.	Lenalidomide	94-106	interferon regulatory factor 4	Homo sapiens	177-181
26430725-1	2015	Recent discoveries suggest that the critical events leading to the anti-proliferative activity of the IMiD immunomodulatory agents lenalidomide and pomalidomide in multiple myeloma (MM) cells are initiated by Cereblon-dependent ubiquitination and proteasomal degradation of substrate proteins Ikaros (IKZF1) and Aiolos (IKZF3).	Lenalidomide	131-143	IKAROS family zinc finger 1	Homo sapiens	293-299
26430725-1	2015	Recent discoveries suggest that the critical events leading to the anti-proliferative activity of the IMiD immunomodulatory agents lenalidomide and pomalidomide in multiple myeloma (MM) cells are initiated by Cereblon-dependent ubiquitination and proteasomal degradation of substrate proteins Ikaros (IKZF1) and Aiolos (IKZF3).	Lenalidomide	131-143	IKAROS family zinc finger 1	Homo sapiens	301-306
26430725-1	2015	Recent discoveries suggest that the critical events leading to the anti-proliferative activity of the IMiD immunomodulatory agents lenalidomide and pomalidomide in multiple myeloma (MM) cells are initiated by Cereblon-dependent ubiquitination and proteasomal degradation of substrate proteins Ikaros (IKZF1) and Aiolos (IKZF3).	Lenalidomide	131-143	IKAROS family zinc finger 3	Homo sapiens	312-318
26430725-1	2015	Recent discoveries suggest that the critical events leading to the anti-proliferative activity of the IMiD immunomodulatory agents lenalidomide and pomalidomide in multiple myeloma (MM) cells are initiated by Cereblon-dependent ubiquitination and proteasomal degradation of substrate proteins Ikaros (IKZF1) and Aiolos (IKZF3).	Lenalidomide	131-143	IKAROS family zinc finger 3	Homo sapiens	320-325
26430725-4	2015	In addition, we found that the half-maximal rate, rather than the final extent of Ikaros and Aiolos degradation, correlated to the relative efficacy of growth inhibition by lenalidomide or pomalidomide.	Lenalidomide	173-185	IKAROS family zinc finger 1	Homo sapiens	82-88
26430725-4	2015	In addition, we found that the half-maximal rate, rather than the final extent of Ikaros and Aiolos degradation, correlated to the relative efficacy of growth inhibition by lenalidomide or pomalidomide.	Lenalidomide	173-185	IKAROS family zinc finger 3	Homo sapiens	93-99
26408680-0	2015	Genes Involved in Maintaining the Bone Marrow Stroma Are Dysregulated in Patients with Myelofibrosis: Lenalidomide Treatment Up-regulates SOCS3.	Lenalidomide	102-114	suppressor of cytokine signaling 3	Homo sapiens	138-143
26408680-5	2015	CONCLUSION: Patients with primary MF showed aberrant expression of several genes involved in maintaining BM homeostasis and our findings suggest that treatment with lenalidomide plus prednisone up-regulates SOCS3.	Lenalidomide	165-177	suppressor of cytokine signaling 3	Homo sapiens	207-212
26450624-0	2015	Lenalidomide enhances the function of chimeric antigen receptor T cells against the epidermal growth factor receptor variant III by enhancing immune synapses.	Lenalidomide	0-12	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-63
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.	Lenalidomide	78-90	nuclear receptor subfamily 1, group I, member 3	Mus musculus	104-107
26450624-8	2015	Lenalidomide also exhibited enhanced immunological synapses between the effector cells and the target cells as determined by CD11a and F-actin polymerization.	Lenalidomide	0-12	integrin alpha L	Mus musculus	125-130
26450624-9	2015	Collectively, lentiviral-mediated transduction of CAR effectors targeting the EGFRvIII showed specific efficacy, and lenalidomide even intensified CAR cell therapy by enhanced formation of immunological synapses.	Lenalidomide	117-129	nuclear receptor subfamily 1, group I, member 3	Mus musculus	147-150
26002042-0	2015	Selection of resistant acute myeloid leukemia SKM-1 and MOLM-13 cells by vincristine-, mitoxantrone- and lenalidomide-induced upregulation of P-glycoprotein activity and downregulation of CD33 cell surface exposure.	Lenalidomide	105-117	sodium voltage-gated channel alpha subunit 4	Homo sapiens	46-51
26002042-0	2015	Selection of resistant acute myeloid leukemia SKM-1 and MOLM-13 cells by vincristine-, mitoxantrone- and lenalidomide-induced upregulation of P-glycoprotein activity and downregulation of CD33 cell surface exposure.	Lenalidomide	105-117	ATP binding cassette subfamily B member 1	Homo sapiens	142-156
26002042-0	2015	Selection of resistant acute myeloid leukemia SKM-1 and MOLM-13 cells by vincristine-, mitoxantrone- and lenalidomide-induced upregulation of P-glycoprotein activity and downregulation of CD33 cell surface exposure.	Lenalidomide	105-117	CD33 molecule	Homo sapiens	188-192
26002042-5	2015	For this purpose, we established drug resistant variants of SKM-1 and MOLM-13 AML cell lines via the selection of parental cells for resistance to vincristine, mitoxantrone and lenalidomide.	Lenalidomide	177-189	sodium voltage-gated channel alpha subunit 4	Homo sapiens	60-65
26378933-8	2015	Furthermore, our clinical analysis suggests that including immunomodulatory agents such as Lenalidomide in the treatment regimen may help to overcome this negative effect, providing an alternative consideration in treatment planning of MM patients with del(8)(p21).	Lenalidomide	91-103	H3 histone pseudogene 16	Homo sapiens	260-263
25999435-0	2015	A Phase I Trial of the Anti-KIR Antibody IPH2101 and Lenalidomide in Patients with Relapsed/Refractory Multiple Myeloma.	Lenalidomide	53-65	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	28-31
26051632-4	2015	Lenalidomide pre-treatment of MM cell lines reduced TReg generation and the concomitant TReg:TEff (CD4(+)CD25(+)FoxP3(-): effector T cells) ratio, as a consequence of reduced ICOSL transcription.	Lenalidomide	0-12	inducible T cell costimulator ligand	Homo sapiens	175-180
26169489-4	2015	The responses to lenalidomide seem to be inversely correlated to the pre-treatment EPO level.	Lenalidomide	17-29	erythropoietin	Homo sapiens	83-86
26195701-4	2015	Tumoricidal effects of lenalidomide are associated with reduced interferon regulatory factor 4, a downstream target of cereblon.	Lenalidomide	23-35	interferon regulatory factor 4	Homo sapiens	64-94
26002965-1	2015	Cereblon (CRBN), a substrate receptor of the Cullin 4 RING E3 ubiquitin ligase complex, is the target of the immunomodulatory drugs lenalidomide and pomalidomide.	Lenalidomide	132-144	cereblon	Homo sapiens	10-14
26002964-3	2015	Here, we report that lenalidomide lowers the threshold for NK-cell activation, causing a 66% decrease in the 50% effective concentration (EC50) for activation through CD16, and a 38% decrease in EC50 for NK group 2 member D (NKG2D)-mediated activation, allowing NK cells to respond to lower doses of ligand.	Lenalidomide	21-33	Fc gamma receptor IIIa	Homo sapiens	167-171
26002964-3	2015	Here, we report that lenalidomide lowers the threshold for NK-cell activation, causing a 66% decrease in the 50% effective concentration (EC50) for activation through CD16, and a 38% decrease in EC50 for NK group 2 member D (NKG2D)-mediated activation, allowing NK cells to respond to lower doses of ligand.	Lenalidomide	21-33	killer cell lectin like receptor K1	Homo sapiens	204-223
26535672-0	2015	Lenalidomide affect expression level of cereblon protein in multiple myeloma cell line RPMI8226.	Lenalidomide	0-12	cereblon	Homo sapiens	40-48
26535672-1	2015	We investigated the mechanisms of action of immuno-modulatory drug (lenalidomide) on the protein expression of cereblon (CRBN) and their therapeutic targets in the multiple myeloma cell line RPMI8226.	Lenalidomide	68-80	cereblon	Homo sapiens	111-119
26535672-1	2015	We investigated the mechanisms of action of immuno-modulatory drug (lenalidomide) on the protein expression of cereblon (CRBN) and their therapeutic targets in the multiple myeloma cell line RPMI8226.	Lenalidomide	68-80	cereblon	Homo sapiens	121-125
26535672-4	2015	However, the protein expression of CRBN decreased signifi-cantly after treatment with lenalidomide, while bortezomib had no effect on the expression of CRBN.	Lenalidomide	86-98	cereblon	Homo sapiens	35-39
25963624-0	2015	Effectiveness of lenalidomide in a patient with refractory anemia with ring sideroblasts and thrombocytosis with JAK2 (V617F) mutation.	Lenalidomide	17-29	Janus kinase 2	Homo sapiens	113-117
26345573-0	2015	[Successful treatment of venous thromboembolism with a Factor Xa inhibitor, edoxaban, in patients with lenalidomide-treated multiple myeloma].	Lenalidomide	103-115	coagulation factor X	Homo sapiens	55-64
26002964-3	2015	Here, we report that lenalidomide lowers the threshold for NK-cell activation, causing a 66% decrease in the 50% effective concentration (EC50) for activation through CD16, and a 38% decrease in EC50 for NK group 2 member D (NKG2D)-mediated activation, allowing NK cells to respond to lower doses of ligand.	Lenalidomide	21-33	killer cell lectin like receptor K1	Homo sapiens	225-230
26002964-4	2015	In addition, lenalidomide augments NK-cell responses, causing a twofold increase in the proportion of primary NK cells producing interferon-gamma (IFN-gamma), and a 20-fold increase in the amount of IFN-gamma produced per cell.	Lenalidomide	13-25	interferon gamma	Homo sapiens	129-145
26002964-4	2015	In addition, lenalidomide augments NK-cell responses, causing a twofold increase in the proportion of primary NK cells producing interferon-gamma (IFN-gamma), and a 20-fold increase in the amount of IFN-gamma produced per cell.	Lenalidomide	13-25	interferon gamma	Homo sapiens	147-156
26002964-4	2015	In addition, lenalidomide augments NK-cell responses, causing a twofold increase in the proportion of primary NK cells producing interferon-gamma (IFN-gamma), and a 20-fold increase in the amount of IFN-gamma produced per cell.	Lenalidomide	13-25	interferon gamma	Homo sapiens	199-208
26002964-7	2015	Of particular clinical importance, lenalidomide also allowed NK cells to be activated by lower doses of rituximab, an anti-CD20 monoclonal antibody (mAb) widely used to treat B-cell malignancies.	Lenalidomide	35-47	keratin 20	Homo sapiens	123-127
26002964-9	2015	Finally, superresolution microscopy revealed that lenalidomide increased the periodicity of cortical actin at immune synapses, resulting in an increase in the area of the actin mesh predicted to be penetrable to vesicles containing IFN-gamma.	Lenalidomide	50-62	interferon gamma	Homo sapiens	232-241
26131937-2	2015	Here, we demonstrate that lenalidomide induces the ubiquitination of casein kinase 1A1 (CK1alpha) by the E3 ubiquitin ligase CUL4-RBX1-DDB1-CRBN (known as CRL4(CRBN)), resulting in CK1alpha degradation.	Lenalidomide	26-38	cereblon	Mus musculus	160-164
26131937-4	2015	We found that mouse cells are resistant to lenalidomide but that changing a single amino acid in mouse Crbn to the corresponding human residue enables lenalidomide-dependent degradation of CK1alpha.	Lenalidomide	43-55	cereblon	Mus musculus	103-107
26131937-4	2015	We found that mouse cells are resistant to lenalidomide but that changing a single amino acid in mouse Crbn to the corresponding human residue enables lenalidomide-dependent degradation of CK1alpha.	Lenalidomide	151-163	cereblon	Mus musculus	103-107
26273440-0	2015	A case of myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN) successfully treated with lenalidomide.	Lenalidomide	99-111	serine protease 27	Homo sapiens	68-71
26273440-4	2015	We report a patient with MDS/MPN who responded well to lenalidomide therapy.	Lenalidomide	55-67	serine protease 27	Homo sapiens	29-32
25915157-7	2015	Moreover, clarithromycin overcame stromal-mediated MM resistance to dexamethasone, suggesting that CYP3A4 inhibition plays a role in its ability to augment the activity of lenalidomide and dexamethasone as part of the BiRd regimen.	Lenalidomide	172-184	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-105
25284710-0	2015	High level of full-length cereblon mRNA in lower risk myelodysplastic syndrome with isolated 5q deletion is implicated in the efficacy of lenalidomide.	Lenalidomide	138-150	cereblon	Homo sapiens	26-34
25284710-1	2015	Downregulation of cereblon (CRBN) gene expression is associated with resistance to the immunomodulatory drug lenalidomide and poor survival outcomes in multiple myeloma (MM) patients.	Lenalidomide	109-121	cereblon	Homo sapiens	18-26
25284710-1	2015	Downregulation of cereblon (CRBN) gene expression is associated with resistance to the immunomodulatory drug lenalidomide and poor survival outcomes in multiple myeloma (MM) patients.	Lenalidomide	109-121	cereblon	Homo sapiens	28-32
25284710-6	2015	High levels of CRBN mRNA were detected in all lenalidomide responders during the course of therapy.	Lenalidomide	46-58	cereblon	Homo sapiens	15-19
25284710-7	2015	A significant decrease of the CRBN mRNA level during lenalidomide treatment is associated with loss of response to treatment and disease progression.	Lenalidomide	53-65	cereblon	Homo sapiens	30-34
25284710-8	2015	These results suggest that, similar to the treatment of MM, high levels of full-length CRBN mRNA in lower risk 5q- patients are necessary for the efficacy of lenalidomide.	Lenalidomide	158-170	cereblon	Homo sapiens	87-91
25287904-3	2015	METHODS: We used miRNA expression microarrays to study changes in miRNA levels in peripheral blood CD14+ monocytes collected from patients before and during lenalidomide treatment and compared them with those from healthy donors.	Lenalidomide	157-169	CD14 molecule	Homo sapiens	99-103
25287904-4	2015	RESULTS: Before treatment, we observed strong upregulation of pro-apoptotic miR-34a and miR-34a* that diminished during lenalidomide exposure.	Lenalidomide	120-132	microRNA 34a	Homo sapiens	76-83
25287904-4	2015	RESULTS: Before treatment, we observed strong upregulation of pro-apoptotic miR-34a and miR-34a* that diminished during lenalidomide exposure.	Lenalidomide	120-132	microRNA 34a	Homo sapiens	88-95
25398450-0	2015	Preclinical Evidence for the Therapeutic Potential of CD38-Targeted Immuno-Chemotherapy in Multiple Myeloma Patients Refractory to Lenalidomide and Bortezomib.	Lenalidomide	131-143	CD38 molecule	Homo sapiens	54-58
27668268-0	2015	Lenalidomide Polarizes Th1-specific Anti-tumor Immune Response and Expands XBP1 Antigen-Specific Central Memory CD3+CD8+ T cells against Various Solid Tumors.	Lenalidomide	0-12	negative elongation factor complex member C/D	Homo sapiens	23-26
27668268-0	2015	Lenalidomide Polarizes Th1-specific Anti-tumor Immune Response and Expands XBP1 Antigen-Specific Central Memory CD3+CD8+ T cells against Various Solid Tumors.	Lenalidomide	0-12	X-box binding protein 1	Homo sapiens	75-79
27668268-2	2015	METHODS: XBP1 antigen-specific cytotoxic T lymphocytes (XBP1-CTL) generated using immunogenic heteroclitic XBP1 US184-192 (YISPWILAV) and XBP1 SP367-375 (YLFPQLISV) peptides or various solid tumor cells over-expressing XBP1 target antigen were evaluated, either alone or in combination with lenalidomide, for phenotype and immune functional activity.	Lenalidomide	291-303	X-box binding protein 1	Homo sapiens	9-13
27668268-2	2015	METHODS: XBP1 antigen-specific cytotoxic T lymphocytes (XBP1-CTL) generated using immunogenic heteroclitic XBP1 US184-192 (YISPWILAV) and XBP1 SP367-375 (YLFPQLISV) peptides or various solid tumor cells over-expressing XBP1 target antigen were evaluated, either alone or in combination with lenalidomide, for phenotype and immune functional activity.	Lenalidomide	291-303	X-box binding protein 1	Homo sapiens	56-60
27668268-2	2015	METHODS: XBP1 antigen-specific cytotoxic T lymphocytes (XBP1-CTL) generated using immunogenic heteroclitic XBP1 US184-192 (YISPWILAV) and XBP1 SP367-375 (YLFPQLISV) peptides or various solid tumor cells over-expressing XBP1 target antigen were evaluated, either alone or in combination with lenalidomide, for phenotype and immune functional activity.	Lenalidomide	291-303	X-box binding protein 1	Homo sapiens	56-60
27668268-2	2015	METHODS: XBP1 antigen-specific cytotoxic T lymphocytes (XBP1-CTL) generated using immunogenic heteroclitic XBP1 US184-192 (YISPWILAV) and XBP1 SP367-375 (YLFPQLISV) peptides or various solid tumor cells over-expressing XBP1 target antigen were evaluated, either alone or in combination with lenalidomide, for phenotype and immune functional activity.	Lenalidomide	291-303	X-box binding protein 1	Homo sapiens	56-60
27668268-2	2015	METHODS: XBP1 antigen-specific cytotoxic T lymphocytes (XBP1-CTL) generated using immunogenic heteroclitic XBP1 US184-192 (YISPWILAV) and XBP1 SP367-375 (YLFPQLISV) peptides or various solid tumor cells over-expressing XBP1 target antigen were evaluated, either alone or in combination with lenalidomide, for phenotype and immune functional activity.	Lenalidomide	291-303	X-box binding protein 1	Homo sapiens	56-60
27668268-3	2015	RESULTS: Lenalidomide treatment of XBP1-CTL increased the proportion of CD45RO+ memory CD3+CD8+ T cells, but not the total CD3+CD8+ T cells.	Lenalidomide	9-21	X-box binding protein 1	Homo sapiens	35-39
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	CD28 molecule	Homo sapiens	89-93
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	CD38 molecule	Homo sapiens	95-99
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	CD40 ligand	Homo sapiens	101-106
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	CD69 molecule	Homo sapiens	108-112
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	inducible T cell costimulator	Homo sapiens	114-118
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	X-box binding protein 1	Homo sapiens	172-176
27668268-4	2015	Lenalidomide upregulated critical T cell activation markers and costimulatory molecules (CD28, CD38, CD40L, CD69, ICOS), especially within the central memory CTL subset of XBP1-CTL, while decreasing TCRalphabeta and T cell checkpoint blockade (CTLA-4, PD-1).	Lenalidomide	0-12	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	244-250
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	X-box binding protein 1	Homo sapiens	52-56
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	negative elongation factor complex member C/D	Homo sapiens	118-121
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	eomesodermin	Homo sapiens	157-162
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	AKT serine/threonine kinase 1	Homo sapiens	168-171
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	interferon gamma	Homo sapiens	214-223
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	granzyme B	Homo sapiens	236-246
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	CD28 molecule	Homo sapiens	273-277
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	CD38 molecule	Homo sapiens	278-282
27668268-5	2015	Lenalidomide increased the anti-tumor activities of XBP1-CTL memory subsets, which were associated with expression of Th1 transcriptional regulators (T-bet, Eomes) and Akt activation, thereby resulting in enhanced IFN-gamma production, granzyme B upregulation and specific CD28/CD38-positive and CTLA-4/PD-1-negative cell proliferation.	Lenalidomide	0-12	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	296-302
27668268-6	2015	CONCLUSIONS: These studies suggest the potential benefit of lenalidomide treatment to boost anti-tumor activities of XBP1-specific CTL against a variety of solid tumors and enhance response to an XBP1-directing cancer vaccine regime.	Lenalidomide	60-72	X-box binding protein 1	Homo sapiens	117-121
27668268-6	2015	CONCLUSIONS: These studies suggest the potential benefit of lenalidomide treatment to boost anti-tumor activities of XBP1-specific CTL against a variety of solid tumors and enhance response to an XBP1-directing cancer vaccine regime.	Lenalidomide	60-72	X-box binding protein 1	Homo sapiens	196-200
25448491-0	2015	Increased serum tumor necrosis factor alpha levels in patients with lenalidomide-induced hypothyroidism.	Lenalidomide	68-80	tumor necrosis factor	Homo sapiens	16-43
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.	Lenalidomide	44-56	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	188-193
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.	Lenalidomide	44-56	interferon regulatory factor 4	Homo sapiens	198-202
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.	Lenalidomide	58-61	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	188-193
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.	Lenalidomide	58-61	interferon regulatory factor 4	Homo sapiens	198-202
25632047-1	2015	PURPOSE: Lenalidomide, an immunomodulatory agent that enhances antibody-dependent cell-mediated cytotoxicity, has the potential to synergize with rituximab, an anti-CD20 mAb.	Lenalidomide	9-21	keratin 20	Homo sapiens	165-169
25643589-9	2015	Maintenance lenalidomide/azacitidine augmented the function of cytotoxic T lymphocytes, particularly in patients with NPM1 mutation.	Lenalidomide	12-24	nucleophosmin 1	Homo sapiens	118-122
25643589-10	2015	The lenalidomide/azacitidine maintenance combination was effective in suppressing residual DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A)-positive disease, resulting in sustained remission in patients with concurrent NPM1 mutation.	Lenalidomide	4-16	DNA methyltransferase 3 alpha	Homo sapiens	136-142
25643589-10	2015	The lenalidomide/azacitidine maintenance combination was effective in suppressing residual DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A)-positive disease, resulting in sustained remission in patients with concurrent NPM1 mutation.	Lenalidomide	4-16	nucleophosmin 1	Homo sapiens	223-227
24738975-0	2015	Intermittent granulocyte colony-stimulating factor for neutropenia management in patients with relapsed or refractory multiple myeloma treated with lenalidomide plus dexamethasone.	Lenalidomide	148-160	colony stimulating factor 3	Homo sapiens	13-50
24738975-7	2015	Intermittent G-CSF may be an effective approach for lenalidomide dose-preservation, which may lead to improved outcomes, although it does not prevent infections or thrombocytopenia-related dose limitations.	Lenalidomide	52-64	colony stimulating factor 3	Homo sapiens	13-18
25395420-5	2015	RSK2 knockdown induced cytotoxicity across a panel of MM cell lines and consistently increased sensitivity to lenalidomide.	Lenalidomide	110-122	ribosomal protein S6 kinase A3	Homo sapiens	0-4
25395420-6	2015	Accordingly, 3 small molecular inhibitors of RSK2 demonstrated synergy with lenalidomide cytotoxicity in MM cells even in the presence of stromal contact.	Lenalidomide	76-88	ribosomal protein S6 kinase A3	Homo sapiens	45-49
25395420-7	2015	Both RSK2 knockdown and small molecule inhibition downregulate interferon regulatory factor 4 and MYC, and provides an explanation for the synergy between lenalidomide and RSK2 inhibition.	Lenalidomide	155-167	ribosomal protein S6 kinase A3	Homo sapiens	5-9
25395420-7	2015	Both RSK2 knockdown and small molecule inhibition downregulate interferon regulatory factor 4 and MYC, and provides an explanation for the synergy between lenalidomide and RSK2 inhibition.	Lenalidomide	155-167	interferon regulatory factor 4	Homo sapiens	63-93
25395420-7	2015	Both RSK2 knockdown and small molecule inhibition downregulate interferon regulatory factor 4 and MYC, and provides an explanation for the synergy between lenalidomide and RSK2 inhibition.	Lenalidomide	155-167	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	98-101
25987070-5	2015	These lenalidomide based regimens included cisplatin, doxorubicin, or GM-CSF.	Lenalidomide	6-18	colony stimulating factor 2	Homo sapiens	70-76
25987070-6	2015	Pooled analysis suggested that, in all patients, the pooled PSA level decline of >=50% was 13.3% (13/98) in lenalidomide based regimens.	Lenalidomide	111-123	aminopeptidase puromycin sensitive	Homo sapiens	60-63
26075044-9	2015	Recurrent TP53 mutations have been associated with an increased risk of disease evolution and with decreased response to the drug lenalidomide in del(5q) MDS patients.	Lenalidomide	130-142	tumor protein p53	Homo sapiens	10-14
25966683-5	2015	Lenalidomide has shown protective effects in an animal model of amyotrophic lateral sclerosis, and its mechanism of action involves modulation of cytokine production and inhibition of NF-kappaB signaling.	Lenalidomide	0-12	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	184-193
25966683-9	2015	Central expression of pro-inflammatory cytokines was diminished in lenalidomide-treated transgenic animals, together with reduction in NF-kappaB activation.	Lenalidomide	67-79	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
26688096-8	2015	Serial sampling and response to lenalidomide treatment showed that CSNK1A1 mutations were highly associated with the del(5q) clone.	Lenalidomide	32-44	casein kinase 1 alpha 1	Homo sapiens	67-74
26688096-9	2015	Only one patient with a CSNK1A1 mutation showed complete cytogenetic response to lenalidomide.	Lenalidomide	81-93	casein kinase 1 alpha 1	Homo sapiens	24-31
26688096-10	2015	Four (57%) of the seven patients carrying a CSNK1A1 mutation showed disease progression coupled with an increase in mutant allele burden (all four were on lenalidomide).	Lenalidomide	155-167	casein kinase 1 alpha 1	Homo sapiens	44-51
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	CD14 molecule	Homo sapiens	64-68
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	ras homolog family member A	Homo sapiens	119-123
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	Rac family small GTPase 1	Homo sapiens	125-129
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	RAP1A, member of RAS oncogene family	Homo sapiens	134-138
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	C-C motif chemokine ligand 2	Homo sapiens	226-230
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	C-C motif chemokine ligand 3	Homo sapiens	232-236
25398834-6	2015	We found that lenalidomide induces high actin polymerization on CD14(+) monocytes through activation of small GTPases, RhoA, Rac1 and Rap1 that correlated with increased adhesion and impaired monocyte migration in response to CCL2, CCL3 and CXCL12.	Lenalidomide	14-26	C-X-C motif chemokine ligand 12	Homo sapiens	241-247
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	C-C motif chemokine ligand 2	Homo sapiens	168-172
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	insulin like growth factor 1	Homo sapiens	174-178
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	C-X-C motif chemokine ligand 12	Homo sapiens	180-186
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	interleukin 2	Homo sapiens	252-255
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	interleukin 10	Homo sapiens	264-268
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	C-X-C motif chemokine ligand 8	Homo sapiens	270-273
25398834-8	2015	Gene expression signature, induced by lenalidomide in nurse-like cells, indicated a reduction of pivotal pro-survival signals for chronic lymphocytic leukemia, such as CCL2, IGF1, CXCL12, HGF1, and supported a modulation towards M1 phenotype with high IL2 and low IL10, IL8 and CD163.	Lenalidomide	38-50	CD163 molecule	Homo sapiens	278-283
25617756-9	2015	In addition, TC11 and lenalidomide, another phthalimide derivative, directly bound to nucleophosmin 1 (NPM1), whose role in MM is unknown.	Lenalidomide	22-34	nucleophosmin 1	Homo sapiens	86-101
25617756-9	2015	In addition, TC11 and lenalidomide, another phthalimide derivative, directly bound to nucleophosmin 1 (NPM1), whose role in MM is unknown.	Lenalidomide	22-34	nucleophosmin 1	Homo sapiens	103-107
25984532-6	2015	Future efforts should aim at targeting the role of NF-kappaB resistance in clinical trials, where novel agents like lenalidomide and proteasome inhibitors with established activity in this perspective will be an important component in combination therapy, along with new monoclonal antibody, BTK-inhibitors, and other novel therapy agents.	Lenalidomide	116-128	Bruton tyrosine kinase	Homo sapiens	292-295
25287778-8	2015	In co-culture assays, TNF-alpha directly increased NK cell activation and myeloma cell death with elotuzumab or elotuzumab plus lenalidomide, and neutralizing TNF-alpha decreased NK cell activation and myeloma cell death with elotuzumab.	Lenalidomide	128-140	tumor necrosis factor	Homo sapiens	22-31
25448491-4	2015	We found a significantly higher rate of therapy-induced hypothyroidism in the DLBCL-len group (25.8% vs. 1.3%), and we found a statistically significant increase in serum tumor necrosis factor alpha in patients with lenalidomide-induced hypothyroidism.	Lenalidomide	216-228	tumor necrosis factor	Homo sapiens	171-198
26763359-0	2015	CD200 Expression on Plasma Cell Myeloma Cells is Associated with the Efficacies of Bortezomib, Lenalidomide and Thalidomide.	Lenalidomide	95-107	CD200 molecule	Homo sapiens	0-5
24721791-4	2014	Lenalidomide was particularly active in this subgroup of tumors, targeting IRF4 expression and plasmacytic differentiation program, thus overcoming bortezomib resistance.	Lenalidomide	0-12	interferon regulatory factor 4	Mus musculus	75-79
25212607-2	2014	EXPERIMENTAL DESIGN: The HGF/cMET pathway was evaluated in ECs from patients with multiple myeloma (multiple myeloma ECs) at diagnosis, at relapse after bortezomib- or lenalidomide-based therapies, or on refractory phase to these drugs; in ECs from patients with MGUS (MGECs); and in those patients from the control group.	Lenalidomide	168-180	hepatocyte growth factor	Homo sapiens	25-28
25212607-2	2014	EXPERIMENTAL DESIGN: The HGF/cMET pathway was evaluated in ECs from patients with multiple myeloma (multiple myeloma ECs) at diagnosis, at relapse after bortezomib- or lenalidomide-based therapies, or on refractory phase to these drugs; in ECs from patients with MGUS (MGECs); and in those patients from the control group.	Lenalidomide	168-180	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	29-33
24813620-9	2014	CONCLUSIONS: These data support the clinical benefits and acceptable safety profile of lenalidomide in transfusion-dependent patients with IPSS-defined Low-/Int-1-risk MDS with isolated del(5q).	Lenalidomide	87-99	Wnt family member 1	Homo sapiens	157-162
25547653-0	2015	Lenalidomide differently modulates CD20 antigen surface expression on chronic lymphocytic leukemia B-cells.	Lenalidomide	0-12	keratin 20	Homo sapiens	35-39
25626322-3	2015	Lenalidomide stimulates T cells and NK-cell through production of Th1 type cytokines IL-2 and IFN-gamma from CD4+ helper-T cells.	Lenalidomide	0-12	interferon gamma	Homo sapiens	94-103
25626322-3	2015	Lenalidomide stimulates T cells and NK-cell through production of Th1 type cytokines IL-2 and IFN-gamma from CD4+ helper-T cells.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	109-112
25469886-0	2014	Lenalidomide induces lipid raft assembly to enhance erythropoietin receptor signaling in myelodysplastic syndrome progenitors.	Lenalidomide	0-12	erythropoietin receptor	Homo sapiens	52-75
25469886-6	2014	Lenalidomide treatment rapidly induced lipid raft formation accompanied by EpoR recruitment into raft fractions together with STAT5, JAK2, and Lyn kinase.	Lenalidomide	0-12	erythropoietin receptor	Homo sapiens	75-79
25469886-6	2014	Lenalidomide treatment rapidly induced lipid raft formation accompanied by EpoR recruitment into raft fractions together with STAT5, JAK2, and Lyn kinase.	Lenalidomide	0-12	signal transducer and activator of transcription 5A	Homo sapiens	126-131
25469886-6	2014	Lenalidomide treatment rapidly induced lipid raft formation accompanied by EpoR recruitment into raft fractions together with STAT5, JAK2, and Lyn kinase.	Lenalidomide	0-12	Janus kinase 2	Homo sapiens	133-137
25469886-6	2014	Lenalidomide treatment rapidly induced lipid raft formation accompanied by EpoR recruitment into raft fractions together with STAT5, JAK2, and Lyn kinase.	Lenalidomide	0-12	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	143-146
25469886-8	2014	Lenalidomide treatment prior to Epo stimulation enhanced both JAK2 and STAT5 phosphorylation in UT7 and primary MDS erythroid progenitors, accompanied by increased STAT5 DNA binding in UT7 cells, and increased erythroid colony forming capacity in both UT7 and primary cells.	Lenalidomide	0-12	Janus kinase 2	Homo sapiens	62-66
25469886-8	2014	Lenalidomide treatment prior to Epo stimulation enhanced both JAK2 and STAT5 phosphorylation in UT7 and primary MDS erythroid progenitors, accompanied by increased STAT5 DNA binding in UT7 cells, and increased erythroid colony forming capacity in both UT7 and primary cells.	Lenalidomide	0-12	signal transducer and activator of transcription 5A	Homo sapiens	71-76
25469886-8	2014	Lenalidomide treatment prior to Epo stimulation enhanced both JAK2 and STAT5 phosphorylation in UT7 and primary MDS erythroid progenitors, accompanied by increased STAT5 DNA binding in UT7 cells, and increased erythroid colony forming capacity in both UT7 and primary cells.	Lenalidomide	0-12	signal transducer and activator of transcription 5A	Homo sapiens	164-169
25550914-7	2014	In a subgroup analysis for therapy regimen, lenalidomide- and bortezomib-based therapies increased the PFS of patients with Amp (1q21) (HR=1.50, 95% CI=0.95-2.36, p=0.084) and t (4; 14) (HR=1.38, 95% CI=0.90-2.11, p=0.143).	Lenalidomide	44-56	adenine phosphoribosyltransferase	Homo sapiens	124-127
25281606-6	2014	In patients with a long REM1 (>=3 years), salvage treatment with either repeat FCR or lenalidomide-based therapy results in subsequent median survival exceeding 5 years; for these patients, FCR rechallenge represents a reasonable standard of care.	Lenalidomide	89-101	RRAD and GEM like GTPase 1	Homo sapiens	24-28
24721791-5	2014	Moreover, repression of the IRF4 target gene MYC in bortezomib-resistant cells by gene knockdown or treatment with CPI203, a BET (bromodomain and extra terminal) bromodomain inhibitor, synergistically induced cell death when combined with lenalidomide.	Lenalidomide	239-251	interferon regulatory factor 4	Mus musculus	28-32
24721791-5	2014	Moreover, repression of the IRF4 target gene MYC in bortezomib-resistant cells by gene knockdown or treatment with CPI203, a BET (bromodomain and extra terminal) bromodomain inhibitor, synergistically induced cell death when combined with lenalidomide.	Lenalidomide	239-251	myelocytomatosis oncogene	Mus musculus	45-48
24721791-7	2014	Together, these results suggest that exacerbated IRF4/MYC signaling is associated to bortezomib resistance in MCL in vivo and warrant clinical evaluation of lenalidomide plus BET inhibitor combination in MCL cases refractory to proteasome inhibition.	Lenalidomide	157-169	interferon regulatory factor 4	Mus musculus	49-53
24721791-7	2014	Together, these results suggest that exacerbated IRF4/MYC signaling is associated to bortezomib resistance in MCL in vivo and warrant clinical evaluation of lenalidomide plus BET inhibitor combination in MCL cases refractory to proteasome inhibition.	Lenalidomide	157-169	myelocytomatosis oncogene	Mus musculus	54-57
25295231-11	2014	Through its inhibitory effect on PP2A, lenalidomide stabilizes MDM2 to restore p53 degradation in erythroid precursors, with subsequent arrest in G2/M.	Lenalidomide	39-51	protein phosphatase 2 phosphatase activator	Homo sapiens	33-37
25295231-11	2014	Through its inhibitory effect on PP2A, lenalidomide stabilizes MDM2 to restore p53 degradation in erythroid precursors, with subsequent arrest in G2/M.	Lenalidomide	39-51	MDM2 proto-oncogene	Homo sapiens	63-67
25295231-11	2014	Through its inhibitory effect on PP2A, lenalidomide stabilizes MDM2 to restore p53 degradation in erythroid precursors, with subsequent arrest in G2/M.	Lenalidomide	39-51	tumor protein p53	Homo sapiens	79-82
24687382-1	2014	Cereblon (CRBN) is essential for the anti-myeloma (MM) activity of immunomodulatory drugs (IMiDs), such as thalidomide and lenalidomide.	Lenalidomide	123-135	cereblon	Homo sapiens	10-14
24990888-0	2014	Lenalidomide inhibits the proliferation of CLL cells via a cereblon/p21(WAF1/Cip1)-dependent mechanism independent of functional p53.	Lenalidomide	0-12	cyclin dependent kinase inhibitor 1A	Homo sapiens	68-81
24990888-2	2014	We examined the direct effect of lenalidomide on CLL-cell proliferation induced by CD154-expressing accessory cells in media containing interleukin-4 and -10.	Lenalidomide	33-45	CD40 ligand	Homo sapiens	83-88
24990888-3	2014	Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).	Lenalidomide	15-27	tumor protein p53	Homo sapiens	115-118
24990888-3	2014	Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).	Lenalidomide	15-27	cyclin dependent kinase inhibitor 1A	Homo sapiens	186-199
24990888-3	2014	Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).	Lenalidomide	15-27	cyclin dependent kinase inhibitor 1A	Homo sapiens	186-189
24990888-4	2014	Silencing p21 with small interfering RNA impaired the capacity of lenalidomide to inhibit CLL-cell proliferation.	Lenalidomide	66-78	cyclin dependent kinase inhibitor 1A	Homo sapiens	10-13
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	48-60	cyclin dependent kinase inhibitor 1A	Homo sapiens	124-127
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	48-60	CD40 ligand	Homo sapiens	137-142
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	48-60	zinc finger protein 266	Homo sapiens	219-247
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	87-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	124-127
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	87-99	CD40 ligand	Homo sapiens	137-142
24990888-5	2014	Silencing cereblon, a known molecular target of lenalidomide, impaired the capacity of lenalidomide to induce expression of p21, inhibit CD154-induced CLL-cell proliferation, or enhance the degradation of Ikaros family zinc finger proteins 1 and 3.	Lenalidomide	87-99	zinc finger protein 266	Homo sapiens	219-247
24990888-6	2014	We isolated CLL cells from the blood of patients before and after short-term treatment with low-dose lenalidomide (5 mg per day) and found the leukemia cells were also induced to express p21 in vivo.	Lenalidomide	101-113	cyclin dependent kinase inhibitor 1A	Homo sapiens	187-190
24990888-7	2014	These results indicate that lenalidomide can directly inhibit proliferation of CLL cells in a cereblon/p21-dependent but p53-independent manner, at concentrations achievable in vivo, potentially contributing to the capacity of this drug to inhibit disease-progression in patients with CLL.	Lenalidomide	28-40	cyclin dependent kinase inhibitor 1A	Homo sapiens	103-106
24990888-7	2014	These results indicate that lenalidomide can directly inhibit proliferation of CLL cells in a cereblon/p21-dependent but p53-independent manner, at concentrations achievable in vivo, potentially contributing to the capacity of this drug to inhibit disease-progression in patients with CLL.	Lenalidomide	28-40	tumor protein p53	Homo sapiens	121-124
25248908-0	2014	[Three cases of lenalidomide-resistant IgA myeloma for which a response was regained after the addition of clarithromycin].	Lenalidomide	16-28	CD79a molecule	Homo sapiens	39-42
24569836-0	2014	SNS01-T modulation of eIF5A inhibits B-cell cancer progression and synergizes with bortezomib and lenalidomide.	Lenalidomide	98-110	eukaryotic translation initiation factor 5A	Homo sapiens	22-27
25108355-0	2014	Structure of the human Cereblon-DDB1-lenalidomide complex reveals basis for responsiveness to thalidomide analogs.	Lenalidomide	37-49	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.	Lenalidomide	86-98	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.	Lenalidomide	86-98	damage specific DNA binding protein 1	Homo sapiens	14-18
25108355-3	2014	Here we present the crystal structure of human CRBN bound to DDB1 and the drug lenalidomide.	Lenalidomide	79-91	cereblon	Homo sapiens	47-51
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.	Lenalidomide	108-120	cereblon	Homo sapiens	64-68
25165875-0	2014	Combination of lenalidomide with vitamin D3 induces apoptosis in mantle cell lymphoma via demethylation of BIK.	Lenalidomide	15-27	BCL2 interacting killer	Homo sapiens	107-110
25043012-4	2014	Here we present crystal structures of the DDB1-CRBN complex bound to thalidomide, lenalidomide and pomalidomide.	Lenalidomide	82-94	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.	Lenalidomide	82-94	cereblon	Homo sapiens	47-51
24757092-0	2014	Lenalidomide-based maintenance therapy reduces TNF receptor 2 on CD4 T cells and enhances immune effector function in acute myeloid leukemia patients.	Lenalidomide	0-12	tumor necrosis factor	Homo sapiens	47-50
24757092-0	2014	Lenalidomide-based maintenance therapy reduces TNF receptor 2 on CD4 T cells and enhances immune effector function in acute myeloid leukemia patients.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	65-68
24757092-7	2014	Our data indicates that although treatment with lenalidomide and azacitidine increased cytokine production by effector T cells in all patients, durable clinical remissions may be observed in patients with a concomitant reduction in TNFR2+ T cells and TNFR2+ Tregs.	Lenalidomide	48-60	TNF receptor superfamily member 1B	Homo sapiens	232-237
24757092-7	2014	Our data indicates that although treatment with lenalidomide and azacitidine increased cytokine production by effector T cells in all patients, durable clinical remissions may be observed in patients with a concomitant reduction in TNFR2+ T cells and TNFR2+ Tregs.	Lenalidomide	48-60	TNF receptor superfamily member 1B	Homo sapiens	251-256
24757092-8	2014	In vitro studies further demonstrated that lenalidomide can reduce TNFR2 expression and can augment effector cytokine production by T cells, which can be further enhanced by azacitidine.	Lenalidomide	43-55	TNF receptor superfamily member 1B	Homo sapiens	67-72
24757092-9	2014	These results indicate that reduction of TNFR2+ T cells in AML postremission phase may result from combined azacitidine/lenalidomide therapy and may contribute to an improved clinical outcome.	Lenalidomide	120-132	TNF receptor superfamily member 1B	Homo sapiens	41-46
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.	Lenalidomide	209-221	cereblon	Homo sapiens	102-106
24712857-3	2014	Lenalidomide therapy was associated with increased amounts of a CD8(+) T cell subset, phenotypically staged between classical central memory T cells (TCM) and effector memory T cells (TEM), consequently termed TCM/TEM.	Lenalidomide	0-12	CD8a molecule	Homo sapiens	64-67
24840055-5	2014	demonstrates that, by binding to CRBN and altering its selectivity, lenalidomide potentiates the ubiquitination and proteolysis of 2 specific proteins, IKZF1 and IKZF3.	Lenalidomide	68-80	cereblon	Homo sapiens	33-37
24840055-5	2014	demonstrates that, by binding to CRBN and altering its selectivity, lenalidomide potentiates the ubiquitination and proteolysis of 2 specific proteins, IKZF1 and IKZF3.	Lenalidomide	68-80	IKAROS family zinc finger 1	Homo sapiens	152-157
24840055-5	2014	demonstrates that, by binding to CRBN and altering its selectivity, lenalidomide potentiates the ubiquitination and proteolysis of 2 specific proteins, IKZF1 and IKZF3.	Lenalidomide	68-80	IKAROS family zinc finger 3	Homo sapiens	162-167
24840055-7	2014	IKZF1 and IKZF3 are transcription factors that are necessary for multiple myeloma, and repression of these transcription factors is a likely mechanism for lenalidomide activity in this disease.	Lenalidomide	155-167	IKAROS family zinc finger 1	Homo sapiens	0-5
24840055-7	2014	IKZF1 and IKZF3 are transcription factors that are necessary for multiple myeloma, and repression of these transcription factors is a likely mechanism for lenalidomide activity in this disease.	Lenalidomide	155-167	IKAROS family zinc finger 3	Homo sapiens	10-15
24712857-5	2014	In addition, lenalidomide-treated patients showed higher abundance of CD14(+) myeloid cells co-expressing CD15.	Lenalidomide	13-25	CD14 molecule	Homo sapiens	70-74
24712857-5	2014	In addition, lenalidomide-treated patients showed higher abundance of CD14(+) myeloid cells co-expressing CD15.	Lenalidomide	13-25	fucosyltransferase 4	Homo sapiens	106-110
24891322-7	2014	Chronic stimulation with LPS accelerated the development of MDS in mDia1 heterozygous and knockout mice that can be rescued by lenalidomide.	Lenalidomide	127-139	diaphanous related formin 1	Mus musculus	67-72
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	72-75
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	CD8a molecule	Homo sapiens	82-85
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	protein tyrosine phosphatase receptor type C	Homo sapiens	88-92
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	C-C motif chemokine receptor 7	Homo sapiens	97-101
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	88-91
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	interferon stimulated exonuclease gene 20	Homo sapiens	165-169
24237448-7	2014	Lenalidomide impaired long-term thymic T-cell reconstitution, decreased CD4 + and CD8 + CD45RA + CCR7 - effector-terminal T-cell absolute counts and increased CD4 + CD25 + CD127 - /low regulatory T-cells.	Lenalidomide	0-12	interleukin 7 receptor	Homo sapiens	172-177
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.	Lenalidomide	0-12	tumor necrosis factor	Mus musculus	176-210
24914135-2	2014	Using 2 different methodologies, we identified 244 CRBN binding proteins and established relevance to MM biology by changes in their abundance after exposure to lenalidomide.	Lenalidomide	161-173	cereblon	Homo sapiens	51-55
24914135-4	2014	After lenalidomide treatment, the abundance of 46 CRBN binding proteins decreased.	Lenalidomide	6-18	cereblon	Homo sapiens	50-54
25610725-0	2014	Lenalidomide induces degradation of IKZF1 and IKZF3.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	36-41
25610725-0	2014	Lenalidomide induces degradation of IKZF1 and IKZF3.	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	46-51
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.	Lenalidomide	0-12	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.	Lenalidomide	0-12	interleukin 2	Homo sapiens	170-174
24982344-7	2014	In RT4 xenografts, lenalidomide significantly reduced tumor size and CD31 expression, and increased expression of CC3 (p<0.05).	Lenalidomide	19-31	platelet and endothelial cell adhesion molecule 1	Homo sapiens	69-73
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.	Lenalidomide	14-22	tumor necrosis factor	Mus musculus	176-210
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	tumor necrosis factor	Mus musculus	40-49
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	BCL2-associated X protein	Mus musculus	51-54
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	B cell leukemia/lymphoma 2	Mus musculus	56-61
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	heat shock protein 5	Mus musculus	63-66
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	caspase 8	Mus musculus	68-77
24739012-9	2014	Western blot analysis revealed elevated TNF-alpha, Bax, Bcl-2, Bip, caspase 8 and caspase 9 in ob/ob mice with various degrees of reversal by lenalidomide treatment.	Lenalidomide	142-154	caspase 9	Mus musculus	82-91
23922218-0	2014	Flow cytometry-based enumeration and functional characterization of CD8 T regulatory cells in patients with multiple myeloma before and after lenalidomide plus dexamethasone treatment.	Lenalidomide	142-154	CD8a molecule	Homo sapiens	68-71
24682512-3	2014	In this study, bone marrow biopsies from 85 patients treated with lenalidomide in the MDS-004 clinical trial were retrospectively assessed for p53 expression by immunohistochemistry in association with outcome.	Lenalidomide	66-78	tumor protein p53	Homo sapiens	143-146
24742716-2	2014	Lenalidomide loaded chitosan nanoparticles (LND-CS-NPs) were in the size range of 220-295 nm and characterized by DLS, TEM, FT-IR, TGA and XRD.	Lenalidomide	0-12	T-box transcription factor 1	Homo sapiens	131-134
24966686-0	2014	Myelodysplastic disorders carrying both isolated del(5q) and JAK2(V617F) mutation: concise review, with focus on lenalidomide therapy.	Lenalidomide	113-125	Janus kinase 2	Homo sapiens	61-71
25189730-5	2014	The rationale of combination of danazol or lenalidomide with ruxolitinib is mainly based on mitigation of anti-JAK2-mediated myelosuppression.	Lenalidomide	43-55	Janus kinase 2	Homo sapiens	111-115
24706190-7	2014	Moreover, bortezomib-induced up-regulation of CHOP was readily enhanced by lenalidomide in contact with stromal cells.	Lenalidomide	75-87	DNA damage inducible transcript 3	Homo sapiens	46-50
24328678-0	2014	Immunomodulatory agents lenalidomide and pomalidomide co-stimulate T cells by inducing degradation of T cell repressors Ikaros and Aiolos via modulation of the E3 ubiquitin ligase complex CRL4(CRBN.).	Lenalidomide	24-36	IKAROS family zinc finger 3	Homo sapiens	131-137
24659021-1	2014	PURPOSE: Lenalidomide, a weak substrate of P-glycoprotein (P-gp) in vitro, is an oral anticancer drug eliminated predominantly via renal excretion as unchanged compound.	Lenalidomide	9-21	ATP binding cassette subfamily B member 1	Homo sapiens	43-57
24659021-1	2014	PURPOSE: Lenalidomide, a weak substrate of P-glycoprotein (P-gp) in vitro, is an oral anticancer drug eliminated predominantly via renal excretion as unchanged compound.	Lenalidomide	9-21	ATP binding cassette subfamily B member 1	Homo sapiens	59-63
24659021-2	2014	The role of P-gp in lenalidomide disposition and the associated clinical relevance were evaluated.	Lenalidomide	20-32	ATP binding cassette subfamily B member 1	Homo sapiens	12-16
24351336-0	2014	Increase in antibody-dependent cellular cytotoxicity (ADCC) in a patient with advanced colorectal carcinoma carrying a KRAS mutation under lenalidomide therapy.	Lenalidomide	139-151	KRAS proto-oncogene, GTPase	Homo sapiens	119-123
24351336-5	2014	In a heavily pretreated patient with advanced colorectal cancer carrying mutations in APC and KRAS genes, we show an early metabolic response and enhanced NK cell activity to monotherapy with lenalidomide.	Lenalidomide	192-204	KRAS proto-oncogene, GTPase	Homo sapiens	94-98
24627193-11	2014	TP53 mutations are important predictors of AML progression and possible resistance to lenalidomide.	Lenalidomide	86-98	tumor protein p53	Homo sapiens	0-4
24606326-11	2014	The ORR and PFS in patients with low-affinity FCGR3A polymorphisms (F/F and F/V) suggest that lenalidomide may improve the activity of rituximab in these patients.	Lenalidomide	94-106	Fc gamma receptor IIIa	Homo sapiens	46-52
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	ATP binding cassette subfamily B member 1	Homo sapiens	51-55
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	57-61
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	ATP binding cassette subfamily C member 2	Homo sapiens	63-67
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	POU class 2 homeobox 2	Homo sapiens	69-73
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	solute carrier family 22 member 6	Homo sapiens	75-79
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	solute carrier family 22 member 8	Homo sapiens	81-85
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	solute carrier organic anion transporter family member 1B1	Homo sapiens	87-94
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	solute carrier organic anion transporter family member 1B3	Homo sapiens	96-103
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	ATP binding cassette subfamily B member 11	Homo sapiens	108-129
24627218-4	2014	Lenalidomide was also evaluated as an inhibitor of P-gp, BCRP, MRP2, OCT2, OAT1, OAT3, OATP1B1, OATP1B3 and bile salt export pump (BSEP).	Lenalidomide	0-12	ATP binding cassette subfamily B member 11	Homo sapiens	131-135
24627218-5	2014	In addition, inhibition of UDP-glucuronosyltransferase 1A1 (UGT1A1) variants by lenalidomide was also assessed.	Lenalidomide	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	27-58
24627218-5	2014	In addition, inhibition of UDP-glucuronosyltransferase 1A1 (UGT1A1) variants by lenalidomide was also assessed.	Lenalidomide	80-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
24627218-7	2014	RESULTS: Results of these studies indicate that the lenalidomide is not a substrate for the transporters examined, except that it is weak substrate of P-gp.	Lenalidomide	52-64	ATP binding cassette subfamily B member 1	Homo sapiens	151-155
24328678-2	2014	T cell co-stimulation by lenalidomide or pomalidomide is cereblon dependent: however, the CRL4(CRBN) substrates responsible for T cell co-stimulation have yet to be identified.	Lenalidomide	25-37	interleukin 17 receptor B	Homo sapiens	90-94
24328678-2	2014	T cell co-stimulation by lenalidomide or pomalidomide is cereblon dependent: however, the CRL4(CRBN) substrates responsible for T cell co-stimulation have yet to be identified.	Lenalidomide	25-37	cereblon	Homo sapiens	95-99
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	IKAROS family zinc finger 1	Homo sapiens	74-79
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	IKAROS family zinc finger 1	Homo sapiens	96-101
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	IKAROS family zinc finger 3	Homo sapiens	112-118
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	IKAROS family zinc finger 3	Homo sapiens	120-125
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	IKAROS family zinc finger 3	Homo sapiens	142-147
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	interleukin 17 receptor B	Homo sapiens	159-163
24328678-3	2014	Here we demonstrate that interaction of the transcription factors Ikaros (IKZF1, encoded by the IKZF1 gene) and Aiolos (IKZF3, encoded by the IKZF3 gene) with CRL4(CRBN) is induced by lenalidomide or pomalidomide.	Lenalidomide	184-196	cereblon	Homo sapiens	164-168
24328678-7	2014	Importantly, Aiolos could serve as a proximal pharmacodynamic marker for lenalidomide and pomalidomide, as healthy human subjects administered lenalidomide demonstrated Aiolos degradation in their peripheral T cells.	Lenalidomide	73-85	IKAROS family zinc finger 3	Homo sapiens	13-19
24328678-7	2014	Importantly, Aiolos could serve as a proximal pharmacodynamic marker for lenalidomide and pomalidomide, as healthy human subjects administered lenalidomide demonstrated Aiolos degradation in their peripheral T cells.	Lenalidomide	143-155	IKAROS family zinc finger 3	Homo sapiens	13-19
24328678-7	2014	Importantly, Aiolos could serve as a proximal pharmacodynamic marker for lenalidomide and pomalidomide, as healthy human subjects administered lenalidomide demonstrated Aiolos degradation in their peripheral T cells.	Lenalidomide	143-155	IKAROS family zinc finger 3	Homo sapiens	169-175
24328678-0	2014	Immunomodulatory agents lenalidomide and pomalidomide co-stimulate T cells by inducing degradation of T cell repressors Ikaros and Aiolos via modulation of the E3 ubiquitin ligase complex CRL4(CRBN.).	Lenalidomide	24-36	interleukin 17 receptor B	Homo sapiens	188-192
24328678-0	2014	Immunomodulatory agents lenalidomide and pomalidomide co-stimulate T cells by inducing degradation of T cell repressors Ikaros and Aiolos via modulation of the E3 ubiquitin ligase complex CRL4(CRBN.).	Lenalidomide	24-36	cereblon	Homo sapiens	193-197
24328678-1	2014	Cereblon (CRBN), the molecular target of lenalidomide and pomalidomide, is a substrate receptor of the cullin ring E3 ubiquitin ligase complex, CRL4(CRBN) .	Lenalidomide	41-53	cereblon	Homo sapiens	10-14
24328678-1	2014	Cereblon (CRBN), the molecular target of lenalidomide and pomalidomide, is a substrate receptor of the cullin ring E3 ubiquitin ligase complex, CRL4(CRBN) .	Lenalidomide	41-53	CDK2 associated cullin domain 1	Homo sapiens	103-109
24328678-1	2014	Cereblon (CRBN), the molecular target of lenalidomide and pomalidomide, is a substrate receptor of the cullin ring E3 ubiquitin ligase complex, CRL4(CRBN) .	Lenalidomide	41-53	interleukin 17 receptor B	Homo sapiens	144-148
24328678-1	2014	Cereblon (CRBN), the molecular target of lenalidomide and pomalidomide, is a substrate receptor of the cullin ring E3 ubiquitin ligase complex, CRL4(CRBN) .	Lenalidomide	41-53	cereblon	Homo sapiens	149-153
24236538-7	2014	This cytotoxic effect and BCL2 downregulation were further potentiated when AT-101 was combined with lenalidomide/dexamethasone (LDA).	Lenalidomide	101-113	BCL2 apoptosis regulator	Homo sapiens	26-30
24297864-7	2014	The HIF-1alpha inhibition by either siRNA or panobinostat impaired the MMECs angiogenesis-related functions both in vitro and in vivo and restored MMEC sensitivity to bortezomib and lenalidomide.	Lenalidomide	182-194	hypoxia inducible factor 1 subunit alpha	Homo sapiens	4-14
24297864-9	2014	CONCLUSIONS: The HIF-1alpha protein in MMECs may induce angiogenesis and resistance to bortezomib and lenalidomide and may be a plausible target for the antiangiogenic management of patients with well-defined relapsed/refractory multiple myeloma.	Lenalidomide	102-114	hypoxia inducible factor 1 subunit alpha	Homo sapiens	17-27
24211319-3	2014	In multiple regression analysis, age, platelet count at time of mobilization, type of GF utilized, and extent of exposure to lenalidomide independently correlated with peripheral blood (PB)-CD34+ and were integrated in a predicting score (PS) for poor mobilizers, defined as PB-CD34+ < 20/mm(3) 4 days after initiation of GF.	Lenalidomide	125-137	CD34 molecule	Homo sapiens	190-194
24211319-3	2014	In multiple regression analysis, age, platelet count at time of mobilization, type of GF utilized, and extent of exposure to lenalidomide independently correlated with peripheral blood (PB)-CD34+ and were integrated in a predicting score (PS) for poor mobilizers, defined as PB-CD34+ < 20/mm(3) 4 days after initiation of GF.	Lenalidomide	125-137	CD34 molecule	Homo sapiens	278-282
24253022-8	2014	Immunotherapy against MM is also being explored, and probably the most attractive example of this approach is the combination of the anti-CS1 MoAb elotuzumab with lenalidomide and dexamethasone, which has produced exciting results in the relapsed/refractory setting.	Lenalidomide	163-175	chorionic somatomammotropin hormone 1	Homo sapiens	138-141
24335103-9	2014	Data from correlative studies on peripheral blood samples suggest that the effects of lenalidomide could be associated with decreased circulating CD25(+) T cells and CD4(+) T-cell numbers.	Lenalidomide	86-98	interleukin 2 receptor subunit alpha	Homo sapiens	146-150
24335103-9	2014	Data from correlative studies on peripheral blood samples suggest that the effects of lenalidomide could be associated with decreased circulating CD25(+) T cells and CD4(+) T-cell numbers.	Lenalidomide	86-98	CD4 molecule	Homo sapiens	166-169
24212063-7	2014	Patients who respond to lenalidomide showed a more pronounced decrease of VEGF and bFGF than did patients with stable or progressive disease (p = 0.007 and p = 0.005).	Lenalidomide	24-36	vascular endothelial growth factor A	Homo sapiens	74-78
24212063-7	2014	Patients who respond to lenalidomide showed a more pronounced decrease of VEGF and bFGF than did patients with stable or progressive disease (p = 0.007 and p = 0.005).	Lenalidomide	24-36	fibroblast growth factor 2	Homo sapiens	83-87
24178620-0	2014	Antitumoral activity of lenalidomide in in vitro and in vivo models of mantle cell lymphoma involves the destabilization of cyclin D1/p27KIP1 complexes.	Lenalidomide	24-36	cyclin D1	Homo sapiens	124-133
23760401-0	2014	Evidence of a role for CD44 and cell adhesion in mediating resistance to lenalidomide in multiple myeloma: therapeutic implications.	Lenalidomide	73-85	CD44 molecule (Indian blood group)	Homo sapiens	23-27
23760401-2	2014	Lenalidomide-resistant models were found to overexpress the hyaluronan (HA)-binding protein CD44, a downstream Wnt/beta-catenin transcriptional target.	Lenalidomide	0-12	CD44 molecule (Indian blood group)	Homo sapiens	92-96
23760401-2	2014	Lenalidomide-resistant models were found to overexpress the hyaluronan (HA)-binding protein CD44, a downstream Wnt/beta-catenin transcriptional target.	Lenalidomide	0-12	catenin beta 1	Homo sapiens	115-127
23760401-3	2014	Consistent with a role of CD44 in cell adhesion-mediated drug resistance (CAM-DR), lenalidomide-resistant myeloma cells were more adhesive to bone marrow stroma and HA-coated plates.	Lenalidomide	83-95	CD44 molecule (Indian blood group)	Homo sapiens	26-30
23760401-4	2014	Blockade of CD44 with monoclonal antibodies, free HA or CD44 knockdown reduced adhesion and sensitized to lenalidomide.	Lenalidomide	106-118	CD44 molecule (Indian blood group)	Homo sapiens	12-16
23760401-4	2014	Blockade of CD44 with monoclonal antibodies, free HA or CD44 knockdown reduced adhesion and sensitized to lenalidomide.	Lenalidomide	106-118	CD44 molecule (Indian blood group)	Homo sapiens	56-60
23760401-5	2014	Wnt/beta-catenin suppression by FH535 enhanced the activity of lenalidomide, as did interleukin-6 neutralization with siltuximab.	Lenalidomide	63-75	catenin beta 1	Homo sapiens	4-16
23760401-6	2014	Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model.	Lenalidomide	189-201	catenin (cadherin associated protein), beta 1	Mus musculus	60-72
23760401-6	2014	Notably, all-trans retinoic acid (ATRA) downregulated total beta-catenin, cell-surface and total CD44, reduced adhesion of lenalidomide-resistant myeloma cells and enhanced the activity of lenalidomide in a lenalidomide-resistant in vivo murine xenograft model.	Lenalidomide	189-201	catenin (cadherin associated protein), beta 1	Mus musculus	60-72
23760401-8	2014	Taken together, our findings support the hypotheses that CD44 and CAM-DR contribute to lenalidomide resistance in multiple myeloma, that CD44 should be evaluated as a putative biomarker of sensitivity to lenalidomide, and that ATRA or other approaches that target CD44 may overcome clinical lenalidomide resistance.	Lenalidomide	87-99	CD44 molecule (Indian blood group)	Homo sapiens	57-61
24292623-0	2014	The myeloma drug lenalidomide promotes the cereblon-dependent destruction of Ikaros proteins.	Lenalidomide	17-29	IKAROS family zinc finger 1	Homo sapiens	77-83
24292623-5	2014	Here we show that lenalidomide-bound cereblon acquires the ability to target for proteasomal degradation two specific B cell transcription factors, Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	18-30	IKAROS family zinc finger 1	Homo sapiens	148-154
24292623-5	2014	Here we show that lenalidomide-bound cereblon acquires the ability to target for proteasomal degradation two specific B cell transcription factors, Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	18-30	zinc finger protein 266	Homo sapiens	162-190
24292623-5	2014	Here we show that lenalidomide-bound cereblon acquires the ability to target for proteasomal degradation two specific B cell transcription factors, Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	18-30	IKAROS family zinc finger 1	Homo sapiens	192-197
24292623-5	2014	Here we show that lenalidomide-bound cereblon acquires the ability to target for proteasomal degradation two specific B cell transcription factors, Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3).	Lenalidomide	18-30	IKAROS family zinc finger 3	Homo sapiens	202-207
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.	Lenalidomide	106-118	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.	Lenalidomide	106-118	IKAROS family zinc finger 3	Homo sapiens	63-68
24292625-0	2014	Lenalidomide causes selective degradation of IKZF1 and IKZF3 in multiple myeloma cells.	Lenalidomide	0-12	IKAROS family zinc finger 1	Homo sapiens	45-50
24292625-0	2014	Lenalidomide causes selective degradation of IKZF1 and IKZF3 in multiple myeloma cells.	Lenalidomide	0-12	IKAROS family zinc finger 3	Homo sapiens	55-60
24292625-2	2014	Using quantitative proteomics, we found that lenalidomide causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase.	Lenalidomide	45-57	IKAROS family zinc finger 1	Homo sapiens	145-150
24292625-2	2014	Using quantitative proteomics, we found that lenalidomide causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase.	Lenalidomide	45-57	IKAROS family zinc finger 3	Homo sapiens	155-160
24292625-4	2014	A single amino acid substitution of IKZF3 conferred resistance to lenalidomide-induced degradation and rescued lenalidomide-induced inhibition of cell growth.	Lenalidomide	66-78	IKAROS family zinc finger 3	Homo sapiens	36-41
24292625-4	2014	A single amino acid substitution of IKZF3 conferred resistance to lenalidomide-induced degradation and rescued lenalidomide-induced inhibition of cell growth.	Lenalidomide	111-123	IKAROS family zinc finger 3	Homo sapiens	36-41
24292625-5	2014	Similarly, we found that lenalidomide-induced interleukin-2 production in T cells is due to depletion of IKZF1 and IKZF3.	Lenalidomide	25-37	interleukin 2	Homo sapiens	46-59
24292625-5	2014	Similarly, we found that lenalidomide-induced interleukin-2 production in T cells is due to depletion of IKZF1 and IKZF3.	Lenalidomide	25-37	IKAROS family zinc finger 1	Homo sapiens	105-110
24292625-5	2014	Similarly, we found that lenalidomide-induced interleukin-2 production in T cells is due to depletion of IKZF1 and IKZF3.	Lenalidomide	25-37	IKAROS family zinc finger 3	Homo sapiens	115-120
24178620-0	2014	Antitumoral activity of lenalidomide in in vitro and in vivo models of mantle cell lymphoma involves the destabilization of cyclin D1/p27KIP1 complexes.	Lenalidomide	24-36	cyclin dependent kinase inhibitor 1B	Homo sapiens	134-141
24178620-2	2014	We investigated whether the expression and subcellular localization of cyclin D1, a major cell-cycle regulator overexpressed in MCL, and the cyclin-dependent kinase inhibitor p27(KIP1), could identify MCL cases sensitive to lenalidomide, and whether the compound could modulate cyclin D1/p27(KIP1) complexes in MCL cells.	Lenalidomide	224-236	cyclin D1	Homo sapiens	71-80
24178620-4	2014	Activity of lenalidomide in vitro and its effect on cyclin D1/p27(KIP1) complexes were evaluated by real-time PCR, immunoprecipitation, immunofluorescence, and Western blot.	Lenalidomide	12-24	cyclin D1	Homo sapiens	52-61
24178620-4	2014	Activity of lenalidomide in vitro and its effect on cyclin D1/p27(KIP1) complexes were evaluated by real-time PCR, immunoprecipitation, immunofluorescence, and Western blot.	Lenalidomide	12-24	interferon alpha inducible protein 27	Homo sapiens	62-65
24178620-4	2014	Activity of lenalidomide in vitro and its effect on cyclin D1/p27(KIP1) complexes were evaluated by real-time PCR, immunoprecipitation, immunofluorescence, and Western blot.	Lenalidomide	12-24	cyclin dependent kinase inhibitor 1B	Homo sapiens	66-70
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	cyclin D1	Homo sapiens	43-52
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	cyclin D1	Homo sapiens	86-95
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	interferon alpha inducible protein 27	Homo sapiens	96-99
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	cyclin dependent kinase inhibitor 1B	Homo sapiens	100-104
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	interferon alpha inducible protein 27	Homo sapiens	155-158
24178620-9	2014	Lenalidomide mechanism of action relied on cyclin D1 downregulation and disruption of cyclin D1/p27(KIP1) complexes, followed by cytosolic accumulation of p27(KIP1), cell proliferation arrest, apoptosis, and angiogenesis inhibition.	Lenalidomide	0-12	cyclin dependent kinase inhibitor 1B	Homo sapiens	159-163
24178620-10	2014	CONCLUSIONS: These results highlight a mechanism of action of lenalidomide in MCL cases with increased tumorigenicity in vivo, which is mediated by the dissociation of cyclin D1/p27(KIP1) complexes, and subsequent proliferation blockade and apoptosis induction.	Lenalidomide	62-74	cyclin D1	Homo sapiens	168-177
24178620-10	2014	CONCLUSIONS: These results highlight a mechanism of action of lenalidomide in MCL cases with increased tumorigenicity in vivo, which is mediated by the dissociation of cyclin D1/p27(KIP1) complexes, and subsequent proliferation blockade and apoptosis induction.	Lenalidomide	62-74	interferon alpha inducible protein 27	Homo sapiens	178-181
24178620-10	2014	CONCLUSIONS: These results highlight a mechanism of action of lenalidomide in MCL cases with increased tumorigenicity in vivo, which is mediated by the dissociation of cyclin D1/p27(KIP1) complexes, and subsequent proliferation blockade and apoptosis induction.	Lenalidomide	62-74	cyclin dependent kinase inhibitor 1B	Homo sapiens	182-186
23573828-7	2014	Our data thus indicate a functional role for the TRAIL/TRAIL-R system in lenalidomide-mediated NK-cell activity against MM cells, but also show that dasatinib is unsuitable to support or boost this effect.	Lenalidomide	73-85	TNF superfamily member 10	Homo sapiens	49-54
24018623-5	2014	Advances in the understanding of the pathogenesis of the disease have suggested that lenalidomide targets aberrant signaling pathways caused by haplosufficiency of specific genes in a commonly deleted region on chromosome 5 (e.g., SPARC, RPS14, Cdc25C, and PP2A).	Lenalidomide	85-97	secreted protein acidic and cysteine rich	Homo sapiens	231-236
24018623-5	2014	Advances in the understanding of the pathogenesis of the disease have suggested that lenalidomide targets aberrant signaling pathways caused by haplosufficiency of specific genes in a commonly deleted region on chromosome 5 (e.g., SPARC, RPS14, Cdc25C, and PP2A).	Lenalidomide	85-97	ribosomal protein S14	Homo sapiens	238-243
24018623-5	2014	Advances in the understanding of the pathogenesis of the disease have suggested that lenalidomide targets aberrant signaling pathways caused by haplosufficiency of specific genes in a commonly deleted region on chromosome 5 (e.g., SPARC, RPS14, Cdc25C, and PP2A).	Lenalidomide	85-97	cell division cycle 25C	Homo sapiens	245-251
24018623-5	2014	Advances in the understanding of the pathogenesis of the disease have suggested that lenalidomide targets aberrant signaling pathways caused by haplosufficiency of specific genes in a commonly deleted region on chromosome 5 (e.g., SPARC, RPS14, Cdc25C, and PP2A).	Lenalidomide	85-97	protein phosphatase 2 phosphatase activator	Homo sapiens	257-261
25313353-6	2014	The effect of lenalidomide on NK cells was secondary to the induction of IL-2 production by CD4 T cells.	Lenalidomide	14-26	interleukin 2	Homo sapiens	73-77
25313353-9	2014	Lenalidomide also upregulated CD20 expression on leukemia cells and, accordingly, it had a synergistic effect with rituximab on promoting antibody-dependent cell-mediated cytotoxicity against primary leukemia cells.	Lenalidomide	0-12	keratin 20	Homo sapiens	30-34
24206017-0	2014	Measuring cereblon as a biomarker of response or resistance to lenalidomide and pomalidomide requires use of standardized reagents and understanding of gene complexity.	Lenalidomide	63-75	cereblon	Homo sapiens	10-18
24206017-1	2014	Cereblon, a member of the cullin 4 ring ligase complex (CRL4), is the molecular target of the immunomodulatory drugs (IMiDs) lenalidomide and pomalidomide and is required for the antiproliferative activity of these agents in multiple myeloma (MM) and immunomodulatory activity in T cells.	Lenalidomide	125-137	cereblon	Homo sapiens	0-8
24206017-1	2014	Cereblon, a member of the cullin 4 ring ligase complex (CRL4), is the molecular target of the immunomodulatory drugs (IMiDs) lenalidomide and pomalidomide and is required for the antiproliferative activity of these agents in multiple myeloma (MM) and immunomodulatory activity in T cells.	Lenalidomide	125-137	interleukin 17 receptor B	Homo sapiens	56-60
24206017-2	2014	Cereblon"s central role as a target of lenalidomide and pomalidomide suggests potential utility as a predictive biomarker of response or resistance to IMiD therapy.	Lenalidomide	39-51	cereblon	Homo sapiens	0-8
24206017-7	2014	In cell lines made resistant to lenalidomide and pomalidomide, cereblon protein is greatly reduced.	Lenalidomide	32-44	cereblon	Homo sapiens	63-71
23573828-7	2014	Our data thus indicate a functional role for the TRAIL/TRAIL-R system in lenalidomide-mediated NK-cell activity against MM cells, but also show that dasatinib is unsuitable to support or boost this effect.	Lenalidomide	73-85	TNF superfamily member 10	Homo sapiens	55-60
23636891-4	2013	Modulation of TNF-alpha expression, either by stimulation using myeloid-related protein (MRP8) or lipopolysaccharide or inhibition using lenalidomide on astrocytes, leads to similar dynamic changes in miR-155 expression.	Lenalidomide	137-149	tumor necrosis factor	Homo sapiens	14-23
23992230-4	2013	We examined HMCL protein expression levels of the lenalidomide target cereblon (CRBN) and its downstream target interferon regulatory factor-4 (IRF4), which have previously been shown to be predictive of lenalidomide response in HMCLs.	Lenalidomide	50-62	cereblon	Homo sapiens	80-84
23992230-4	2013	We examined HMCL protein expression levels of the lenalidomide target cereblon (CRBN) and its downstream target interferon regulatory factor-4 (IRF4), which have previously been shown to be predictive of lenalidomide response in HMCLs.	Lenalidomide	204-216	cereblon	Homo sapiens	80-84
23992230-4	2013	We examined HMCL protein expression levels of the lenalidomide target cereblon (CRBN) and its downstream target interferon regulatory factor-4 (IRF4), which have previously been shown to be predictive of lenalidomide response in HMCLs.	Lenalidomide	204-216	interferon regulatory factor 4	Homo sapiens	112-142
23992230-4	2013	We examined HMCL protein expression levels of the lenalidomide target cereblon (CRBN) and its downstream target interferon regulatory factor-4 (IRF4), which have previously been shown to be predictive of lenalidomide response in HMCLs.	Lenalidomide	204-216	interferon regulatory factor 4	Homo sapiens	144-148
23992230-10	2013	While CRBN and IRF4 have been shown to be associated with response to lenalidomide in patients, these findings do not translate back to HMCLs, which could be attributable to factors present in the bone marrow microenvironment.	Lenalidomide	70-82	cereblon	Homo sapiens	6-10
23992230-10	2013	While CRBN and IRF4 have been shown to be associated with response to lenalidomide in patients, these findings do not translate back to HMCLs, which could be attributable to factors present in the bone marrow microenvironment.	Lenalidomide	70-82	interferon regulatory factor 4	Homo sapiens	15-19
24210217-6	2013	Bortezomib, thalidomide or lenalidomide extended OS of FGFR3 and/or c-MAF-positive patients.	Lenalidomide	27-39	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.	Lenalidomide	27-39	MAF bZIP transcription factor	Homo sapiens	68-73
24244261-0	2013	Phase II open-label study to assess efficacy and safety of lenalidomide in combination with cetuximab in KRAS-mutant metastatic colorectal cancer.	Lenalidomide	59-71	KRAS proto-oncogene, GTPase	Homo sapiens	105-109
24244261-1	2013	UNLABELLED: This study aimed to assess the efficacy and safety of combination treatment with lenalidomide and cetuximab in KRAS-mutant metastatic colorectal cancer patients.	Lenalidomide	93-105	KRAS proto-oncogene, GTPase	Homo sapiens	123-127
24244687-0	2013	Immunomodulatory effects in a phase II study of lenalidomide combined with cetuximab in refractory KRAS-mutant metastatic colorectal cancer patients.	Lenalidomide	48-60	KRAS proto-oncogene, GTPase	Homo sapiens	99-103
24244687-3	2013	In addition, lenalidomide decreased the percentage of circulating CD19(+) B cells 2.6-fold (p<0.0001).	Lenalidomide	13-25	CD19 molecule	Homo sapiens	66-70
24189071-6	2013	Disease progression is attenuated in a Rhoh(-/-) mouse model of chronic lymphocytic leukemia and treatment of primary human chronic lymphocytic leukemia cells with Lenalidomide results in reduced RhoH protein levels.	Lenalidomide	164-176	ras homolog family member H	Mus musculus	39-43
24189071-6	2013	Disease progression is attenuated in a Rhoh(-/-) mouse model of chronic lymphocytic leukemia and treatment of primary human chronic lymphocytic leukemia cells with Lenalidomide results in reduced RhoH protein levels.	Lenalidomide	164-176	ras homolog family member H	Homo sapiens	196-200
23545991-1	2013	Lenalidomide-rituximab therapy is effective in grade 1-2 follicular and mantle cell lymphoma, but its efficacy in diffuse large B-cell lymphoma (DLBCL), transformed large cell lymphoma (TL) and grade 3 follicular lymphoma (FLG3) is unknown.	Lenalidomide	0-12	hornerin	Homo sapiens	223-227
24482747-4	2013	In particular, lenalidomide has been shown to stimulate the cytotoxic functions of T lymphocytes and natural killer cells, to limit the immunosuppressive impact of regulatory T cells, and to modulate the secretion of a wide range of cytokines, including tumor necrosis factor alpha, interferon gamma as well as interleukin (IL)-6, IL-10, and IL-12.	Lenalidomide	15-27	tumor necrosis factor	Homo sapiens	254-281
24482747-4	2013	In particular, lenalidomide has been shown to stimulate the cytotoxic functions of T lymphocytes and natural killer cells, to limit the immunosuppressive impact of regulatory T cells, and to modulate the secretion of a wide range of cytokines, including tumor necrosis factor alpha, interferon gamma as well as interleukin (IL)-6, IL-10, and IL-12.	Lenalidomide	15-27	interferon gamma	Homo sapiens	283-299
24482747-4	2013	In particular, lenalidomide has been shown to stimulate the cytotoxic functions of T lymphocytes and natural killer cells, to limit the immunosuppressive impact of regulatory T cells, and to modulate the secretion of a wide range of cytokines, including tumor necrosis factor alpha, interferon gamma as well as interleukin (IL)-6, IL-10, and IL-12.	Lenalidomide	15-27	interleukin 10	Homo sapiens	331-336
23982484-0	2013	Lenalidomide overcomes suppression of human natural killer cell anti-tumor functions by neuroblastoma microenvironment-associated IL-6 and TGFbeta1.	Lenalidomide	0-12	interleukin 6	Homo sapiens	130-134
23982484-0	2013	Lenalidomide overcomes suppression of human natural killer cell anti-tumor functions by neuroblastoma microenvironment-associated IL-6 and TGFbeta1.	Lenalidomide	0-12	transforming growth factor beta 1	Homo sapiens	139-147
23982484-8	2013	Lenalidomide blocks IL-6 and TGFbeta1 activation of these signaling pathways and inhibits their suppression of NK cells.	Lenalidomide	0-12	interleukin 6	Homo sapiens	20-24
23982484-8	2013	Lenalidomide blocks IL-6 and TGFbeta1 activation of these signaling pathways and inhibits their suppression of NK cells.	Lenalidomide	0-12	transforming growth factor beta 1	Homo sapiens	29-37
23982484-11	2013	CONCLUSION: Immunotherapy with anti-tumor cell antibodies may be improved by lenalidomide, which enhances activation of NK cells and inhibits their suppression by IL-6 and TGFbeta1.	Lenalidomide	77-89	interleukin 6	Homo sapiens	163-167
23982484-11	2013	CONCLUSION: Immunotherapy with anti-tumor cell antibodies may be improved by lenalidomide, which enhances activation of NK cells and inhibits their suppression by IL-6 and TGFbeta1.	Lenalidomide	77-89	transforming growth factor beta 1	Homo sapiens	172-180
24170980-0	2013	Effects of MRP8, LPS, and lenalidomide on the expressions of TNF-alpha , brain-enriched, and inflammation-related microRNAs in the primary astrocyte culture.	Lenalidomide	26-38	tumor necrosis factor	Rattus norvegicus	61-70
24170980-4	2013	Further, we inhibited the expression of TNF- alpha in the astrocytes by using TNF- alpha inhibitor (lenalidomide) and tested for the first time the effect of this inhibition on the expressions of the same tested miRNAs.	Lenalidomide	100-112	tumor necrosis factor	Rattus norvegicus	40-50
24170980-4	2013	Further, we inhibited the expression of TNF- alpha in the astrocytes by using TNF- alpha inhibitor (lenalidomide) and tested for the first time the effect of this inhibition on the expressions of the same tested miRNAs.	Lenalidomide	100-112	tumor necrosis factor	Rattus norvegicus	78-88
24170980-6	2013	TNF- alpha inhibition with lenalidomide leads to opposite expressions of the tested miRNAs.	Lenalidomide	27-39	tumor necrosis factor	Rattus norvegicus	0-10
24043769-0	2013	TP53 suppression promotes erythropoiesis in del(5q) MDS, suggesting a targeted therapeutic strategy in lenalidomide-resistant patients.	Lenalidomide	103-115	tumor protein p53	Homo sapiens	0-4
24043769-7	2013	We conclude that targeted suppression of p53 could support effective erythropoiesis in lenalidomide-resistant del(5q) MDS.	Lenalidomide	87-99	tumor protein p53	Homo sapiens	41-44
23893930-0	2013	Flow cytometry based enumeration and functional characterization of CD8 T regulatory cells in patients with multiple myeloma before and after lenalidomide plus dexamethasone treatment.	Lenalidomide	142-154	CD8a molecule	Homo sapiens	68-71
23334269-7	2013	The data support the current International Multiple Myeloma Working Group guidelines recommending the use of cyclophosphamide and G-CSF based mobilization for patients previously exposed to lenalidomide.	Lenalidomide	190-202	colony stimulating factor 3	Homo sapiens	130-135
23417027-4	2013	Our findings demonstrate that lenalidomide acts directly on bone marrow stromal cells via an Akt-mediated increase in Jun N-terminal kinase-dependent signaling resulting in activin A secretion, with consequent inhibition of osteoblastogenesis.	Lenalidomide	30-42	AKT serine/threonine kinase 1	Homo sapiens	93-96
23614682-10	2013	This study reveals the importance of a low baseline platelet count, karyotypic complexity and TP53 mutational status for response to lenalidomide treatment.	Lenalidomide	133-145	tumor protein p53	Homo sapiens	94-98
23614682-11	2013	It supports the molecular study of TP53 in MDS patients treated with lenalidomide.	Lenalidomide	69-81	tumor protein p53	Homo sapiens	35-39
23252419-0	2013	Response to lenalidomide of a patient with t(2;3)(p23;q29) and JAK2 non-mutated refractory anemia with ring sideroblasts and thrombocytosis.	Lenalidomide	12-24	Janus kinase 2	Homo sapiens	63-67
23434730-0	2013	A G polymorphism in the CRBN gene acts as a biomarker of response to treatment with lenalidomide in low/int-1 risk MDS without del(5q).	Lenalidomide	84-96	cereblon	Homo sapiens	24-28
23692564-9	2013	In conclusion, RBP with lenalidomide 25 mg/d, days 1-21 and bendamustine 75 mg/m(2) days 1-2 is well tolerated in patients with relapsed/refractory MM.	Lenalidomide	24-36	SURP and G-patch domain containing 1	Homo sapiens	15-18
23609417-0	2013	Association of Th1 and Th2 cytokines with transient inflammatory reaction during lenalidomide plus dexamethasone therapy in multiple myeloma.	Lenalidomide	81-93	negative elongation factor complex member C/D	Homo sapiens	15-18
23565715-4	2013	CRBN expression levels correlated significantly with response to lenalidomide treatment (r = 0 48; P < 0 001).	Lenalidomide	65-77	cereblon	Homo sapiens	0-4
23565715-7	2013	Overall, a statistically significant association between baseline CRBN expression and response in MM patients treated with lenalidomide is shown.	Lenalidomide	123-135	cereblon	Homo sapiens	66-70
23506134-0	2013	Low RPS14 expression in MDS without 5q - aberration confers higher apoptosis rate of nucleated erythrocytes and predicts prolonged survival and possible response to lenalidomide in lower risk non-5q- patients.	Lenalidomide	165-177	ribosomal protein S14	Homo sapiens	4-9
23506134-14	2013	Additionally, lower RPS14 predicts prolonged survival and possible response to lenalidomide in lower risk MDS patients.	Lenalidomide	79-91	ribosomal protein S14	Homo sapiens	20-25
23434730-0	2013	A G polymorphism in the CRBN gene acts as a biomarker of response to treatment with lenalidomide in low/int-1 risk MDS without del(5q).	Lenalidomide	84-96	Wnt family member 1	Homo sapiens	104-109
23609417-6	2013	Furthermore, Len enhanced the production of both Th1 and Th2 cytokines in normal peripheral blood mononuclear cells and in patient bone marrow mononuclear cells containing primary myeloma cells and lymphocytes.	Lenalidomide	13-16	negative elongation factor complex member C/D	Homo sapiens	49-52
23138185-0	2013	Lenalidomide-induced upregulation of CXCR4 in CD34+ hematopoietic cells, a potential mechanism of decreased hematopoietic progenitor mobilization.	Lenalidomide	0-12	C-X-C motif chemokine receptor 4	Homo sapiens	37-42
23138185-0	2013	Lenalidomide-induced upregulation of CXCR4 in CD34+ hematopoietic cells, a potential mechanism of decreased hematopoietic progenitor mobilization.	Lenalidomide	0-12	CD34 molecule	Homo sapiens	46-50
23632478-8	2013	CONCLUSION: Lenalidomide favours a uniform TNF-alpha and IL-8 inflammatory and IGF-1 secretory profile of myeloma cells, an observation that raises important questions for therapeutic approaches incorporating the agent.	Lenalidomide	12-24	insulin like growth factor 1	Homo sapiens	79-84
23565715-0	2013	High expression of cereblon (CRBN) is associated with improved clinical response in patients with multiple myeloma treated with lenalidomide and dexamethasone.	Lenalidomide	128-140	cereblon	Homo sapiens	19-27
23565715-0	2013	High expression of cereblon (CRBN) is associated with improved clinical response in patients with multiple myeloma treated with lenalidomide and dexamethasone.	Lenalidomide	128-140	cereblon	Homo sapiens	29-33
23565715-1	2013	Cereblon (CRBN) has recently been identified as a target for immunomodulatory drugs (IMiDs) and its downregulation has been linked to resistance to lenalidomide.	Lenalidomide	148-160	cereblon	Homo sapiens	0-8
23565715-1	2013	Cereblon (CRBN) has recently been identified as a target for immunomodulatory drugs (IMiDs) and its downregulation has been linked to resistance to lenalidomide.	Lenalidomide	148-160	cereblon	Homo sapiens	10-14
23565715-2	2013	Here, we studied CRBN expression by real time polymerase chain reaction in 49 bone marrow samples of newly diagnosed patients with multiple myeloma treated with lenalidomide and dexamethasone.	Lenalidomide	161-173	cereblon	Homo sapiens	17-21
23325833-0	2013	Chronic lymphocytic leukemia cells induce defective LFA-1-directed T-cell motility by altering Rho GTPase signaling that is reversible with lenalidomide.	Lenalidomide	140-152	integrin subunit alpha L	Homo sapiens	52-57
23696885-8	2013	When Len is given in combination with Dex, PCA may be induced on endothelial cells and monocytes through TF expression and PS exposure.	Lenalidomide	5-8	coagulation factor III, tissue factor	Homo sapiens	105-107
23632478-8	2013	CONCLUSION: Lenalidomide favours a uniform TNF-alpha and IL-8 inflammatory and IGF-1 secretory profile of myeloma cells, an observation that raises important questions for therapeutic approaches incorporating the agent.	Lenalidomide	12-24	tumor necrosis factor	Homo sapiens	43-52
23632478-8	2013	CONCLUSION: Lenalidomide favours a uniform TNF-alpha and IL-8 inflammatory and IGF-1 secretory profile of myeloma cells, an observation that raises important questions for therapeutic approaches incorporating the agent.	Lenalidomide	12-24	C-X-C motif chemokine ligand 8	Homo sapiens	57-61
23178378-0	2013	Immunomodulatory drugs lenalidomide and pomalidomide inhibit multiple myeloma-induced osteoclast formation and the RANKL/OPG ratio in the myeloma microenvironment targeting the expression of adhesion molecules.	Lenalidomide	23-35	TNF superfamily member 11	Homo sapiens	115-120
23178378-0	2013	Immunomodulatory drugs lenalidomide and pomalidomide inhibit multiple myeloma-induced osteoclast formation and the RANKL/OPG ratio in the myeloma microenvironment targeting the expression of adhesion molecules.	Lenalidomide	23-35	TNF receptor superfamily member 11b	Homo sapiens	121-124
23178378-3	2013	We found that in vivo concentrations of both lenalidomide (LEN) and pomalidomide (POM) significantly blunted RANKL upregulation normalizing the RANKL/OPG ratio in human osteoprogenitor cells (PreOBs) when co-cultured with MM cells and also inhibited CCL3 production by MM cells.	Lenalidomide	45-57	TNF superfamily member 11	Homo sapiens	109-114
23178378-3	2013	We found that in vivo concentrations of both lenalidomide (LEN) and pomalidomide (POM) significantly blunted RANKL upregulation normalizing the RANKL/OPG ratio in human osteoprogenitor cells (PreOBs) when co-cultured with MM cells and also inhibited CCL3 production by MM cells.	Lenalidomide	45-57	TNF superfamily member 11	Homo sapiens	144-149
23252516-0	2013	Lenalidomide efficacy in activated B-cell-like subtype diffuse large B-cell lymphoma is dependent upon IRF4 and cereblon expression.	Lenalidomide	0-12	interferon regulatory factor 4	Homo sapiens	103-107
22929976-0	2013	Correlation of clinical response and response duration with miR-145 induction by lenalidomide in CD34(+) cells from patients with del(5q) myelodysplastic syndrome.	Lenalidomide	81-93	microRNA 145	Homo sapiens	60-67
22929976-0	2013	Correlation of clinical response and response duration with miR-145 induction by lenalidomide in CD34(+) cells from patients with del(5q) myelodysplastic syndrome.	Lenalidomide	81-93	CD34 molecule	Homo sapiens	97-101
22929976-1	2013	We examined whether lenalidomide exposure up-regulates miRNAs and mRNAs, previously shown to play a role in the disease phenotype of del(5q) myelodysplastic syndrome, in pre-treatment CD34(+) marrow cells.	Lenalidomide	20-32	CD34 molecule	Homo sapiens	184-188
22929976-7	2013	Lenalidomide selectively abrogated progenitor activity in cells depleted of miR-143 and miR-145 supporting a key role for miR-143/145 in the sensitivity to lenalidomide of del(5q) myelodysplastic syndrome patients.	Lenalidomide	0-12	microRNA 143	Homo sapiens	76-83
22929976-7	2013	Lenalidomide selectively abrogated progenitor activity in cells depleted of miR-143 and miR-145 supporting a key role for miR-143/145 in the sensitivity to lenalidomide of del(5q) myelodysplastic syndrome patients.	Lenalidomide	0-12	microRNA 145	Homo sapiens	88-95
22929976-7	2013	Lenalidomide selectively abrogated progenitor activity in cells depleted of miR-143 and miR-145 supporting a key role for miR-143/145 in the sensitivity to lenalidomide of del(5q) myelodysplastic syndrome patients.	Lenalidomide	0-12	microRNA 143	Homo sapiens	122-129
22525275-0	2013	Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion.	Lenalidomide	0-12	tumor protein p53	Homo sapiens	22-25
22525275-0	2013	Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion.	Lenalidomide	0-12	MDM2 proto-oncogene	Homo sapiens	52-56
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	31-43	MDM2 proto-oncogene	Homo sapiens	68-72
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	31-43	tumor protein p53	Homo sapiens	95-98
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	45-48	MDM2 proto-oncogene	Homo sapiens	68-72
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	45-48	tumor protein p53	Homo sapiens	95-98
23178378-3	2013	We found that in vivo concentrations of both lenalidomide (LEN) and pomalidomide (POM) significantly blunted RANKL upregulation normalizing the RANKL/OPG ratio in human osteoprogenitor cells (PreOBs) when co-cultured with MM cells and also inhibited CCL3 production by MM cells.	Lenalidomide	45-57	TNF receptor superfamily member 11b	Homo sapiens	150-153
23178378-3	2013	We found that in vivo concentrations of both lenalidomide (LEN) and pomalidomide (POM) significantly blunted RANKL upregulation normalizing the RANKL/OPG ratio in human osteoprogenitor cells (PreOBs) when co-cultured with MM cells and also inhibited CCL3 production by MM cells.	Lenalidomide	45-57	C-C motif chemokine ligand 3	Homo sapiens	250-254
23252516-6	2013	IRF4 inhibition by lenalidomide induced downregulation of B-cell receptor (BCR)-dependent NF-kappaB.	Lenalidomide	19-31	interferon regulatory factor 4	Homo sapiens	0-4
23252516-7	2013	Whereas IRF4-specific small, interfering RNA mimicked the effects of lenalidomide reducing NF-kappaB activation, IRF4 overexpression enhanced NF-kappaB activation and conferred resistance to lenalidomide.	Lenalidomide	69-81	interferon regulatory factor 4	Homo sapiens	8-12
23252516-7	2013	Whereas IRF4-specific small, interfering RNA mimicked the effects of lenalidomide reducing NF-kappaB activation, IRF4 overexpression enhanced NF-kappaB activation and conferred resistance to lenalidomide.	Lenalidomide	191-203	interferon regulatory factor 4	Homo sapiens	113-117
23252516-8	2013	These findings indicate the crucial role of IRF4 inhibition in lenalidomide efficacy in ABC cells.	Lenalidomide	63-75	interferon regulatory factor 4	Homo sapiens	44-48
23252516-9	2013	Furthermore, lenalidomide-induced IRF4 downregulation required the expression of cereblon, a molecular target of lenalidomide.	Lenalidomide	13-25	interferon regulatory factor 4	Homo sapiens	34-38
23252516-9	2013	Furthermore, lenalidomide-induced IRF4 downregulation required the expression of cereblon, a molecular target of lenalidomide.	Lenalidomide	113-125	interferon regulatory factor 4	Homo sapiens	34-38
23252516-10	2013	Taken together, these findings suggest that lenalidomide has direct antitumour activity against DLBCL cells, preferentially ABC-DLBCL cells, by blocking IRF4 expression and the BCR-NF-kappaB signalling pathway in a cereblon-dependent manner.	Lenalidomide	44-56	interferon regulatory factor 4	Homo sapiens	153-157
23233657-1	2013	Recently, cereblon (CRBN) expression was found to be essential for the activity of thalidomide and lenalidomide.	Lenalidomide	99-111	cereblon	Homo sapiens	20-24
23420263-8	2013	In addition, array-based gene expression analysis revealed that lenalidomide regulated the expression of several genes associated with cell survival, apoptosis and development, including BH3-interacting domain death agonist (BID), v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) and NK2 homeobox1 (NKX2-1).	Lenalidomide	64-76	BH3 interacting domain death agonist	Mus musculus	225-228
23420263-8	2013	In addition, array-based gene expression analysis revealed that lenalidomide regulated the expression of several genes associated with cell survival, apoptosis and development, including BH3-interacting domain death agonist (BID), v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) and NK2 homeobox1 (NKX2-1).	Lenalidomide	64-76	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	233-236
23420263-8	2013	In addition, array-based gene expression analysis revealed that lenalidomide regulated the expression of several genes associated with cell survival, apoptosis and development, including BH3-interacting domain death agonist (BID), v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) and NK2 homeobox1 (NKX2-1).	Lenalidomide	64-76	FBJ osteosarcoma oncogene	Mus musculus	285-288
23420263-8	2013	In addition, array-based gene expression analysis revealed that lenalidomide regulated the expression of several genes associated with cell survival, apoptosis and development, including BH3-interacting domain death agonist (BID), v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) and NK2 homeobox1 (NKX2-1).	Lenalidomide	64-76	NK2 homeobox 1	Mus musculus	294-307
23420263-8	2013	In addition, array-based gene expression analysis revealed that lenalidomide regulated the expression of several genes associated with cell survival, apoptosis and development, including BH3-interacting domain death agonist (BID), v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS) and NK2 homeobox1 (NKX2-1).	Lenalidomide	64-76	NK2 homeobox 1	Mus musculus	309-315
23420263-9	2013	BID and FOS, which are known apoptosis activators, were upregulated by lenalidomide treatment, whereas NKX2-1, which is used as an immunohistochemistry marker for NSCLC, was downregulated.	Lenalidomide	71-83	BH3 interacting domain death agonist	Homo sapiens	0-3
23420263-9	2013	BID and FOS, which are known apoptosis activators, were upregulated by lenalidomide treatment, whereas NKX2-1, which is used as an immunohistochemistry marker for NSCLC, was downregulated.	Lenalidomide	71-83	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	8-11
23100311-6	2013	Furthermore, we show that lenalidomide, a drug approved for myelodysplastic syndromes and multiple myeloma, enhances translation of the C/EBPalpha-p30 isoform, resulting in higher miR-181a levels.	Lenalidomide	26-38	centromere protein V	Homo sapiens	147-150
23100311-6	2013	Furthermore, we show that lenalidomide, a drug approved for myelodysplastic syndromes and multiple myeloma, enhances translation of the C/EBPalpha-p30 isoform, resulting in higher miR-181a levels.	Lenalidomide	26-38	microRNA 181a-2	Mus musculus	180-188
23100311-8	2013	Similarly, lenalidomide exhibits antitumorigenic activity paralleled by increased miR-181a expression.	Lenalidomide	11-23	microRNA 181a-2	Mus musculus	82-90
23100311-10	2013	Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients, and suggest that lenalidomide treatment enhancing the C/EBPalpha-p30 protein levels and in turn miR-181a may sensitize AML blasts to chemotherapy.	Lenalidomide	148-160	CCAAT enhancer binding protein alpha	Homo sapiens	100-105
23100311-10	2013	Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients, and suggest that lenalidomide treatment enhancing the C/EBPalpha-p30 protein levels and in turn miR-181a may sensitize AML blasts to chemotherapy.	Lenalidomide	148-160	CCAAT enhancer binding protein alpha	Homo sapiens	185-195
23100311-10	2013	Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients, and suggest that lenalidomide treatment enhancing the C/EBPalpha-p30 protein levels and in turn miR-181a may sensitize AML blasts to chemotherapy.	Lenalidomide	148-160	centromere protein V	Homo sapiens	196-199
23100311-10	2013	Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients, and suggest that lenalidomide treatment enhancing the C/EBPalpha-p30 protein levels and in turn miR-181a may sensitize AML blasts to chemotherapy.	Lenalidomide	148-160	microRNA 181a-2	Mus musculus	227-235
22975686-0	2013	BTK inhibitor ibrutinib is cytotoxic to myeloma and potently enhances bortezomib and lenalidomide activities through NF-kappaB.	Lenalidomide	85-97	Bruton tyrosine kinase	Homo sapiens	0-3
24163824-3	2013	This review discusses the potential mechanism of action and efficacy of lenalidomide, alone or in combination, in treatment of CLL and its toxic effects such as tumor lysis syndrome (TLS) and tumor flare reaction (TFR), that make its management different from other hematologic malignancies.	Lenalidomide	72-84	transferrin receptor	Homo sapiens	214-217
22733396-4	2013	We demonstrate that exposure to lenalidomide in the context of T-cell expansion with direct ligation of CD3/CD28 complex results in polarization toward a Th1 phenotype characterized by increased IFN-gamma, but not IL-10 expression.	Lenalidomide	32-44	CD28 molecule	Homo sapiens	108-112
22733396-4	2013	We demonstrate that exposure to lenalidomide in the context of T-cell expansion with direct ligation of CD3/CD28 complex results in polarization toward a Th1 phenotype characterized by increased IFN-gamma, but not IL-10 expression.	Lenalidomide	32-44	interferon gamma	Homo sapiens	195-204
22733396-4	2013	We demonstrate that exposure to lenalidomide in the context of T-cell expansion with direct ligation of CD3/CD28 complex results in polarization toward a Th1 phenotype characterized by increased IFN-gamma, but not IL-10 expression.	Lenalidomide	32-44	interleukin 10	Homo sapiens	214-219
22522886-1	2012	Lenalidomide is a potent immunomodulatory agent capable of downregulating proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and upregulating anti-inflammatory cytokines.	Lenalidomide	0-12	tumor necrosis factor	Mus musculus	108-135
22552008-0	2012	Cereblon is a direct protein target for immunomodulatory and antiproliferative activities of lenalidomide and pomalidomide.	Lenalidomide	93-105	cereblon	Homo sapiens	0-8
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.	Lenalidomide	42-54	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.	Lenalidomide	42-54	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.	Lenalidomide	42-54	damage specific DNA binding protein 1	Homo sapiens	177-181
22552008-4	2012	CRBN mediated antiproliferative activities of lenalidomide and pomalidomide in myeloma cells, as well as lenalidomide- and pomalidomide-induced cytokine production in T cells.	Lenalidomide	46-58	cereblon	Homo sapiens	0-4
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).	Lenalidomide	0-12	cereblon	Homo sapiens	62-66
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).	Lenalidomide	0-12	cereblon	Homo sapiens	135-139
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).	Lenalidomide	0-12	cereblon	Homo sapiens	135-139
22552008-7	2012	Long-term selection for lenalidomide resistance in H929 myeloma cell lines was accompanied by a reduction in CRBN, while in DF15R myeloma cells resistant to both pomalidomide and lenalidomide, CRBN protein was undetectable.	Lenalidomide	24-36	cereblon	Homo sapiens	109-113
22552008-7	2012	Long-term selection for lenalidomide resistance in H929 myeloma cell lines was accompanied by a reduction in CRBN, while in DF15R myeloma cells resistant to both pomalidomide and lenalidomide, CRBN protein was undetectable.	Lenalidomide	24-36	cereblon	Homo sapiens	193-197
22552008-8	2012	Our biophysical, biochemical and gene silencing studies show that CRBN is a proximate, therapeutically important molecular target of lenalidomide and pomalidomide.	Lenalidomide	133-145	cereblon	Homo sapiens	66-70
22623160-3	2012	The combination of Enzastaurin and Lenalidomide, at doses as low as 1 muM, showed strong synergism against indolent lymphomas by reducing cell growth, producing an increase in G0-G1 phase followed by significant decrease in S phase, increasing apoptosis, and inhibiting PI3K/AKT, PKC and MAPK/ERK pathways.	Lenalidomide	35-47	latexin	Homo sapiens	70-73
22623160-3	2012	The combination of Enzastaurin and Lenalidomide, at doses as low as 1 muM, showed strong synergism against indolent lymphomas by reducing cell growth, producing an increase in G0-G1 phase followed by significant decrease in S phase, increasing apoptosis, and inhibiting PI3K/AKT, PKC and MAPK/ERK pathways.	Lenalidomide	35-47	AKT serine/threonine kinase 1	Homo sapiens	275-278
22623160-3	2012	The combination of Enzastaurin and Lenalidomide, at doses as low as 1 muM, showed strong synergism against indolent lymphomas by reducing cell growth, producing an increase in G0-G1 phase followed by significant decrease in S phase, increasing apoptosis, and inhibiting PI3K/AKT, PKC and MAPK/ERK pathways.	Lenalidomide	35-47	proline rich transmembrane protein 2	Homo sapiens	280-283
22623160-3	2012	The combination of Enzastaurin and Lenalidomide, at doses as low as 1 muM, showed strong synergism against indolent lymphomas by reducing cell growth, producing an increase in G0-G1 phase followed by significant decrease in S phase, increasing apoptosis, and inhibiting PI3K/AKT, PKC and MAPK/ERK pathways.	Lenalidomide	35-47	mitogen-activated protein kinase 1	Homo sapiens	293-296
22608605-1	2012	UNLABELLED: We used microarray profiling to investigate the direct effects of lenalidomide on gene expression in isolated CD14(+) monocytes from 6 patients with del(5q).	Lenalidomide	78-90	CD14 molecule	Homo sapiens	122-126
22608605-2	2012	Our data demonstrate that changes in genes involved the tumor necrosis factor (TNF) signaling pathway and the bone marrow stroma, suggesting that treatment with lenalidomide may help restore the damaged niche and suppress the TNF signaling pathway.	Lenalidomide	161-173	tumor necrosis factor	Homo sapiens	56-77
22608605-2	2012	Our data demonstrate that changes in genes involved the tumor necrosis factor (TNF) signaling pathway and the bone marrow stroma, suggesting that treatment with lenalidomide may help restore the damaged niche and suppress the TNF signaling pathway.	Lenalidomide	161-173	tumor necrosis factor	Homo sapiens	79-82
22608605-2	2012	Our data demonstrate that changes in genes involved the tumor necrosis factor (TNF) signaling pathway and the bone marrow stroma, suggesting that treatment with lenalidomide may help restore the damaged niche and suppress the TNF signaling pathway.	Lenalidomide	161-173	tumor necrosis factor	Homo sapiens	226-229
22608605-4	2012	MATERIALS AND METHODS: We used gene expression profiling to study the effect of lenalidomide therapy in peripheral blood CD14(+) monocytes of 6 patients with del(5q) and MDS.	Lenalidomide	80-92	CD14 molecule	Homo sapiens	121-125
22608605-5	2012	RESULTS: After lenalidomide treatment, genes involved in the tumor necrosis factor (TNF) signaling pathway that were upregulated in the patients before treatment decreased to the healthy control baseline expression level.	Lenalidomide	15-27	tumor necrosis factor	Homo sapiens	61-82
22608605-5	2012	RESULTS: After lenalidomide treatment, genes involved in the tumor necrosis factor (TNF) signaling pathway that were upregulated in the patients before treatment decreased to the healthy control baseline expression level.	Lenalidomide	15-27	tumor necrosis factor	Homo sapiens	84-87
23100311-0	2013	Lenalidomide-mediated enhanced translation of C/EBPalpha-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia.	Lenalidomide	0-12	CCAAT enhancer binding protein alpha	Homo sapiens	46-56
23100311-0	2013	Lenalidomide-mediated enhanced translation of C/EBPalpha-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia.	Lenalidomide	0-12	centromere protein V	Homo sapiens	57-60
23100311-6	2013	Furthermore, we show that lenalidomide, a drug approved for myelodysplastic syndromes and multiple myeloma, enhances translation of the C/EBPalpha-p30 isoform, resulting in higher miR-181a levels.	Lenalidomide	26-38	CCAAT enhancer binding protein alpha	Homo sapiens	136-146
22933333-9	2012	Our findings also suggest that sequencing of the TP53 gene should be included in the study of patients with del(5q) as a single abnormality or in complex karyotype before lenalidomide treatment.	Lenalidomide	171-183	tumor protein p53	Homo sapiens	49-53
23012246-7	2012	RSK2(Ser227) inhibition resulting from BI-D1870 treatment restored lenalidomide-induced direct cytotoxicity of myeloma cells from interleukin-6-mediated cell protection, showed no cross-resistance to bortezomib, and exerted additive/synergistic antiproliferative effects in conjunction with the mTOR, histone deacetylase, and BH3-mimicking BCL2/BCLX(L) inhibitors.	Lenalidomide	67-79	ribosomal protein S6 kinase A3	Homo sapiens	0-4
23012246-7	2012	RSK2(Ser227) inhibition resulting from BI-D1870 treatment restored lenalidomide-induced direct cytotoxicity of myeloma cells from interleukin-6-mediated cell protection, showed no cross-resistance to bortezomib, and exerted additive/synergistic antiproliferative effects in conjunction with the mTOR, histone deacetylase, and BH3-mimicking BCL2/BCLX(L) inhibitors.	Lenalidomide	67-79	interleukin 6	Homo sapiens	130-143
23012246-7	2012	RSK2(Ser227) inhibition resulting from BI-D1870 treatment restored lenalidomide-induced direct cytotoxicity of myeloma cells from interleukin-6-mediated cell protection, showed no cross-resistance to bortezomib, and exerted additive/synergistic antiproliferative effects in conjunction with the mTOR, histone deacetylase, and BH3-mimicking BCL2/BCLX(L) inhibitors.	Lenalidomide	67-79	mechanistic target of rapamycin kinase	Homo sapiens	295-299
23012246-7	2012	RSK2(Ser227) inhibition resulting from BI-D1870 treatment restored lenalidomide-induced direct cytotoxicity of myeloma cells from interleukin-6-mediated cell protection, showed no cross-resistance to bortezomib, and exerted additive/synergistic antiproliferative effects in conjunction with the mTOR, histone deacetylase, and BH3-mimicking BCL2/BCLX(L) inhibitors.	Lenalidomide	67-79	BCL2 apoptosis regulator	Homo sapiens	340-344
23012246-7	2012	RSK2(Ser227) inhibition resulting from BI-D1870 treatment restored lenalidomide-induced direct cytotoxicity of myeloma cells from interleukin-6-mediated cell protection, showed no cross-resistance to bortezomib, and exerted additive/synergistic antiproliferative effects in conjunction with the mTOR, histone deacetylase, and BH3-mimicking BCL2/BCLX(L) inhibitors.	Lenalidomide	67-79	BCL2 like 1	Homo sapiens	345-349
22936658-1	2012	The erythropoietic effects of lenalidomide are cytokine dependent, suggesting that the erythroid hematologic improvement (HI-E) rate may be augmented by combined treatment (CT) with recombinant human erythropoietin (rhu-EPO) in myelodysplastic syndrome (MDS).	Lenalidomide	30-42	erythropoietin	Homo sapiens	200-214
22936658-1	2012	The erythropoietic effects of lenalidomide are cytokine dependent, suggesting that the erythroid hematologic improvement (HI-E) rate may be augmented by combined treatment (CT) with recombinant human erythropoietin (rhu-EPO) in myelodysplastic syndrome (MDS).	Lenalidomide	30-42	erythropoietin	Homo sapiens	220-223
22522886-1	2012	Lenalidomide is a potent immunomodulatory agent capable of downregulating proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and upregulating anti-inflammatory cytokines.	Lenalidomide	0-12	tumor necrosis factor	Mus musculus	137-146
22522886-9	2012	ob/ob mice displayed elevated serum TNF-alpha and IL-6 levels, fat composition and glucose intolerance, the effects of which except glucose intolerance and fat composition were attenuated by lenalidomide.	Lenalidomide	191-203	tumor necrosis factor	Mus musculus	36-45
22522886-9	2012	ob/ob mice displayed elevated serum TNF-alpha and IL-6 levels, fat composition and glucose intolerance, the effects of which except glucose intolerance and fat composition were attenuated by lenalidomide.	Lenalidomide	191-203	interleukin 6	Mus musculus	50-54
22766978-0	2012	Multiple myeloma cells expressing low levels of CD138 have an immature             phenotype and reduced sensitivity to lenalidomide.	Lenalidomide	120-132	syndecan 1	Homo sapiens	48-53
22150117-0	2012	Severe dermatologic adverse reactions after exposure to lenalidomide in multiple myeloma patients with a positive HLA-DRB1*1501 and HLA-DQB1*0602.	Lenalidomide	56-68	major histocompatibility complex, class II, DR beta 1	Homo sapiens	114-122
22150117-0	2012	Severe dermatologic adverse reactions after exposure to lenalidomide in multiple myeloma patients with a positive HLA-DRB1*1501 and HLA-DQB1*0602.	Lenalidomide	56-68	major histocompatibility complex, class II, DQ beta 1	Homo sapiens	132-140
22766978-10	2012	CD138- cells sorted from the KYMM-2 cell             line also showed high BCL6, low IRF4 expression and decreased sensitivity to lenalidomide             compared with CD138+ cells.	Lenalidomide	130-142	syndecan 1	Homo sapiens	0-5
22766978-11	2012	Our observations suggest that low CD138 expression             relates to i) poor prognosis, ii) immature phenotype and iii) low sensitivity             to lenalidomide.	Lenalidomide	156-168	syndecan 1	Homo sapiens	34-39
22640031-2	2012	Preclinical data showed that the Akt inhibitor, perifosine, sensitized MM cells to lenalidomide and dexamethasone, providing the rationale for this Phase I, multicentre, single-arm study to assess the safety and determine the maximum-tolerated dose (MTD) of perifosine-lenalidomide-dexamethasone in relapsed and relapsed/refractory MM.	Lenalidomide	83-95	AKT serine/threonine kinase 1	Homo sapiens	33-36
22640031-2	2012	Preclinical data showed that the Akt inhibitor, perifosine, sensitized MM cells to lenalidomide and dexamethasone, providing the rationale for this Phase I, multicentre, single-arm study to assess the safety and determine the maximum-tolerated dose (MTD) of perifosine-lenalidomide-dexamethasone in relapsed and relapsed/refractory MM.	Lenalidomide	269-281	AKT serine/threonine kinase 1	Homo sapiens	33-36
21750922-5	2012	Despite their inhibition of CFU formation, perifosine, bortezomib and lenalidomide induced only slight or moderate cytotoxicity in CD34(+) selected HPC, as assessed using different assays such as flow cytometry-based detection of activated caspases and immunohistochemistry studies (e.g., Ki-67 staining).	Lenalidomide	70-82	CD34 molecule	Homo sapiens	131-135
22774993-0	2012	Lenalidomide enhancement of human T cell functions in human immunodeficiency virus (HIV)-infected and HIV-negative CD4 T lymphocytopenic patients.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	115-118
22774993-5	2012	Significant enhancement of chemotaxis to S1P and CCL21 was induced by 100-1000 nM lenalidomide only for normal T cells at a low CD4 : CD8 ratio.	Lenalidomide	82-94	C-C motif chemokine ligand 21	Homo sapiens	49-54
22774993-5	2012	Significant enhancement of chemotaxis to S1P and CCL21 was induced by 100-1000 nM lenalidomide only for normal T cells at a low CD4 : CD8 ratio.	Lenalidomide	82-94	CD4 molecule	Homo sapiens	128-131
22774993-5	2012	Significant enhancement of chemotaxis to S1P and CCL21 was induced by 100-1000 nM lenalidomide only for normal T cells at a low CD4 : CD8 ratio.	Lenalidomide	82-94	CD8a molecule	Homo sapiens	134-137
22774993-7	2012	Lenalidomide at 30-1000 nM significantly enhanced chemotaxis to S1P and IL-2 generation for T cells from HIV-negative CD4 T lymphocytopenic patients as from HIV-infected patients, with less effect on CCL21-elicited chemotaxis and none for IFN-gamma generation.	Lenalidomide	0-12	interleukin 2	Homo sapiens	72-76
22774993-7	2012	Lenalidomide at 30-1000 nM significantly enhanced chemotaxis to S1P and IL-2 generation for T cells from HIV-negative CD4 T lymphocytopenic patients as from HIV-infected patients, with less effect on CCL21-elicited chemotaxis and none for IFN-gamma generation.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	118-121
22774993-7	2012	Lenalidomide at 30-1000 nM significantly enhanced chemotaxis to S1P and IL-2 generation for T cells from HIV-negative CD4 T lymphocytopenic patients as from HIV-infected patients, with less effect on CCL21-elicited chemotaxis and none for IFN-gamma generation.	Lenalidomide	0-12	interferon gamma	Homo sapiens	239-248
22474168-4	2012	Unexpectedly, A2A and beta2AR agonists also synergize with melphalan, lenalidomide, bortezomib, and doxorubicin.	Lenalidomide	70-82	immunoglobulin kappa variable 2D-29	Homo sapiens	14-17
22474168-4	2012	Unexpectedly, A2A and beta2AR agonists also synergize with melphalan, lenalidomide, bortezomib, and doxorubicin.	Lenalidomide	70-82	adrenoceptor beta 2	Homo sapiens	22-29
22617388-6	2012	Furthermore, we explored the expression of HO-1 in multiple myeloma cells in response to the key anti-myeloma drugs bortezomib and lenalidomide.	Lenalidomide	131-143	heme oxygenase 1	Homo sapiens	43-47
22617388-8	2012	Moreover, we also observe that HO-1 is increased in lenalidomide-resistant MM cell lines.	Lenalidomide	52-64	heme oxygenase 1	Homo sapiens	31-35
22698399-3	2012	Lenalidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncogenic MYD88 mutations in these lymphomas.	Lenalidomide	0-12	interferon beta 1	Homo sapiens	49-64
22698399-3	2012	Lenalidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncogenic MYD88 mutations in these lymphomas.	Lenalidomide	0-12	interferon beta 1	Homo sapiens	66-73
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.	Lenalidomide	134-146	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.	Lenalidomide	134-146	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.	Lenalidomide	134-146	tumor necrosis factor	Homo sapiens	187-190
22698399-2	2012	Lenalidomide is an active agent in the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), but its mechanism of action is unknown.	Lenalidomide	0-12	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	62-65
22698399-3	2012	Lenalidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncogenic MYD88 mutations in these lymphomas.	Lenalidomide	0-12	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	19-22
21968939-5	2012	RESULTS: Lenalidomide decreased the IC(50) of docetaxel by up to 50% (P < 0.05) and also decreased invasion in PC3, LNCaP, and DU145 cells and anchorage independent growth in PC3 cells (P < 0.01).	Lenalidomide	9-21	chromobox 8	Homo sapiens	114-117
21968939-5	2012	RESULTS: Lenalidomide decreased the IC(50) of docetaxel by up to 50% (P < 0.05) and also decreased invasion in PC3, LNCaP, and DU145 cells and anchorage independent growth in PC3 cells (P < 0.01).	Lenalidomide	9-21	chromobox 8	Homo sapiens	178-181
21968939-6	2012	Apoptosis in lenalidomide/docetaxel-treated cells was increased by 2.2-fold over single agent docetaxel and a corresponding increase in p53, p38, and BAD activation was observed in Western blots (P < 0.001).	Lenalidomide	13-25	tumor protein p53	Homo sapiens	136-139
21968939-6	2012	Apoptosis in lenalidomide/docetaxel-treated cells was increased by 2.2-fold over single agent docetaxel and a corresponding increase in p53, p38, and BAD activation was observed in Western blots (P < 0.001).	Lenalidomide	13-25	mitogen-activated protein kinase 14	Homo sapiens	141-144
21968939-7	2012	When PC3 challenged mice were treated with lenalidomide and docetaxel, median survival increased from 48 to 59 days and the rate of tumor growth was significantly reduced (P < 0.05).	Lenalidomide	43-55	chromobox 8	Mus musculus	5-8
22474251-7	2012	These findings in the Rhoh(-/-) CLL cells were subsequently demonstrated to closely resemble changes in GTPase activation observed in human CLL samples after in vitro and in vivo treatment with lenalidomide, an agent with known influence on microenvironment protection, and suggest that RhoH plays a critical role in prosurvival CLL cell-cell and cell-microenvironment interactions with this agent.	Lenalidomide	194-206	ras homolog family member H	Homo sapiens	22-26
22474251-7	2012	These findings in the Rhoh(-/-) CLL cells were subsequently demonstrated to closely resemble changes in GTPase activation observed in human CLL samples after in vitro and in vivo treatment with lenalidomide, an agent with known influence on microenvironment protection, and suggest that RhoH plays a critical role in prosurvival CLL cell-cell and cell-microenvironment interactions with this agent.	Lenalidomide	194-206	ras homolog family member H	Homo sapiens	287-291
22698399-3	2012	Lenalidomide kills ABC DLBCL cells by augmenting interferon beta (IFNbeta) production, owing to the oncogenic MYD88 mutations in these lymphomas.	Lenalidomide	0-12	MYD88 innate immune signal transduction adaptor	Homo sapiens	110-115
22698399-4	2012	In a cereblon-dependent fashion, lenalidomide downregulates IRF4 and SPIB, transcription factors that together prevent IFNbeta production by repressing IRF7 and amplify prosurvival NF-kappaB signaling by transactivating CARD11.	Lenalidomide	33-45	interferon regulatory factor 4	Homo sapiens	60-64
22698399-4	2012	In a cereblon-dependent fashion, lenalidomide downregulates IRF4 and SPIB, transcription factors that together prevent IFNbeta production by repressing IRF7 and amplify prosurvival NF-kappaB signaling by transactivating CARD11.	Lenalidomide	33-45	Spi-B transcription factor	Homo sapiens	69-73
22698399-4	2012	In a cereblon-dependent fashion, lenalidomide downregulates IRF4 and SPIB, transcription factors that together prevent IFNbeta production by repressing IRF7 and amplify prosurvival NF-kappaB signaling by transactivating CARD11.	Lenalidomide	33-45	interferon beta 1	Homo sapiens	119-126
22698399-4	2012	In a cereblon-dependent fashion, lenalidomide downregulates IRF4 and SPIB, transcription factors that together prevent IFNbeta production by repressing IRF7 and amplify prosurvival NF-kappaB signaling by transactivating CARD11.	Lenalidomide	33-45	interferon regulatory factor 7	Homo sapiens	152-156
22698399-4	2012	In a cereblon-dependent fashion, lenalidomide downregulates IRF4 and SPIB, transcription factors that together prevent IFNbeta production by repressing IRF7 and amplify prosurvival NF-kappaB signaling by transactivating CARD11.	Lenalidomide	33-45	caspase recruitment domain family member 11	Homo sapiens	220-226
22698399-5	2012	Blockade of B cell receptor signaling using the BTK inhibitor ibrutinib also downregulates IRF4 and consequently synergizes with lenalidomide in killing ABC DLBCLs, suggesting attractive therapeutic strategies.	Lenalidomide	129-141	Bruton tyrosine kinase	Homo sapiens	48-51
22698399-5	2012	Blockade of B cell receptor signaling using the BTK inhibitor ibrutinib also downregulates IRF4 and consequently synergizes with lenalidomide in killing ABC DLBCLs, suggesting attractive therapeutic strategies.	Lenalidomide	129-141	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	153-156
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.	Lenalidomide	180-192	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.	Lenalidomide	180-192	vascular endothelial growth factor A	Homo sapiens	61-65
22171982-0	2012	Downregulation of BCL2 by AT-101 enhances the antileukaemic effect of lenalidomide both by an immune dependant and independent manner.	Lenalidomide	70-82	BCL2 apoptosis regulator	Homo sapiens	18-22
22171982-3	2012	Lenalidomide, an immunomodulator, is clinically effective in CLL and can enhance the anti-CLL effects of CD20 targeting monoclonal antibody, rituximab.	Lenalidomide	0-12	keratin 20	Homo sapiens	105-109
21080211-2	2012	The in vitro cytotoxicity of perifosine, bortezomib and lenalidomide against 6 cell lines derived from hematological malignancies was investigated using trypan blue staining, flow cytometry-based detection of activated caspases, Annexin V assays, immunohistochemistry studies (KI-67 and caspase-3 staining) and the immature-myeloid-information (IMI) technique.	Lenalidomide	56-68	annexin A5	Homo sapiens	229-238
21080211-2	2012	The in vitro cytotoxicity of perifosine, bortezomib and lenalidomide against 6 cell lines derived from hematological malignancies was investigated using trypan blue staining, flow cytometry-based detection of activated caspases, Annexin V assays, immunohistochemistry studies (KI-67 and caspase-3 staining) and the immature-myeloid-information (IMI) technique.	Lenalidomide	56-68	caspase 3	Homo sapiens	287-296
21520044-7	2012	In addition, the pretreatment of LLL12 blocked the promotion of the cell proliferation and resistance to lenalidomide by IL-6.	Lenalidomide	105-117	interleukin 6	Homo sapiens	121-125
21748755-0	2012	Lenalidomide modulates IL-8 and anti-prostate antibody levels in men with biochemically recurrent prostate cancer.	Lenalidomide	0-12	C-X-C motif chemokine ligand 8	Homo sapiens	23-27
21748755-6	2012	RESULTS: Treatment with lenalidomide was associated with global changes in immunoreactivity to a number of prostate-associated antigens, as well as with changes in circulating levels of the T(H) 2 cytokines IL-4, IL-5, IL-10, and IL-13.	Lenalidomide	24-36	interleukin 4	Homo sapiens	207-211
21748755-6	2012	RESULTS: Treatment with lenalidomide was associated with global changes in immunoreactivity to a number of prostate-associated antigens, as well as with changes in circulating levels of the T(H) 2 cytokines IL-4, IL-5, IL-10, and IL-13.	Lenalidomide	24-36	interleukin 5	Homo sapiens	213-217
21748755-6	2012	RESULTS: Treatment with lenalidomide was associated with global changes in immunoreactivity to a number of prostate-associated antigens, as well as with changes in circulating levels of the T(H) 2 cytokines IL-4, IL-5, IL-10, and IL-13.	Lenalidomide	24-36	interleukin 10	Homo sapiens	219-224
21748755-6	2012	RESULTS: Treatment with lenalidomide was associated with global changes in immunoreactivity to a number of prostate-associated antigens, as well as with changes in circulating levels of the T(H) 2 cytokines IL-4, IL-5, IL-10, and IL-13.	Lenalidomide	24-36	interleukin 13	Homo sapiens	230-235
23556117-4	2012	Other recent advances include a better understanding of the pathogenesis of disease including haplodeficiency of several candidate genes, and elucidation of the lenalidomide-specific effect on two phosphatases ultimately leading to p53 degradation in the erythroid progenitors and cell cycle arrest in earlier myeloid progenitors.	Lenalidomide	161-173	tumor protein p53	Homo sapiens	232-235
22301101-4	2012	In particular, GDF15 conferred resistance to melphalan, bortezomib, and to a lesser extent, lenalidomide in both stroma-dependent and stroma-independent multiple myeloma cells.	Lenalidomide	92-104	growth differentiation factor 15	Homo sapiens	15-20
22261445-0	2012	p53 nuclear expression correlates with hemizygous TP53 deletion and predicts an adverse outcome for patients with relapsed/refractory multiple myeloma treated with lenalidomide.	Lenalidomide	164-176	tumor protein p53	Homo sapiens	0-3
22261445-1	2012	del(17p13)(TP53) seems to be an independent poor prognostic factor in patients with relapsed/refractory multiple myeloma (MM) receiving lenalidomide.	Lenalidomide	136-148	tumor protein p53	Homo sapiens	11-15
22261445-2	2012	However, whether aberrant p53 nuclear expression detected by immunohistochemical analysis can be used as a surrogate marker for del(17p13)(TP53) in prognostic evaluation of lenalidomide-treated relapsed/refractory MM remains unclear.	Lenalidomide	173-185	tumor protein p53	Homo sapiens	26-29
22261445-7	2012	Our results suggest that p53 nuclear expression is associated with adverse outcome in patients with relapsed/refractory MM receiving lenalidomide-based therapy and that p53 immunohistochemical analysis may serve as a simple, rapid method to predict del(17p13)(TP53) in this patient subgroup.	Lenalidomide	133-145	tumor protein p53	Homo sapiens	25-28
22109882-0	2012	The immunomodulatory drug lenalidomide restores a vitamin D sensitive phenotype to the vitamin D resistant breast cancer cell line MDA-MB-231 through inhibition of BCL-2: potential for breast cancer therapeutics.	Lenalidomide	26-38	BCL2 apoptosis regulator	Homo sapiens	164-169
22109882-8	2012	Whereas lenalidomide alone had no effect on cell growth, a 50% inhibition of cell growth by 1,25-D3 was achieved with additional 1 muM lenalidomide in resistant cells.	Lenalidomide	135-147	latexin	Homo sapiens	131-134
22109882-10	2012	An apoptosis protein array showed that the 1,25-D3 and lenalidomide combination increased pro-apoptotic proteins (phosphorylated p53) and decreased BCL-2 expression.	Lenalidomide	55-67	tumor protein p53	Homo sapiens	129-132
22109882-10	2012	An apoptosis protein array showed that the 1,25-D3 and lenalidomide combination increased pro-apoptotic proteins (phosphorylated p53) and decreased BCL-2 expression.	Lenalidomide	55-67	BCL2 apoptosis regulator	Homo sapiens	148-153
22001752-9	2012	In conclusion, salvage mobilization with plerixafor plus G-CSF is successful in the majority of patients with MM previously treated with lenalidomide.	Lenalidomide	137-149	colony stimulating factor 3	Homo sapiens	57-62
21860026-0	2011	Cereblon expression is required for the antimyeloma activity of lenalidomide and pomalidomide.	Lenalidomide	64-76	cereblon	Homo sapiens	0-8
22792112-8	2012	Preliminary data regarding the role of lenalidomide in addition to chemoimmunotherapy (R-CHOP) in first line clinical trials were discussed; data of safety, feasibility and efficacy were promising.	Lenalidomide	39-51	DNA damage inducible transcript 3	Homo sapiens	89-93
22919394-5	2012	The molecular mechanisms and targets of lenalidomide remain largely unknown, but recent evidence shows cereblon (CRBN) as a possible mediator of its therapeutical effects.	Lenalidomide	40-52	cereblon	Homo sapiens	113-117
22997574-3	2012	Lenalidomide has the potential to invoke changes in TNF-alpha with less toxicity than thalidomide.	Lenalidomide	0-12	tumor necrosis factor	Homo sapiens	52-61
22997574-4	2012	This pilot study evaluated lenalidomide at reduction of TNF-alpha and improvement of behavior and language in children with autism with elevated TNF-alpha.	Lenalidomide	27-39	tumor necrosis factor	Homo sapiens	56-65
22997574-4	2012	This pilot study evaluated lenalidomide at reduction of TNF-alpha and improvement of behavior and language in children with autism with elevated TNF-alpha.	Lenalidomide	27-39	tumor necrosis factor	Homo sapiens	145-154
22997574-5	2012	Subjects with elevated TNF-alpha were given 2.5 mgs lenalidomide daily for 12-weeks.	Lenalidomide	52-64	tumor necrosis factor	Homo sapiens	23-32
22666210-0	2012	PSA Response to Lenalidomide Therapy in a Pre-Treated Patient with Metastatic Prostate Cancer Refractory to Hormones and Chemotherapy: A Case Report.	Lenalidomide	16-28	aminopeptidase puromycin sensitive	Homo sapiens	0-3
22666210-4	2012	In this paper, we report that lenalidomide showed antitumoral activity in a patient with HRPC and bone metastases pre-treated with chemotherapy, decreased the PSA level and improved the patient"s health status for the first 5 months.	Lenalidomide	30-42	aminopeptidase puromycin sensitive	Homo sapiens	159-162
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.	Lenalidomide	214-226	DNA methyltransferase 1	Homo sapiens	143-147
22161851-0	2011	Effect of combined dexamethasone/lenalidomide therapy on NK cell-receptor levels in myeloma patients.	Lenalidomide	33-45	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	57-73
21860026-3	2011	CRBN depletion is initially cytotoxic to human myeloma cells, but surviving cells with stable CRBN depletion become highly resistant to both lenalidomide and pomalidomide, but not to the unrelated drugs bortezomib, dexamethasone, and melphalan.	Lenalidomide	141-153	cereblon	Homo sapiens	0-4
21860026-4	2011	Acquired deletion of CRBN was found to be the primary genetic event differentiating isogenic MM1.S cell lines cultured to be sensitive or resistant to lenalidomide and pomalidomide.	Lenalidomide	151-163	cereblon	Homo sapiens	21-25
21802139-0	2011	Anti-myelin associated glycoprotein neuropathy responding to lenalidomide.	Lenalidomide	61-73	myelin associated glycoprotein	Homo sapiens	5-35
21812019-0	2011	Inflammation, TNFalpha and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia.	Lenalidomide	56-68	tumor necrosis factor	Homo sapiens	14-22
21812019-10	2011	In patients with lenalidomide-related DVTs, TNFalpha, and sVCAM-1 were more strongly upregulated than in all other patients (p < 0.05) and TNFalpha and sVCAM-1 levels were significantly correlated (r = 0.65, p < 0.001).	Lenalidomide	17-29	tumor necrosis factor	Homo sapiens	44-52
21812019-10	2011	In patients with lenalidomide-related DVTs, TNFalpha, and sVCAM-1 were more strongly upregulated than in all other patients (p < 0.05) and TNFalpha and sVCAM-1 levels were significantly correlated (r = 0.65, p < 0.001).	Lenalidomide	17-29	tumor necrosis factor	Homo sapiens	142-150
21812019-11	2011	These data link lenalidomide associated DVTs with TNFalpha upregulation and endothelial cell dysfunction and suggest that aspirin may have a role for DVT prophylaxis in these patients.	Lenalidomide	16-28	tumor necrosis factor	Homo sapiens	50-58
22110196-9	2011	Western blot analysis showed lenalidomide significantly reduced pERK expression in all cell lines (p<0.05).	Lenalidomide	29-41	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	64-68
22010965-5	2011	Lenalidomide was unable to directly induce apoptosis in CLL cells in vitro, however it modulated costimulatory (CD80, CD83, CD86) surface molecules on CLL cells in vitro and in vivo.	Lenalidomide	0-12	CD80 molecule	Homo sapiens	112-116
22010965-5	2011	Lenalidomide was unable to directly induce apoptosis in CLL cells in vitro, however it modulated costimulatory (CD80, CD83, CD86) surface molecules on CLL cells in vitro and in vivo.	Lenalidomide	0-12	CD83 molecule	Homo sapiens	118-122
22010965-5	2011	Lenalidomide was unable to directly induce apoptosis in CLL cells in vitro, however it modulated costimulatory (CD80, CD83, CD86) surface molecules on CLL cells in vitro and in vivo.	Lenalidomide	0-12	CD86 molecule	Homo sapiens	124-128
22010965-7	2011	Cytokine analysis showed increase in levels of TNF-alpha post-lenalidomide treatment, consistent with acute inflammatory reaction.	Lenalidomide	62-74	tumor necrosis factor	Homo sapiens	47-56
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	C-X-C motif chemokine ligand 8	Homo sapiens	46-50
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	C-X-C motif chemokine ligand 9	Homo sapiens	52-55
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	C-X-C motif chemokine ligand 10	Homo sapiens	57-62
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	interleukin 4	Homo sapiens	67-71
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	interleukin 5	Homo sapiens	87-91
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	C-C motif chemokine ligand 3	Homo sapiens	93-98
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	C-C motif chemokine ligand 4	Homo sapiens	100-105
22010965-8	2011	Furthermore, the basal cytokine profile (high IL-8, MIG, IP-10 and IL-4 levels and low IL-5, MIP1a, MIP1b, IL12/p70) was predictive of clinical response to lenalidomide.	Lenalidomide	156-168	annexin A6	Homo sapiens	112-115
21860026-5	2011	Gene expression changes induced by lenalidomide were dramatically suppressed in the presence of CRBN depletion, further demonstrating that CRBN is required for lenalidomide activity.	Lenalidomide	35-47	cereblon	Homo sapiens	96-100
21860026-5	2011	Gene expression changes induced by lenalidomide were dramatically suppressed in the presence of CRBN depletion, further demonstrating that CRBN is required for lenalidomide activity.	Lenalidomide	35-47	cereblon	Homo sapiens	139-143
21860026-5	2011	Gene expression changes induced by lenalidomide were dramatically suppressed in the presence of CRBN depletion, further demonstrating that CRBN is required for lenalidomide activity.	Lenalidomide	160-172	cereblon	Homo sapiens	96-100
21860026-5	2011	Gene expression changes induced by lenalidomide were dramatically suppressed in the presence of CRBN depletion, further demonstrating that CRBN is required for lenalidomide activity.	Lenalidomide	160-172	cereblon	Homo sapiens	139-143
21860026-6	2011	Downstream targets of CRBN include interferon regulatory factor 4 (IRF4) previously reported to also be a target of lenalidomide.	Lenalidomide	116-128	cereblon	Homo sapiens	22-26
21860026-6	2011	Downstream targets of CRBN include interferon regulatory factor 4 (IRF4) previously reported to also be a target of lenalidomide.	Lenalidomide	116-128	interferon regulatory factor 4	Homo sapiens	35-65
21860026-6	2011	Downstream targets of CRBN include interferon regulatory factor 4 (IRF4) previously reported to also be a target of lenalidomide.	Lenalidomide	116-128	interferon regulatory factor 4	Homo sapiens	67-71
21860026-7	2011	Patients exposed to, and putatively resistant to, lenalidomide had lower CRBN levels in paired samples before and after therapy.	Lenalidomide	50-62	cereblon	Homo sapiens	73-77
21523725-10	2011	CONCLUSIONS: TFR is a unique immune-mediated phenomenon noted with lenalidomide treatment only in patients with CLL that correlates with clinical response.	Lenalidomide	67-79	transferrin receptor	Homo sapiens	13-16
21630308-0	2011	Lenalidomide, cyclophosphamide and dexamethasone (CRd) for newly diagnosed multiple myeloma: results from a phase 2 trial.	Lenalidomide	0-12	cone-rod homeobox	Homo sapiens	50-53
21707574-0	2011	Lenalidomide downregulates the cell survival factor, interferon regulatory factor-4, providing a potential mechanistic link for predicting response.	Lenalidomide	0-12	interferon regulatory factor 4	Homo sapiens	53-83
21707574-4	2011	This study showed that lenalidomide downregulated IRF4 levels in MM cell lines and bone marrow samples within 8 h of drug exposure.	Lenalidomide	23-35	interferon regulatory factor 4	Homo sapiens	50-54
21707574-6	2011	In eight MM cell lines, high IRF4 levels correlated with increased lenalidomide sensitivity.	Lenalidomide	67-79	interferon regulatory factor 4	Homo sapiens	29-33
21707574-8	2011	Among MM patients with high levels of IRF4 expression, treatment with lenalidomide led to a significantly longer overall survival than other therapies in a retrospective analysis.	Lenalidomide	70-82	interferon regulatory factor 4	Homo sapiens	38-42
21707574-9	2011	These data confirm the central role of IRF4 in MM pathogenesis; indicate that this is an important mechanism by which lenalidomide exerts its antitumour effects; and may provide a mechanistic biomarker to predict response to lenalidomide.	Lenalidomide	118-130	interferon regulatory factor 4	Homo sapiens	39-43
21707574-9	2011	These data confirm the central role of IRF4 in MM pathogenesis; indicate that this is an important mechanism by which lenalidomide exerts its antitumour effects; and may provide a mechanistic biomarker to predict response to lenalidomide.	Lenalidomide	225-237	interferon regulatory factor 4	Homo sapiens	39-43
21677134-0	2011	Lenalidomide enhances antigen-specific activity and decreases CD45RA expression of T cells from patients with multiple myeloma.	Lenalidomide	0-12	protein tyrosine phosphatase receptor type C	Homo sapiens	62-66
21677134-1	2011	The aim of this study was to investigate whether the specific T cell response against the multiple myeloma Ag HM1.24 is enhanced by the immunomodulatory drug lenalidomide (Revlimid).	Lenalidomide	158-170	cholinergic receptor muscarinic 1	Homo sapiens	110-113
21677134-1	2011	The aim of this study was to investigate whether the specific T cell response against the multiple myeloma Ag HM1.24 is enhanced by the immunomodulatory drug lenalidomide (Revlimid).	Lenalidomide	172-180	cholinergic receptor muscarinic 1	Homo sapiens	110-113
21677134-5	2011	We found that activation of HM1.24-specific T cells from healthy donors and patients with plasma cell dyscrasias was enhanced significantly by lenalidomide and furthermore that the impact of lenalidomide on T cells depends on the duration of the exposure.	Lenalidomide	143-155	cholinergic receptor muscarinic 1	Homo sapiens	28-31
21677134-5	2011	We found that activation of HM1.24-specific T cells from healthy donors and patients with plasma cell dyscrasias was enhanced significantly by lenalidomide and furthermore that the impact of lenalidomide on T cells depends on the duration of the exposure.	Lenalidomide	191-203	cholinergic receptor muscarinic 1	Homo sapiens	28-31
21677134-6	2011	Notably, lenalidomide supports the downregulation of CD45RA on T cells upon activation, observed in healthy donors and in patients in vitro and also in patients during lenalidomide therapy in vivo.	Lenalidomide	9-21	protein tyrosine phosphatase receptor type C	Homo sapiens	53-57
21677134-6	2011	Notably, lenalidomide supports the downregulation of CD45RA on T cells upon activation, observed in healthy donors and in patients in vitro and also in patients during lenalidomide therapy in vivo.	Lenalidomide	168-180	protein tyrosine phosphatase receptor type C	Homo sapiens	53-57
21677134-7	2011	We showed for the first time, to our knowledge, that lenalidomide enhances the Ag-specific activation of T cells and the subsequent downregulation of CD45RA expression of T cells in vitro and in vivo.	Lenalidomide	53-65	protein tyrosine phosphatase receptor type C	Homo sapiens	150-154
21856771-9	2011	In mice treated with lenalidomide, BNKL levels of active caspase-3 were significantly augmented, thus showing proapoptotic and cytotoxic effects of this drug in vivo.	Lenalidomide	21-33	caspase 3	Mus musculus	57-66
21825263-2	2011	The preclinical combination of lenalidomide with the mTOR inhibitor CCI-779 has displayed synergy in vitro and represents a novel combination in MM.	Lenalidomide	31-43	mechanistic target of rapamycin kinase	Homo sapiens	53-57
21825263-9	2011	Detailed mechanistic interrogation of this pharmacokinetic interaction demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate.	Lenalidomide	89-101	ATP binding cassette subfamily B member 1	Homo sapiens	109-114
21825263-9	2011	Detailed mechanistic interrogation of this pharmacokinetic interaction demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate.	Lenalidomide	89-101	ATP binding cassette subfamily B member 1	Homo sapiens	116-130
21825263-9	2011	Detailed mechanistic interrogation of this pharmacokinetic interaction demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate.	Lenalidomide	89-101	ATP binding cassette subfamily B member 1	Homo sapiens	132-136
21825263-11	2011	Pharmacokinetic and clinical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating lenalidomide was an ABCB1 (P-gp) substrate.	Lenalidomide	122-134	ATP binding cassette subfamily B member 1	Homo sapiens	142-147
21825263-11	2011	Pharmacokinetic and clinical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating lenalidomide was an ABCB1 (P-gp) substrate.	Lenalidomide	122-134	ATP binding cassette subfamily B member 1	Homo sapiens	149-153
21825263-12	2011	To our knowledge, this is the first report of a clinically significant P-gp-based drug-drug interaction with lenalidomide.	Lenalidomide	109-121	ATP binding cassette subfamily B member 1	Homo sapiens	71-75
21658626-7	2011	Other agents inhibit various cellular pathways including those triggered by the B-cell receptor, including spleen tyrosine kinase (Syk) and Bruton"s tyrosine kinase, and other intracellular pathways such as the mammalian target of rapamycin (mTOR), PI3-kinase, and apoptosis, and drugs that target the tumor microenvironment, notably the immunomodulatory agent lenalidomide.	Lenalidomide	361-373	mechanistic target of rapamycin kinase	Homo sapiens	211-240
21347656-2	2011	MP plus thalidomide (MPT), bortezomib (VMP), or lenalidomide (MPR), as induction plus maintenance, have proved to be superior to MP and are currently the treatment of choice for this population.	Lenalidomide	48-60	progesterone receptor membrane component 1	Homo sapiens	62-65
21551245-6	2011	Moreover, E2A knockdown synergizes with the immunomodulatory drug lenalidomide to reduce CLL viability.	Lenalidomide	66-78	transcription factor 3	Homo sapiens	10-13
21523725-1	2011	BACKGROUND: In patients with chronic lymphocytic leukemia (CLL), treatment with lenalidomide induces a unique, previously uncharacterized, immune response called tumor flare reaction (TFR).	Lenalidomide	80-92	transferrin receptor	Homo sapiens	184-187
21523726-0	2011	Chromosomal aberrations +1q21 and del(17p13) predict survival in patients with recurrent multiple myeloma treated with lenalidomide and dexamethasone.	Lenalidomide	119-131	H3 histone pseudogene 6	Homo sapiens	40-43
21307145-7	2011	Lenalidomide-treated MMECs showed changes in VEGF/VEGFR2 signaling pathway and several proteins controlling EC motility, cytoskeleton remodeling, and energy metabolism pathways.	Lenalidomide	0-12	vascular endothelial growth factor A	Homo sapiens	45-49
21389327-6	2011	Down-regulation of IRF4 by lenalidomide was confirmed by longitudinal studies of bone marrow samples from 23 patients obtained before and during lenalidomide treatment using CD138+/IRF4+ double labeling.	Lenalidomide	27-39	interferon regulatory factor 4	Homo sapiens	19-23
21389327-6	2011	Down-regulation of IRF4 by lenalidomide was confirmed by longitudinal studies of bone marrow samples from 23 patients obtained before and during lenalidomide treatment using CD138+/IRF4+ double labeling.	Lenalidomide	27-39	interferon regulatory factor 4	Homo sapiens	181-185
21389327-6	2011	Down-regulation of IRF4 by lenalidomide was confirmed by longitudinal studies of bone marrow samples from 23 patients obtained before and during lenalidomide treatment using CD138+/IRF4+ double labeling.	Lenalidomide	145-157	interferon regulatory factor 4	Homo sapiens	19-23
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	AKT serine/threonine kinase 1	Homo sapiens	126-129
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	glycogen synthase kinase 3 alpha	Homo sapiens	131-141
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	mitogen-activated protein kinase kinase 1	Homo sapiens	148-152
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	tumor protein p53	Homo sapiens	161-164
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	ribosomal protein S6 kinase B1	Homo sapiens	170-176
21378270-3	2011	Here we demonstrate that lenalidomide activation of CLL cells depends on the phosphatidylinositol 3-kinase p110delta (PI3K-delta) pathway.	Lenalidomide	25-37	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	77-116
21378270-3	2011	Here we demonstrate that lenalidomide activation of CLL cells depends on the phosphatidylinositol 3-kinase p110delta (PI3K-delta) pathway.	Lenalidomide	25-37	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	118-128
21378270-4	2011	Inhibition of PI3K-delta signaling by the PI3K-delta-inhibiting drug, CAL-101, or by siRNA knockdown of p110delta, abrogates CLL cell activation, costimulatory molecule expression, and vascular endothelial growth factor and basic fibroblast growth factor gene expression that is induced by lenalidomide.	Lenalidomide	290-302	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	14-24
21378270-4	2011	Inhibition of PI3K-delta signaling by the PI3K-delta-inhibiting drug, CAL-101, or by siRNA knockdown of p110delta, abrogates CLL cell activation, costimulatory molecule expression, and vascular endothelial growth factor and basic fibroblast growth factor gene expression that is induced by lenalidomide.	Lenalidomide	290-302	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	42-52
21378270-4	2011	Inhibition of PI3K-delta signaling by the PI3K-delta-inhibiting drug, CAL-101, or by siRNA knockdown of p110delta, abrogates CLL cell activation, costimulatory molecule expression, and vascular endothelial growth factor and basic fibroblast growth factor gene expression that is induced by lenalidomide.	Lenalidomide	290-302	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	104-113
21378270-6	2011	Collectively, these data demonstrate the importance of PI3K-delta signaling for lenalidomide immune modulation.	Lenalidomide	80-92	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	55-65
21307145-7	2011	Lenalidomide-treated MMECs showed changes in VEGF/VEGFR2 signaling pathway and several proteins controlling EC motility, cytoskeleton remodeling, and energy metabolism pathways.	Lenalidomide	0-12	kinase insert domain receptor	Homo sapiens	50-56
21189262-0	2011	Evidence of a role for activation of Wnt/beta-catenin signaling in the resistance of plasma cells to lenalidomide.	Lenalidomide	101-113	catenin beta 1	Homo sapiens	41-53
21575928-3	2011	The type of anti-MM therapy represents a key factor, with a substantially elevated VTE risk in patients treated with the immunomodulatory drugs (IMiDs) thalidomide or lenalidomide in combination with dexamethasone and/or chemotherapy; VTE risk with lenalidomide-dexamethasone is further increased with concomitant erythropoietin.	Lenalidomide	167-179	erythropoietin	Homo sapiens	314-328
21189262-7	2011	Components of the beta-catenin destruction complex were also impacted by lenalidomide, which suppressed casein kinase 1alpha expression while augmenting glycogen synthase kinase 3alpha/beta phosphorylation.	Lenalidomide	73-85	catenin beta 1	Homo sapiens	18-30
21189262-8	2011	Stimulation of Wnt/beta-catenin signaling with recombinant Wnt-3a, or by overexpression of beta-catenin, reduced the anti-proliferative activity of lenalidomide.	Lenalidomide	148-160	catenin beta 1	Homo sapiens	19-31
21189262-8	2011	Stimulation of Wnt/beta-catenin signaling with recombinant Wnt-3a, or by overexpression of beta-catenin, reduced the anti-proliferative activity of lenalidomide.	Lenalidomide	148-160	Wnt family member 3A	Homo sapiens	59-65
21189262-8	2011	Stimulation of Wnt/beta-catenin signaling with recombinant Wnt-3a, or by overexpression of beta-catenin, reduced the anti-proliferative activity of lenalidomide.	Lenalidomide	148-160	catenin beta 1	Homo sapiens	91-103
21189262-9	2011	Conversely, suppression of beta-catenin with small hairpin RNAs restored plasma cell sensitivity to lenalidomide.	Lenalidomide	100-112	catenin beta 1	Homo sapiens	27-39
21189262-10	2011	Together, these findings support the hypothesis that lenalidomide mediates activation of Wnt/beta-catenin signaling in plasma cells as a mechanism of inducible chemoresistance through effects at the transcriptional and post-translational levels.	Lenalidomide	53-65	catenin beta 1	Homo sapiens	93-105
20421869-2	2011	Recent reports have suggested decreases in the number of CD34+ cells collected and increases in the failure rate among patients whose initial therapy contained lenalidomide when mobilized with G-CSF alone.	Lenalidomide	160-172	colony stimulating factor 3	Homo sapiens	193-198
20479709-8	2011	These data suggest that CD34+ hematopoietic stem cells can be successfully and predictably collected with combination plerixafor plus G-CSF for primary or secondary mobilization in the majority of patients with MM who have been previously treated with lenalidomide.	Lenalidomide	252-264	CD34 molecule	Homo sapiens	24-28
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.	Lenalidomide	20-23	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.	Lenalidomide	67-70	coagulation factor III, tissue factor	Homo sapiens	132-134
20978269-7	2011	Lymphocyte subset depletion experiments revealed that lenalidomide"s enhancement of NK cell-mediated cytotoxicity was mediated by CD4(+) T-cell production of interleukin 2 and that dexamethasone acted by suppressing interleukin-2 production.	Lenalidomide	54-66	CD4 molecule	Homo sapiens	130-133
20978269-7	2011	Lymphocyte subset depletion experiments revealed that lenalidomide"s enhancement of NK cell-mediated cytotoxicity was mediated by CD4(+) T-cell production of interleukin 2 and that dexamethasone acted by suppressing interleukin-2 production.	Lenalidomide	54-66	interleukin 2	Homo sapiens	158-171
20978269-7	2011	Lymphocyte subset depletion experiments revealed that lenalidomide"s enhancement of NK cell-mediated cytotoxicity was mediated by CD4(+) T-cell production of interleukin 2 and that dexamethasone acted by suppressing interleukin-2 production.	Lenalidomide	54-66	interleukin 2	Homo sapiens	216-229
20978269-8	2011	Similarly, the reduced ability of NK cells from patients with MM to respond to lenalidomide was also due to impaired CD4 T-cell function.	Lenalidomide	79-91	CD4 molecule	Homo sapiens	117-120
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).	Lenalidomide	105-117	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).	Lenalidomide	105-117	interleukin 6	Homo sapiens	235-253
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	latexin	Homo sapiens	8-11
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	latexin	Homo sapiens	17-20
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	interleukin 2	Homo sapiens	58-62
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	interferon gamma	Homo sapiens	67-76
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	latexin	Homo sapiens	17-20
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	latexin	Homo sapiens	17-20
21130040-2	2011	At 0.03 muM to 1 muM, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 muM and 1 muM suppressed IL-17 generation.	Lenalidomide	22-34	interleukin 17A	Homo sapiens	231-236
21130040-3	2011	The same concentrations of lenalidomide enhanced IL-2 and IFN-gamma generation by stimulated T cells of old subjects more, with greater respective maximal increases of up to 120-fold and six-fold, without suppressing IL-17 generation.	Lenalidomide	27-39	interleukin 2	Homo sapiens	49-53
21130040-3	2011	The same concentrations of lenalidomide enhanced IL-2 and IFN-gamma generation by stimulated T cells of old subjects more, with greater respective maximal increases of up to 120-fold and six-fold, without suppressing IL-17 generation.	Lenalidomide	27-39	interferon gamma	Homo sapiens	58-67
21130040-4	2011	Lenalidomide enhanced proliferation and suppressed apoptosis of stimulated T cells from old subjects, by IL-2-dependent mechanisms, and restored diminished T cell chemotactic responses to CCL21 and sphingosine 1-phosphate.	Lenalidomide	0-12	interleukin 2	Homo sapiens	105-109
21130040-4	2011	Lenalidomide enhanced proliferation and suppressed apoptosis of stimulated T cells from old subjects, by IL-2-dependent mechanisms, and restored diminished T cell chemotactic responses to CCL21 and sphingosine 1-phosphate.	Lenalidomide	0-12	C-C motif chemokine ligand 21	Homo sapiens	188-193
21273172-9	2011	When controlling for the number of previous antimyeloma therapies, beta2-microglobulin levels, and Durie-Salmon stage (which adversely affected survival in these patients), continued lenalidomide treatment (HR, 0.137; 95% CI, 0.045-0.417; P=.0005) or each additional cycle of lenalidomide (HR, 0.921; 95% CI, 0.886-0.957; P<.0001) were both associated with longer survival.	Lenalidomide	183-195	beta-2-microglobulin	Homo sapiens	67-86
21322779-6	2011	Disease-specific sensitivity to lenalidomide results from the drug"s inhibitory effect on two haplodeficient phosphatases, PP2Acalpha and CDC25c, which are coregulators of the G(2)/M checkpoint.	Lenalidomide	32-44	cell division cycle 25C	Homo sapiens	138-144
23556075-9	2011	Correlative studies and/or retrospective analysis of lenalidomide-treated patients had identified several biomarkers associated with clinical endpoints in CLL (i.e. changes in tumor necrosis factor alpha [TNF-alpha] or vascular endothelial growth factor [VEGF] levels) or DLBCL (non-GCB phenotype) patients, but need to be validated.	Lenalidomide	53-65	tumor necrosis factor	Homo sapiens	176-203
23556075-9	2011	Correlative studies and/or retrospective analysis of lenalidomide-treated patients had identified several biomarkers associated with clinical endpoints in CLL (i.e. changes in tumor necrosis factor alpha [TNF-alpha] or vascular endothelial growth factor [VEGF] levels) or DLBCL (non-GCB phenotype) patients, but need to be validated.	Lenalidomide	53-65	tumor necrosis factor	Homo sapiens	205-214
20848094-8	2011	The extent of ADCC and its enhancement by lenalidomide correlated with NK cell expression of NKG2D and DNAM-1, and tumor cell expression of PVR and MIC-A.	Lenalidomide	42-54	CD226 molecule	Homo sapiens	103-109
20848094-11	2011	Lenalidomide enhances the ability of IgG1-isotype antibodies to mediate ADCC of solid tumor cells, the extent of which is largely dependent on NKG2D-NKG2D ligand interactions, but appears to be independent of MIC-A/B.	Lenalidomide	0-12	killer cell lectin like receptor K1	Homo sapiens	143-148
20848094-11	2011	Lenalidomide enhances the ability of IgG1-isotype antibodies to mediate ADCC of solid tumor cells, the extent of which is largely dependent on NKG2D-NKG2D ligand interactions, but appears to be independent of MIC-A/B.	Lenalidomide	0-12	killer cell lectin like receptor K1	Homo sapiens	149-154
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.	Lenalidomide	223-235	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.	Lenalidomide	223-235	cereblon	Homo sapiens	128-132
21127185-0	2010	Increases in B-type natriuretic peptide (BNP) during treatment with lenalidomide in AL amyloidosis.	Lenalidomide	68-80	natriuretic peptide B	Homo sapiens	13-39
20848094-8	2011	The extent of ADCC and its enhancement by lenalidomide correlated with NK cell expression of NKG2D and DNAM-1, and tumor cell expression of PVR and MIC-A.	Lenalidomide	42-54	killer cell lectin like receptor K1	Homo sapiens	93-98
21127185-0	2010	Increases in B-type natriuretic peptide (BNP) during treatment with lenalidomide in AL amyloidosis.	Lenalidomide	68-80	natriuretic peptide B	Homo sapiens	41-44
19965642-0	2010	Lenalidomide treatment promotes CD154 expression on CLL cells and enhances production of antibodies by normal B cells through a PI3-kinase-dependent pathway.	Lenalidomide	0-12	CD40 ligand	Homo sapiens	32-37
20689431-6	2010	The chemokine receptor 4 (CXCR4) inhibitor, AMD-3100, is recommended for patients who have received lenalidomide and failed to mobilize stem cells after G-SCF and cyclophosphamide.	Lenalidomide	100-112	C-X-C motif chemokine receptor 4	Homo sapiens	26-31
20491881-0	2010	Changes in RPS14 expression levels during lenalidomide treatment in Low- and Intermediate-1-risk myelodysplastic syndromes with chromosome 5q deletion.	Lenalidomide	42-54	ribosomal protein S14	Homo sapiens	11-16
20594187-6	2010	Several drugs effective for the treatment of MM, including proteasome inhibitors, thalidomide, lenalidomide and arsenic trioxide, block NF-kappaB activation.	Lenalidomide	95-107	nuclear factor kappa B subunit 1	Homo sapiens	136-145
20846100-0	2010	Response to lenalidomide in a patient with myelodysplastic syndrome with isolated del(5q) and JAK2 V617F mutation.	Lenalidomide	12-24	Janus kinase 2	Homo sapiens	94-98
20460501-6	2010	We show that lenalidomide down-regulates PD-L1 on primary MM cells and may augment CT-011"s enhancement of NK-cell function against MM.	Lenalidomide	13-25	CD274 molecule	Homo sapiens	41-46
20194893-0	2010	Efficacy of single-agent lenalidomide in patients with JAK2 (V617F) mutated refractory anemia with ring sideroblasts and thrombocytosis.	Lenalidomide	25-37	Janus kinase 2	Homo sapiens	55-59
19965642-4	2010	Here, we demonstrate that lenalidomide induces expression of functional CD154 antigen on CLL cells both in vitro and in vivo.	Lenalidomide	26-38	CD40 ligand	Homo sapiens	72-77
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	CD40 ligand	Homo sapiens	60-65
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	BH3 interacting domain death agonist	Homo sapiens	99-102
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	TNF receptor superfamily member 10b	Homo sapiens	104-107
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	tumor protein p73	Homo sapiens	113-116
19965642-7	2010	In CLL patients receiving lenalidomide, similar evidence of CD154 activation is observed including BID, DR5, and p73 induction and also development of anti-ROR1 tumor-directed antibodies.	Lenalidomide	26-38	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	156-160
19965642-8	2010	Our data demonstrate that lenalidomide promotes CD154 expression on CLL cells with subsequent activation phenotype, and may therefore reverse the humoral immune defect observed in this disease.	Lenalidomide	26-38	CD40 ligand	Homo sapiens	48-53
19965623-2	2010	We show that IMiDs down-regulate PU.1, a key transcription factor involved in granulocyte differentiation in vitro and in patients treated with lenalidomide.	Lenalidomide	144-156	Spi-1 proto-oncogene	Homo sapiens	33-37
20359632-5	2010	In del(5q) patients, lenalidomide suppresses the clone by inhibiting the nuclear sequestration of the haplodeficient cell cycle regulatory protein cdc25c, thereby promoting selective G2 arrest and apoptosis.	Lenalidomide	21-33	cell division cycle 25C	Homo sapiens	147-153
20088798-2	2010	The effect of dexamethasone on the immunomodulatory activities of lenalidomide such as T cell and natural killer (NK) cell activation was measured via interleukin [IL]-2 production, and interferon-gamma and granzyme B production respectively.	Lenalidomide	66-78	granzyme B	Homo sapiens	207-217
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	early growth response 1	Homo sapiens	114-118
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	early growth response 2	Homo sapiens	120-124
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	early growth response 3	Homo sapiens	126-130
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	cyclin dependent kinase inhibitor 2B	Homo sapiens	132-135
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	H3 histone pseudogene 16	Homo sapiens	137-140
20088798-5	2010	Mechanistically, lenalidomide plus dexamethasone synergistically induced expression of the tumor suppressor genes Egr1, Egr2, Egr3, p15, p21, and p27 in MM cell lines and MM patient cells.	Lenalidomide	17-29	interferon alpha inducible protein 27	Homo sapiens	146-149
20088798-7	2010	Lenalidomide alone increased T cell production of IL-2, and NK cell production of interferon-gamma and granzyme B.	Lenalidomide	0-12	interleukin 2	Homo sapiens	50-54
20088798-7	2010	Lenalidomide alone increased T cell production of IL-2, and NK cell production of interferon-gamma and granzyme B.	Lenalidomide	0-12	interferon gamma	Homo sapiens	82-98
20088798-7	2010	Lenalidomide alone increased T cell production of IL-2, and NK cell production of interferon-gamma and granzyme B.	Lenalidomide	0-12	granzyme B	Homo sapiens	103-113
19773257-4	2010	RESULTS: Compared to baseline, lenalidomide treatment significantly decreased the proportion of bone marrow CD34+ cells, increased the proportion of CD36(+)/GlycoA(+) and CD36(-)/GlycoA(+) erythroid cells and the percentage of apoptotic cells within these cell compartments.	Lenalidomide	31-43	CD34 molecule	Homo sapiens	108-112
19773257-8	2010	CONCLUSIONS: The beneficial effect of lenalidomide in patients with lower risk myelodysplastic syndrome with del(5q) is associated with significant increases in the proportion of bone marrow erythroid precursor cells and in the frequency of clonogenic progenitor cells, a substantial improvement in the hematopoiesis-supporting potential of bone marrow stroma and significant alterations in the adhesion profile of bone marrow CD34(+) cells.	Lenalidomide	38-50	CD34 molecule	Homo sapiens	427-431
19584825-0	2010	Lenalidomide as salvage therapy after allo-SCT for multiple myeloma is effective and leads to an increase of activated NK (NKp44(+)) and T (HLA-DR(+)) cells.	Lenalidomide	0-12	natural cytotoxicity triggering receptor 2	Homo sapiens	123-128
19584825-9	2010	Immunomonitoring after lenalidomide showed significant increase of activated NK (NKp44(+)) and T (HLA-DR(+)) cells, as well as regulatory T cells (CD4(+), CD25(+), CD127(lo)), supporting an immunomodulating anti-myeloma effect of lenalidomide.	Lenalidomide	23-35	natural cytotoxicity triggering receptor 2	Homo sapiens	81-86
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	53-62
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 9	Homo sapiens	70-79
19965674-5	2010	Furthermore, studies using biochemical inhibitors of caspase-8 versus caspase-9 demonstrate that NPI-0052 plus lenalidomide-triggered apoptosis is primarily dependent on caspase-8 signaling.	Lenalidomide	111-123	caspase 8	Homo sapiens	170-179
20621290-0	2010	Lenalidomide down regulates the production of interferon-gamma and the expression of inhibitory cytotoxic receptors of human Natural Killer cells.	Lenalidomide	0-12	interferon gamma	Homo sapiens	46-62
20621290-2	2010	The effect of Lenalidomide towards Peripheral Blood Mononuclear Cells (PBMC) has been studied and direct effects towards T cells have been described, such as an increase of interferon-gamma (IFN-gamma) and interleukin (IL)-2 production.	Lenalidomide	14-26	interferon gamma	Homo sapiens	173-189
20621290-5	2010	Here we show that Lenalidomide can inhibit the production of IFN-gamma by NK cells from healthy donors.	Lenalidomide	18-30	interferon gamma	Homo sapiens	61-70
19738071-0	2009	Pomalidomide and lenalidomide induce p21 WAF-1 expression in both lymphoma and multiple myeloma through a LSD1-mediated epigenetic mechanism.	Lenalidomide	17-29	cyclin dependent kinase inhibitor 1A	Homo sapiens	37-40
19733563-6	2009	We previously reported the neuroprotective effects of lenalidomide, when treatment was started 2 months prior to onset of disease in the G93A SOD1 transgenic mouse model of ALS.	Lenalidomide	54-66	superoxide dismutase 1, soluble	Mus musculus	142-146
19733563-7	2009	Since in ALS patients, treatment can only begin after the appearance of symptoms, we sought to determine the efficacy of lenalidomide administration starting at symptom onset in the G93A SOD1 mice.	Lenalidomide	121-133	superoxide dismutase 1	Homo sapiens	187-191
19733563-10	2009	Qualitative histological analysis showed that lenalidomide treatment modestly reduced the expression of the proinflammatory cytokines Fas Ligand, IL-1beta, TNF-alpha and CD40 ligand.	Lenalidomide	46-58	Fas ligand (TNF superfamily, member 6)	Mus musculus	134-144
19733563-10	2009	Qualitative histological analysis showed that lenalidomide treatment modestly reduced the expression of the proinflammatory cytokines Fas Ligand, IL-1beta, TNF-alpha and CD40 ligand.	Lenalidomide	46-58	interleukin 1 alpha	Mus musculus	146-154
19733563-10	2009	Qualitative histological analysis showed that lenalidomide treatment modestly reduced the expression of the proinflammatory cytokines Fas Ligand, IL-1beta, TNF-alpha and CD40 ligand.	Lenalidomide	46-58	tumor necrosis factor	Mus musculus	156-165
19797731-0	2009	Clonal heterogeneity in the 5q- syndrome: p53 expressing progenitors prevail during lenalidomide treatment and expand at disease progression.	Lenalidomide	84-96	tumor protein p53	Homo sapiens	42-45
19728370-3	2009	The authors reported the results of a phase 2/3 study comparing the safety and efficacy of 2 doses of lenalidomide in patients with relapsed metastatic melanoma disease refractory to previous treatment with dacarbazine, temozolomide, interleukin-2, or interferon-alpha.	Lenalidomide	102-114	interleukin 2	Homo sapiens	234-247
19738071-8	2009	Based on our findings, we propose a model in which pomalidomide and lenalidomide modify the chromatin structure of the p21(WAF-1) promoter through demethylation and acetylation of H3K9.	Lenalidomide	68-80	cyclin dependent kinase inhibitor 1A	Homo sapiens	119-122
19738071-8	2009	Based on our findings, we propose a model in which pomalidomide and lenalidomide modify the chromatin structure of the p21(WAF-1) promoter through demethylation and acetylation of H3K9.	Lenalidomide	68-80	cyclin dependent kinase inhibitor 1A	Homo sapiens	123-128
19738071-0	2009	Pomalidomide and lenalidomide induce p21 WAF-1 expression in both lymphoma and multiple myeloma through a LSD1-mediated epigenetic mechanism.	Lenalidomide	17-29	cyclin dependent kinase inhibitor 1A	Homo sapiens	41-46
19738071-0	2009	Pomalidomide and lenalidomide induce p21 WAF-1 expression in both lymphoma and multiple myeloma through a LSD1-mediated epigenetic mechanism.	Lenalidomide	17-29	lysine demethylase 1A	Homo sapiens	106-110
19738071-7	2009	Interestingly, lysine-specific demethylase-1 (LSD1) silencing reduced both pomalidomide and lenalidomide up-regulation of p21(WAF-1), suggesting that this histone demethylase is involved in the priming of the p21(WAF-1) promoter.	Lenalidomide	92-104	lysine demethylase 1A	Homo sapiens	15-44
19738071-7	2009	Interestingly, lysine-specific demethylase-1 (LSD1) silencing reduced both pomalidomide and lenalidomide up-regulation of p21(WAF-1), suggesting that this histone demethylase is involved in the priming of the p21(WAF-1) promoter.	Lenalidomide	92-104	lysine demethylase 1A	Homo sapiens	46-50
19738071-7	2009	Interestingly, lysine-specific demethylase-1 (LSD1) silencing reduced both pomalidomide and lenalidomide up-regulation of p21(WAF-1), suggesting that this histone demethylase is involved in the priming of the p21(WAF-1) promoter.	Lenalidomide	92-104	cyclin dependent kinase inhibitor 1A	Homo sapiens	122-125
19738071-7	2009	Interestingly, lysine-specific demethylase-1 (LSD1) silencing reduced both pomalidomide and lenalidomide up-regulation of p21(WAF-1), suggesting that this histone demethylase is involved in the priming of the p21(WAF-1) promoter.	Lenalidomide	92-104	cyclin dependent kinase inhibitor 1A	Homo sapiens	126-131
19734418-0	2009	Lenalidomide-induced upregulation of CD80 on tumor cells correlates with T-cell activation, the rapid onset of a cytokine release syndrome and leukemic cell clearance in chronic lymphocytic leukemia.	Lenalidomide	0-12	CD80 molecule	Homo sapiens	37-41
19734418-5	2009	RESULTS: Lenalidomide upregulated the co-stimulatory molecule CD80 on chronic lymphocytic leukemia and mantle cell lymphoma cells but not on normal peripheral blood B cells in vitro.	Lenalidomide	9-21	CD80 molecule	Homo sapiens	62-66
19734418-7	2009	Strong CD80 upregulation and T-cell activation predicted more severe side effects, manifesting in 83% of patients as a cytokine release syndrome within 8-72 h after the first dose of lenalidomide.	Lenalidomide	183-195	CD80 molecule	Homo sapiens	7-11
19734418-11	2009	CONCLUSIONS: Upregulation of CD80 on tumor cells and T-cell activation correlate with unique toxicities of lenalidomide in chronic lymphocytic leukemia.	Lenalidomide	107-119	CD80 molecule	Homo sapiens	29-33
19470455-2	2009	Although haploinsufficiency for the RPS14 gene and others encoded within the common deleted region (CDR) have been implicated in the pathogenesis of the del(5q) phenotype, the molecular basis of the karyotype specificity of lenalidomide remains unexplained.	Lenalidomide	224-236	ribosomal protein S14	Homo sapiens	36-41
19470455-4	2009	We show that the dual specificity phosphatases, Cdc25C and PP2Acalpha, which are coregulators of the G(2)-M checkpoint, are inhibited by lenalidomide.	Lenalidomide	137-149	cell division cycle 25C	Homo sapiens	48-54
19470455-6	2009	Lenalidomide inhibited phosphatase activity either directly (Cdc25C) or indirectly (PP2A) with corresponding retention of inhibitory phospho-tyrosine residues.	Lenalidomide	0-12	cell division cycle 25C	Homo sapiens	61-67
19470455-6	2009	Lenalidomide inhibited phosphatase activity either directly (Cdc25C) or indirectly (PP2A) with corresponding retention of inhibitory phospho-tyrosine residues.	Lenalidomide	0-12	protein phosphatase 2 phosphatase activator	Homo sapiens	84-88
19470455-8	2009	Small interfering RNA (shRNA) suppression of Cdc25C and PP2Acalpha gene expression recapitulated del(5q) susceptibility to lenalidomide with induction of G(2) arrest and apoptosis in both U937 and primary nondel(5q) MDS cells.	Lenalidomide	123-135	cell division cycle 25C	Homo sapiens	45-51
19470455-9	2009	These data establish a role for allelic haplodeficiency of the lenalidomide inhibitable Cdc25C and PP2Acalpha phosphatases in the selective drug sensitivity of del(5q) MDS.	Lenalidomide	63-75	cell division cycle 25C	Homo sapiens	88-94
19183192-0	2009	The humanized CD40 antibody SGN-40 demonstrates pre-clinical activity that is enhanced by lenalidomide in chronic lymphocytic leukaemia.	Lenalidomide	90-102	CD40 molecule	Homo sapiens	14-18
19717386-2	2009	We describe a case of an elderly patient who presented with extramedullary, IgA-lambda-secreting multiple myeloma with plasmablastic features who demonstrated impressive clinical response to single-agent lenalidomide.	Lenalidomide	204-216	CD79a molecule	Homo sapiens	76-79
19525184-3	2009	Here, we describe 6 patients with International Prognostic Scoring System low- or intermediate-1-risk MDS who began lenalidomide therapy between April 2002 and June 2003 as part of the MDS-001 study and who have maintained long-term therapy.	Lenalidomide	116-128	BBX high mobility group box domain containing	Homo sapiens	185-192
19302559-2	2009	Multivariate analysis showed that fewer prior therapies, along with beta(2)-microglobulin (< or = 2.5 mg/L), predicted a better time to progression (TTP; study end-point) with lenalidomide plus dexamethasone treatment.	Lenalidomide	179-191	beta-2-microglobulin	Homo sapiens	68-89
19030860-0	2009	Lenalidomide: in vitro evaluation of the metabolism and assessment of cytochrome P450 inhibition and induction.	Lenalidomide	0-12	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	70-85
19030860-1	2009	PURPOSE: To assess the potential for drug-drug interactions between lenalidomide and substrates and inhibitors of cytochrome P450 (CYP) isozymes.	Lenalidomide	68-80	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	131-134
19030860-3	2009	The inhibitory and inductive effects of lenalidomide on the CYP activities were evaluated in human liver microsomes and cultured human hepatocytes, respectively.	Lenalidomide	40-52	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-63
19406725-1	2009	BACKGROUND: Initial analysis of the combination melphalan, prednisone, plus lenalidomide (MPR) showed significant antimyeloma activity in patients with untreated multiple myeloma, with neutropenia and thrombocytopenia as the most frequent side effects.	Lenalidomide	76-88	progesterone receptor membrane component 1	Homo sapiens	90-93
19509231-3	2009	A drug screen for anti-MM agents that decrease Hif-1alpha and c-Myc levels identified a variety of compounds, including bortezomib, lenalidomide, enzastaurin, and adaphostin.	Lenalidomide	132-144	MYC proto-oncogene, bHLH transcription factor a	Danio rerio	62-67
19183192-7	2009	Previous studies by our group and others have demonstrated that lenalidomide upregulates CD40 expression on primary B CLL cells and activates NK-cells.	Lenalidomide	64-76	CD40 molecule	Homo sapiens	89-93
19778857-2	2009	The MDS-003 multicenter registration trial in deletion of chromosome 5q (del[5q]) showed that lenalidomide suppresses the del(5q) clone in patients who achieve transfusion independence and is a prerequisite for sustained restoration of effective erythropoiesis.	Lenalidomide	94-106	proteasome assembly chaperone 2	Homo sapiens	4-11
19181778-0	2009	The response to lenalidomide of myelodysplastic syndrome patients with deletion del(5q) can be sequentially monitored in CD34+ progenitor cells.	Lenalidomide	16-28	CD34 molecule	Homo sapiens	121-125
18784738-0	2009	Lenalidomide alone or in combination with dexamethasone is highly effective in patients with relapsed multiple myeloma following allogeneic stem cell transplantation and increases the frequency of CD4+Foxp3+ T cells.	Lenalidomide	0-12	CD4 molecule	Homo sapiens	197-200
18784738-0	2009	Lenalidomide alone or in combination with dexamethasone is highly effective in patients with relapsed multiple myeloma following allogeneic stem cell transplantation and increases the frequency of CD4+Foxp3+ T cells.	Lenalidomide	0-12	forkhead box P3	Homo sapiens	201-206
18805433-5	2009	We also found an inhibitory effect of lenalidomide on the associations between cadherin 5, beta-catenin and CD31, adherens junction proteins whose interaction is critical for endothelial cell cord formation.	Lenalidomide	38-50	cadherin 5	Homo sapiens	79-89
18805433-5	2009	We also found an inhibitory effect of lenalidomide on the associations between cadherin 5, beta-catenin and CD31, adherens junction proteins whose interaction is critical for endothelial cell cord formation.	Lenalidomide	38-50	catenin beta 1	Homo sapiens	91-103
18805433-5	2009	We also found an inhibitory effect of lenalidomide on the associations between cadherin 5, beta-catenin and CD31, adherens junction proteins whose interaction is critical for endothelial cell cord formation.	Lenalidomide	38-50	platelet and endothelial cell adhesion molecule 1	Homo sapiens	108-112
18805433-6	2009	Furthermore, lenalidomide inhibited VEGF-induced PI3K-Akt pathway signaling, which is known to regulate adherens junction formation.	Lenalidomide	13-25	vascular endothelial growth factor A	Homo sapiens	36-40
18805433-7	2009	We also found a strong inhibitory effect of lenalidomide on hypoxia-induced endothelial cell formation of cords and HIF-1 alpha expression, the main mediator of hypoxia-mediated effects and a key driver of angiogenesis and metastasis.	Lenalidomide	44-56	hypoxia inducible factor 1 subunit alpha	Homo sapiens	116-127
19707399-3	2009	In the near future melphalan-prednisone-lenalidomide (Revlimid((R)), MPR) will also provide a third therapeutic option (MPT, MPV, and MPR), in elderly multiple myeloma, eventually.	Lenalidomide	40-52	progesterone receptor membrane component 1	Homo sapiens	134-137
19707399-3	2009	In the near future melphalan-prednisone-lenalidomide (Revlimid((R)), MPR) will also provide a third therapeutic option (MPT, MPV, and MPR), in elderly multiple myeloma, eventually.	Lenalidomide	54-62	progesterone receptor membrane component 1	Homo sapiens	134-137
18950461-3	2008	In a study of the immunomodulatory combination BiRD, (lenalidomide and dexamethasone with clarithromycin), we frequently detected the emergence of mono- and oligo-clonal immunoglobulins unrelated to the baseline diagnostic M-protein.	Lenalidomide	54-66	myomesin 2	Homo sapiens	223-232
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).	Lenalidomide	199-211	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	74-79
19067746-6	2009	A significant decrease of DKK-1 after therapy was seen in the following groups: Bortezomib (4059 pg/mL vs. 1862 pg/mL, P = 0.016), lenalidomide (11837 pg/mL vs. 4374 pg/mL, P = 0.039), AD (1668 pg/mL vs. 1241 pg/mL, P = 0.016), and AD + HDCT + ASCT (2446 pg/mL vs. 1082 pg/mL, P = 0.001).	Lenalidomide	131-143	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	26-31
18772452-0	2008	Lenalidomide down-regulates the CD20 antigen and antagonizes direct and antibody-dependent cellular cytotoxicity of rituximab on primary chronic lymphocytic leukemia cells.	Lenalidomide	0-12	keratin 20	Homo sapiens	32-36
18772452-2	2008	The anti-CD20 antibody rituximab is active in CLL and represents a rational agent to combine with lenalidomide.	Lenalidomide	98-110	keratin 20	Homo sapiens	9-13
18772452-4	2008	In contrast to previous reports using CD20-positive lymphoma cell lines, lenalidomide down-regulated CD20 surface antigen expression in CLL patient cells via enhanced internalization, without influencing transcription.	Lenalidomide	73-85	keratin 20	Homo sapiens	101-105
18772452-6	2008	In addition, CD20 surface antigen down-modulation by lenalidomide in CLL was accompanied by diminished rituximab-mediated apoptosis and ADCC.	Lenalidomide	53-65	keratin 20	Homo sapiens	13-17
18772452-8	2008	In addition, they suggest that lenalidomide therapy might be useful to enhance targeted delivery of RNAi-based therapies using CD20 immunoliposomes in B-cell malignancies.	Lenalidomide	31-43	keratin 20	Homo sapiens	127-131
18799726-4	2008	Lenalidomide + dexamethasone led to higher overall response rate (ORR), longer time to progression (TTP), and progression-free survival (PFS) versus placebo + dexamethasone despite prior thalidomide exposure.	Lenalidomide	0-12	ZFP36 ring finger protein	Homo sapiens	100-103
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).	Lenalidomide	6-18	ZFP36 ring finger protein	Homo sapiens	155-158
18980990-9	2008	Importantly, lenalidomide further augmented the Th1 polarization by iNKT cell lines via increased Th1 cytokine production and reduced Th2 cytokine production.	Lenalidomide	13-25	negative elongation factor complex member C/D	Homo sapiens	48-51
18980990-9	2008	Importantly, lenalidomide further augmented the Th1 polarization by iNKT cell lines via increased Th1 cytokine production and reduced Th2 cytokine production.	Lenalidomide	13-25	negative elongation factor complex member C/D	Homo sapiens	98-101
18427150-10	2008	In vitro studies demonstrated lenalidomide-induced B-cell activation (upregulation of CD40 and CD86) corresponding to degree of tumor flare, possibly explaining the tumor flare observation.	Lenalidomide	30-42	CD40 molecule	Homo sapiens	86-90
18713253-2	2008	TE risk may be elevated with combination regimens, notably thalidomide/lenalidomide plus high-dose dexamethasone; concomitant erythropoietin appears to further increase the risk with lenalidomide-dexamethasone.	Lenalidomide	183-195	erythropoietin	Homo sapiens	126-140
18628480-0	2008	lenalidomide enhances natural killer cell and monocyte-mediated antibody-dependent cellular cytotoxicity of rituximab-treated CD20+ tumor cells.	Lenalidomide	0-12	keratin 20	Homo sapiens	126-130
18628480-5	2008	RESULTS: Lenalidomide directly enhanced IFN-gamma production via Fc-gamma receptor-mediated signaling in response to IgG.	Lenalidomide	9-21	interferon gamma	Homo sapiens	40-49
18628480-5	2008	RESULTS: Lenalidomide directly enhanced IFN-gamma production via Fc-gamma receptor-mediated signaling in response to IgG.	Lenalidomide	9-21	Fc gamma receptor Ia	Homo sapiens	65-82
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.	Lenalidomide	104-116	nuclear factor kappa B subunit 1	Homo sapiens	178-187
18596740-6	2008	We identified PU.1 and pERK as major targets of lenalidomide, and nuclear factor of activated T cells of bortezomib, resulting in inhibition of osteoclastogenesis.	Lenalidomide	48-60	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	23-27
18596740-9	2008	Importantly, in serum from MM patients treated with lenalidomide, the essential bone-remodeling factor RANKL, as well as the RANKL/OPG ratio, were significantly reduced, whereas osteoprotegerin (OPG) was increased.	Lenalidomide	52-64	TNF superfamily member 11	Homo sapiens	103-108
18596740-9	2008	Importantly, in serum from MM patients treated with lenalidomide, the essential bone-remodeling factor RANKL, as well as the RANKL/OPG ratio, were significantly reduced, whereas osteoprotegerin (OPG) was increased.	Lenalidomide	52-64	TNF superfamily member 11	Homo sapiens	125-130
18596740-9	2008	Importantly, in serum from MM patients treated with lenalidomide, the essential bone-remodeling factor RANKL, as well as the RANKL/OPG ratio, were significantly reduced, whereas osteoprotegerin (OPG) was increased.	Lenalidomide	52-64	TNF receptor superfamily member 11b	Homo sapiens	131-134
18596740-9	2008	Importantly, in serum from MM patients treated with lenalidomide, the essential bone-remodeling factor RANKL, as well as the RANKL/OPG ratio, were significantly reduced, whereas osteoprotegerin (OPG) was increased.	Lenalidomide	52-64	TNF receptor superfamily member 11b	Homo sapiens	178-193
18596740-9	2008	Importantly, in serum from MM patients treated with lenalidomide, the essential bone-remodeling factor RANKL, as well as the RANKL/OPG ratio, were significantly reduced, whereas osteoprotegerin (OPG) was increased.	Lenalidomide	52-64	TNF receptor superfamily member 11b	Homo sapiens	195-198
18427150-10	2008	In vitro studies demonstrated lenalidomide-induced B-cell activation (upregulation of CD40 and CD86) corresponding to degree of tumor flare, possibly explaining the tumor flare observation.	Lenalidomide	30-42	CD86 molecule	Homo sapiens	95-99
17906467-5	2007	Results from the MDS-003 multicenter deletion 5q registration study show that lenalidomide suppresses the deletion 5q clone, and in higher risk myelodysplastic syndrome patients, may also alter the natural history of disease.	Lenalidomide	78-90	proteasome assembly chaperone 2	Homo sapiens	17-24
18067473-0	2008	Should prophylactic granulocyte-colony stimulating factor be used in multiple myeloma patients developing neutropenia under lenalidomide-based therapy?	Lenalidomide	124-136	colony stimulating factor 3	Homo sapiens	20-57
18064299-0	2008	Pomalidomide and lenalidomide regulate erythropoiesis and fetal hemoglobin production in human CD34+ cells.	Lenalidomide	17-29	CD34 molecule	Homo sapiens	95-99
17576924-0	2007	Lenalidomide inhibits the malignant clone and up-regulates the SPARC gene mapping to the commonly deleted region in 5q- syndrome patients.	Lenalidomide	0-12	secreted protein acidic and cysteine rich	Homo sapiens	63-68
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.	Lenalidomide	9-21	interferon gamma	Homo sapiens	155-171
17686058-5	2007	Caution should be exercised when lenalidomide therapy is commenced and CrCl should be incorporated as a determinant of the initial dosing of lenalidomide in MM patients.	Lenalidomide	141-153	CRCL	Homo sapiens	71-75
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<0.001), average daily collection (P<0.001), day 1 collection (P<0.001) and increased number of aphereses (P=0.004) in patients treated with lenalidomide compared to those receiving dexamethasone, thalidomide-dexamethasone or VAD.	Lenalidomide	298-310	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<0.001), average daily collection (P<0.001), day 1 collection (P<0.001) and increased number of aphereses (P=0.004) in patients treated with lenalidomide compared to those receiving dexamethasone, thalidomide-dexamethasone or VAD.	Lenalidomide	298-310	colony stimulating factor 3	Homo sapiens	66-71
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.	Lenalidomide	9-21	interleukin 2	Homo sapiens	136-149
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	V-set and immunoglobulin domain containing 4	Homo sapiens	127-132
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	peptidylprolyl isomerase C	Homo sapiens	134-138
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	trophoblast glycoprotein	Homo sapiens	140-144
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	secreted protein acidic and cysteine rich	Homo sapiens	161-166
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	hemoglobin subunit alpha 2	Homo sapiens	268-272
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	glycophorin A (MNS blood group)	Homo sapiens	274-278
17576924-6	2007	Moreover, lenalidomide significantly influenced the pattern of gene expression in del(5q) intermediate erythroblasts, with the VSIG4, PPIC, TPBG, activin A, and SPARC genes up-regulated by >2-fold in all samples and many genes involved in erythropoiesis, including HBA2, GYPA, and KLF1, down-regulated in most samples.	Lenalidomide	10-22	Kruppel like factor 1	Homo sapiens	284-288
17576924-9	2007	We conclude that lenalidomide inhibits growth of del(5q) erythroid progenitors and that the up-regulation of SPARC and activin A may underlie the potent effects of lenalidomide in MDS with del(5)(q31).	Lenalidomide	164-176	secreted protein acidic and cysteine rich	Homo sapiens	109-114
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.	Lenalidomide	367-379	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	130-134
17255789-5	2007	Furthermore, lenalidomide induces a direct cytotoxic effect against 5q- clones in leukemia cell lines and enhances ligand-induced erythropoietin receptor signaling in erythroid progenitors.	Lenalidomide	13-25	erythropoietin	Homo sapiens	130-144
17234786-0	2007	Lenalidomide and CC-4047 inhibit the proliferation of malignant B cells while expanding normal CD34+ progenitor cells.	Lenalidomide	0-12	CD34 molecule	Homo sapiens	95-99
17234786-6	2007	Finally, CC-4047 and lenalidomide had synergistic effects with valproic acid [a histone deacetylase (HDAC) inhibitor] by increasing the apoptosis of Namalwa cells and enhancing CD34+ cell expansion.	Lenalidomide	21-33	CD34 molecule	Homo sapiens	177-181
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.	Lenalidomide	25-37	tumor necrosis factor	Homo sapiens	120-129
17168657-4	2006	It seems that lenalidomide and CC-4047 are more powerful in inhibiting TNFalpha and have, except for myelosuppression, less side effects than Thal.	Lenalidomide	14-26	tumor necrosis factor	Homo sapiens	71-79
17242661-6	2006	These studies identified lenalidomide as a highly active erythropoietic- and cytogenetic-remitting agent in lower-risk MDS patients who otherwise would not be expected to benefit from recombinant erythropoietin therapy.	Lenalidomide	25-37	erythropoietin	Homo sapiens	196-210
17242663-7	2006	The costs of lenalidomide therapy were substantially offset by reduced blood transfusion and EPO costs.	Lenalidomide	13-25	erythropoietin	Homo sapiens	93-96
16494942-0	2006	Lenalidomide inhibits proliferation of Namalwa CSN.70 cells and interferes with Gab1 phosphorylation and adaptor protein complex assembly.	Lenalidomide	0-12	GRB2 associated binding protein 1	Homo sapiens	80-84
16990762-0	2006	Hematologic and cytogenetic response to lenalidomide monotherapy in acute myeloid leukemia arising from JAK2(V617F) positive, del(5)(q13q33) myelodysplastic syndrome.	Lenalidomide	40-52	Janus kinase 2	Homo sapiens	104-114
17076650-3	2006	Lenalidomide (CC-5013; Revlimid), a second generation IMiD, has shown significant erythropoietic activity in patients with lower risk MDS that have failed or are not candidates for recombinant erythropoietin treatment.	Lenalidomide	0-12	erythropoietin	Homo sapiens	193-207
17076650-3	2006	Lenalidomide (CC-5013; Revlimid), a second generation IMiD, has shown significant erythropoietic activity in patients with lower risk MDS that have failed or are not candidates for recombinant erythropoietin treatment.	Lenalidomide	14-21	erythropoietin	Homo sapiens	193-207
17076650-3	2006	Lenalidomide (CC-5013; Revlimid), a second generation IMiD, has shown significant erythropoietic activity in patients with lower risk MDS that have failed or are not candidates for recombinant erythropoietin treatment.	Lenalidomide	23-31	erythropoietin	Homo sapiens	193-207
17076650-4	2006	Unlike cytokine therapy, lenalidomide suppresses select MDS clones and enhances erythropoietin receptor signaling to restore erythropoiesis.	Lenalidomide	25-37	erythropoietin	Homo sapiens	80-94
17076650-10	2006	A phase III Intergroup trial (ECOG 2905) will test the capacity to potentiate erythropoietin response by comparing response to lenalidomide monotherapy to the combination of darbepoetin and lenalidomide in non-deletion 5q MDS patients.	Lenalidomide	127-139	erythropoietin	Homo sapiens	78-92
17076650-10	2006	A phase III Intergroup trial (ECOG 2905) will test the capacity to potentiate erythropoietin response by comparing response to lenalidomide monotherapy to the combination of darbepoetin and lenalidomide in non-deletion 5q MDS patients.	Lenalidomide	190-202	erythropoietin	Homo sapiens	78-92
16569772-7	2006	Together these data demonstrate that LEN and its analogues enhance CD1d-mediated presentation of glycolipid antigens and support combining these agents with NKT targeted approaches for protection against tumors.	Lenalidomide	37-40	CD1d molecule	Homo sapiens	67-71
16494942-5	2006	In the most lenalidomide-sensitive chromosome 5 deleted cell line, Namalwa CSN.70, the compound induced G0/G1 cell cycle arrest, inhibited Akt and Gab1 phosphorylation, and inhibited the ability of Gab1 to associate with a receptor tyrosine kinase.	Lenalidomide	12-24	AKT serine/threonine kinase 1	Homo sapiens	139-142
16494942-5	2006	In the most lenalidomide-sensitive chromosome 5 deleted cell line, Namalwa CSN.70, the compound induced G0/G1 cell cycle arrest, inhibited Akt and Gab1 phosphorylation, and inhibited the ability of Gab1 to associate with a receptor tyrosine kinase.	Lenalidomide	12-24	GRB2 associated binding protein 1	Homo sapiens	147-151
16494942-5	2006	In the most lenalidomide-sensitive chromosome 5 deleted cell line, Namalwa CSN.70, the compound induced G0/G1 cell cycle arrest, inhibited Akt and Gab1 phosphorylation, and inhibited the ability of Gab1 to associate with a receptor tyrosine kinase.	Lenalidomide	12-24	GRB2 associated binding protein 1	Homo sapiens	198-202
16357183-0	2005	Immunomodulatory drug lenalidomide (CC-5013, IMiD3) augments anti-CD40 SGN-40-induced cytotoxicity in human multiple myeloma: clinical implications.	Lenalidomide	22-34	CD40 molecule	Homo sapiens	66-70
16735711-4	2006	Lenalidomide is particularly active in treating the anemia of del(5q) MDS, which is especially relevant given the low response rate to erythropoietin in this group of patients.	Lenalidomide	0-12	erythropoietin	Homo sapiens	135-149
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.	Lenalidomide	67-79	tumor necrosis factor	Mus musculus	135-144
16357183-7	2005	Lenalidomide also up-regulated CD40L on CD56(+)CD3(-) NK cells, facilitating IL-2-mediated activation of NK cells.	Lenalidomide	0-12	CD40 ligand	Homo sapiens	31-36
16357183-7	2005	Lenalidomide also up-regulated CD40L on CD56(+)CD3(-) NK cells, facilitating IL-2-mediated activation of NK cells.	Lenalidomide	0-12	neural cell adhesion molecule 1	Homo sapiens	40-44
16357183-7	2005	Lenalidomide also up-regulated CD40L on CD56(+)CD3(-) NK cells, facilitating IL-2-mediated activation of NK cells.	Lenalidomide	0-12	interleukin 2	Homo sapiens	77-81
16357183-8	2005	In addition, lenalidomide induced the CD56(dim) NK subset, which are more potent mediators of ADCC against target MM cells than the CD56(bright) NK subset.	Lenalidomide	13-25	neural cell adhesion molecule 1	Homo sapiens	38-42
16357183-9	2005	Finally, pretreatment of both effector and target MM cells with lenalidomide markedly enhanced SGN-40-mediated ADCC against CD40-expressing MM cells.	Lenalidomide	64-76	CD40 molecule	Homo sapiens	124-128
17124060-5	2006	Lenalidomide can lead to RBC transfusion independence in at least two thirds of cases of the 5q- syndrome, two thirds of those responses persisting after 2 years of treatment.	Lenalidomide	0-12	RNA, 7SL, cytoplasmic 263, pseudogene	Homo sapiens	25-28
16357183-2	2005	Here, we studied the clinical significance of an immunomodulatory drug lenalidomide on SGN-40-induced cytotoxicity against CD138(+)CD40(+) MM lines and patient MM cells.	Lenalidomide	71-83	CD40 molecule	Homo sapiens	131-135
16357183-4	2005	Combined lenalidomide and SGN-40 significantly induced MM apoptosis, evidenced by enhanced cleavage of caspase-3/8/poly(ADP-ribose)polymerase and increased sub-G(0) cells, compared with either single agent at the same doses.	Lenalidomide	9-21	poly(ADP-ribose) polymerase 1	Homo sapiens	103-141
16357183-5	2005	Pretreatment of effector cells with lenalidomide augmented SGN-40-induced MM cell lysis, associated with an increased number of CD56(+)CD3(-) natural killer (NK) cells expressing CD16 and LFA-1.	Lenalidomide	36-48	neural cell adhesion molecule 1	Homo sapiens	128-132
16357183-5	2005	Pretreatment of effector cells with lenalidomide augmented SGN-40-induced MM cell lysis, associated with an increased number of CD56(+)CD3(-) natural killer (NK) cells expressing CD16 and LFA-1.	Lenalidomide	36-48	Fc gamma receptor IIIa	Homo sapiens	179-183
16357183-5	2005	Pretreatment of effector cells with lenalidomide augmented SGN-40-induced MM cell lysis, associated with an increased number of CD56(+)CD3(-) natural killer (NK) cells expressing CD16 and LFA-1.	Lenalidomide	36-48	integrin subunit alpha L	Homo sapiens	188-193
15703420-13	2005	CONCLUSIONS: Lenalidomide has hematologic activity in patients with low-risk myelodysplastic syndromes who have no response to erythropoietin or who are unlikely to benefit from conventional therapy.	Lenalidomide	13-25	erythropoietin	Homo sapiens	127-141
16085015-8	2005	In nonclinical studies, the effects of lenalidomide include potentiation of clonogenic response to erythropoietin, activation of integrin-mediated adhesion, cell cycle arrest, sensitization to apoptotic signals, and abrogation of cellular response to receptor-initiated trophic signals.	Lenalidomide	39-51	erythropoietin	Homo sapiens	99-113
15797261-0	2005	Orally administered lenalidomide (CC-5013) is anti-angiogenic in vivo and inhibits endothelial cell migration and Akt phosphorylation in vitro.	Lenalidomide	20-32	AKT serine/threonine kinase 1	Rattus norvegicus	114-117
15797261-0	2005	Orally administered lenalidomide (CC-5013) is anti-angiogenic in vivo and inhibits endothelial cell migration and Akt phosphorylation in vitro.	Lenalidomide	34-41	AKT serine/threonine kinase 1	Rattus norvegicus	114-117
15797261-4	2005	We now show that oral administration of lenalidomide attenuates growth factor-induced angiogenesis in vivo; the rat mesenteric window assay was utilized to show that lenalidomide significantly inhibits vascularization in a dose-dependent manner.	Lenalidomide	40-52	myotrophin	Rattus norvegicus	64-77
15797261-4	2005	We now show that oral administration of lenalidomide attenuates growth factor-induced angiogenesis in vivo; the rat mesenteric window assay was utilized to show that lenalidomide significantly inhibits vascularization in a dose-dependent manner.	Lenalidomide	166-178	myotrophin	Rattus norvegicus	64-77
15797261-5	2005	We also found that lenalidomide significantly inhibits growth factor-induced endothelial cell migration.	Lenalidomide	19-31	myotrophin	Rattus norvegicus	55-68
15797261-6	2005	This correlates with the inhibitory effect of lenalidomide on growth factor-induced Akt phosphorylation, thereby providing a potential mechanism for its anti-migratory and subsequent anti-angiogenic effects.	Lenalidomide	46-58	myotrophin	Rattus norvegicus	62-75
15797261-6	2005	This correlates with the inhibitory effect of lenalidomide on growth factor-induced Akt phosphorylation, thereby providing a potential mechanism for its anti-migratory and subsequent anti-angiogenic effects.	Lenalidomide	46-58	AKT serine/threonine kinase 1	Rattus norvegicus	84-87
34952465-0	2022	Lenalidomide attenuates post-inflammation pulmonary fibrosis through blocking NF-kappaB signaling pathway.	Lenalidomide	0-12	nuclear factor kappa B subunit 1	Homo sapiens	78-87
33770460-7	2021	Combination of lenalidomide and rituximab has been a safe and effective immune modality for patients with refractory indolent lymphomas; it is currently being used as a backbone to bring other targeted agents such as tazemetostat (EZH2 inhibitor) into earlier lines of treatment.	Lenalidomide	15-27	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	231-235
32859220-5	2020	ATLL cell lines were also sensitive to lenalidomide, which repressed IRF4 expression.	Lenalidomide	39-51	interferon regulatory factor 4	Homo sapiens	69-73
32859220-8	2020	CONCLUSIONS: These data support the pursuit of IRF4 as a therapeutic target in ATLL with the use of either ASOs or lenalidomide.	Lenalidomide	115-127	interferon regulatory factor 4	Homo sapiens	47-51
34952465-8	2022	In vitro study revealed that lenalidomide inhibited NF-kappaB signaling in LPS-induced macrophage, and further attenuated macrophage-induced myofibroblast activation.	Lenalidomide	29-41	nuclear factor kappa B subunit 1	Homo sapiens	52-61
34952465-9	2022	Meanwhile, lenalidomide could inhibit TGF-beta1-induced myofibroblast activation through suppressing TGF-beta1 downstream MAPK signaling.	Lenalidomide	11-23	transforming growth factor beta 1	Homo sapiens	38-47
34952465-9	2022	Meanwhile, lenalidomide could inhibit TGF-beta1-induced myofibroblast activation through suppressing TGF-beta1 downstream MAPK signaling.	Lenalidomide	11-23	transforming growth factor beta 1	Homo sapiens	101-110
34952465-10	2022	In vivo study showed that lenalidomide inhibited pro-inflammatory cytokines TNF-alpha and IL-6 while enhanced anti-fibrotic cytokines IFN-gamma and IL-10 in bleomycin-induced inflammation model, and attenuated pulmonary fibrosis and collagen deposition in the following fibrosis stage.	Lenalidomide	26-38	tumor necrosis factor	Homo sapiens	76-85
34952465-10	2022	In vivo study showed that lenalidomide inhibited pro-inflammatory cytokines TNF-alpha and IL-6 while enhanced anti-fibrotic cytokines IFN-gamma and IL-10 in bleomycin-induced inflammation model, and attenuated pulmonary fibrosis and collagen deposition in the following fibrosis stage.	Lenalidomide	26-38	interleukin 6	Homo sapiens	90-94
34952465-10	2022	In vivo study showed that lenalidomide inhibited pro-inflammatory cytokines TNF-alpha and IL-6 while enhanced anti-fibrotic cytokines IFN-gamma and IL-10 in bleomycin-induced inflammation model, and attenuated pulmonary fibrosis and collagen deposition in the following fibrosis stage.	Lenalidomide	26-38	interferon gamma	Homo sapiens	134-143
34952465-10	2022	In vivo study showed that lenalidomide inhibited pro-inflammatory cytokines TNF-alpha and IL-6 while enhanced anti-fibrotic cytokines IFN-gamma and IL-10 in bleomycin-induced inflammation model, and attenuated pulmonary fibrosis and collagen deposition in the following fibrosis stage.	Lenalidomide	26-38	interleukin 10	Homo sapiens	148-153
34952465-11	2022	In conclusion, our results demonstrate that lenalidomide possesses potential anti-fibrotic effects through suppressing NF-kappaB signaling.	Lenalidomide	44-56	nuclear factor kappa B subunit 1	Homo sapiens	119-128
34936696-1	2022	Immunomodulatory (IMiD) agents like lenalidomide and pomalidomide induce the recruitment of IKZF1 and other targets to the CRL4CRBN E3 ubiquitin ligase, resulting in their ubiquitination and degradation.	Lenalidomide	36-48	IKAROS family zinc finger 1	Homo sapiens	92-97
34936696-9	2022	Moreover, lenalidomide-sensitive TCLs can acquire stable resistance via ZFP91 rewiring, which involves casein kinase 2 (CK2) mediated c-Jun inactivation.	Lenalidomide	10-22	ZFP91 zinc finger protein, atypical E3 ubiquitin ligase	Homo sapiens	72-77
34936696-9	2022	Moreover, lenalidomide-sensitive TCLs can acquire stable resistance via ZFP91 rewiring, which involves casein kinase 2 (CK2) mediated c-Jun inactivation.	Lenalidomide	10-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	134-139
34588172-0	2021	Caspase-8 regulates the anti-myeloma activity of bortezomib and lenalidomide.	Lenalidomide	64-76	caspase 8	Homo sapiens	0-9
34667029-0	2021	An allogeneic multiple myeloma GM-CSF-secreting vaccine with lenalidomide induces long-term immunity and durable clinical responses in patients in near complete remission.	Lenalidomide	61-73	colony stimulating factor 2	Homo sapiens	31-37
34674611-0	2021	Lenalidomide improves the antitumor activity of CAR-T cells directed toward the intracellular Wilms Tumor 1 antigen.	Lenalidomide	0-12	nuclear receptor subfamily 1, group I, member 3	Mus musculus	48-51
34674611-9	2021	Our data demonstrated that LEN improved the anti-tumor activity of CAR-T cells in vivo by increasing the infiltration of tumors with CD3+ and CD8+ T cells.	Lenalidomide	27-30	nuclear receptor subfamily 1, group I, member 3	Mus musculus	67-70
34674611-11	2021	CONCLUSION: These results demonstrate that lenalidomide potentiates WT1 CAR-T activity and paves the way to evaluate the combination of LEN with CAR-T for a planned clinical trial.	Lenalidomide	43-55	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-75
34588172-5	2021	Either inhibition or genetic depletion of CASP-8 decreased the CRBN cleavage upon Btz treatment, which could potentiate the anti-myeloma activity of IMiD lenalidomide (Len).	Lenalidomide	168-171	caspase 8	Homo sapiens	42-48
34588172-5	2021	Either inhibition or genetic depletion of CASP-8 decreased the CRBN cleavage upon Btz treatment, which could potentiate the anti-myeloma activity of IMiD lenalidomide (Len).	Lenalidomide	168-171	cereblon	Homo sapiens	63-67
34588172-6	2021	This work suggests that administration of CASP-8 inhibitors might enhance the overall effectiveness of Btz/Len-based therapeutic treatment for myeloma patients.	Lenalidomide	107-110	caspase 8	Homo sapiens	42-48
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	caspase 8	Homo sapiens	23-32
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	cereblon	Homo sapiens	97-105
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	IKAROS family zinc finger 1	Homo sapiens	230-235
34588172-7	2021	Significance Statement Caspase-8 activation upon bortezomib treatment results in the cleavage of cereblon, a substrate receptor of the cullin 4-RING E3 ligase, which is responsible for the degradation of two transcription factors IKZF1 and IKZF3 in the presence of immunomodulatory drugs including lenalidomide.	Lenalidomide	298-310	IKAROS family zinc finger 3	Homo sapiens	240-245
34588172-8	2021	The administration of caspase-8 inhibitor may enhance the anti-myeloma activity of the combination therapy with bortezomib and lenalidomide to multiple myeloma.	Lenalidomide	127-139	caspase 8	Homo sapiens	22-31
34151705-0	2021	Efficacy of lenalidomide in a patient with systemic mastocytosis associated with SF3B1-mutant myelodysplastic syndrome.	Lenalidomide	12-24	splicing factor 3b subunit 1	Homo sapiens	81-86
34885822-3	2021	In this study, a series of novel CRBN-recruiting HDAC PROTACs were designed and synthesized by linking hydroxamic acid and benzamide with lenalidomide, pomalidomide, and CC-220 through linkers of different lengths and types.	Lenalidomide	138-150	cereblon	Homo sapiens	33-37
34885822-3	2021	In this study, a series of novel CRBN-recruiting HDAC PROTACs were designed and synthesized by linking hydroxamic acid and benzamide with lenalidomide, pomalidomide, and CC-220 through linkers of different lengths and types.	Lenalidomide	138-150	histone deacetylase 9	Homo sapiens	49-53
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.	Lenalidomide	104-116	cereblon	Homo sapiens	38-42
34780623-2	2022	The CD30-targeted antibody-drug conjugate brentuximab vedotin (BV) and the immunomodulator lenalidomide (Len) have demonstrated promising activity as single agents in this population.	Lenalidomide	91-103	TNF receptor superfamily member 8	Homo sapiens	4-8
34780623-2	2022	The CD30-targeted antibody-drug conjugate brentuximab vedotin (BV) and the immunomodulator lenalidomide (Len) have demonstrated promising activity as single agents in this population.	Lenalidomide	105-108	TNF receptor superfamily member 8	Homo sapiens	4-8
34392531-6	2021	Moreover, CRBN depletion significantly impairs the ability of NK cells to migrate and reduces the enhancing effect of Lenalidomide on NK cell migration.	Lenalidomide	118-130	cereblon	Homo sapiens	10-14
34392531-9	2021	Altogether our data identify a critical role for CRBN in regulating NK cell functions and suggest that this protein may mediate the stimulatory effect of Lenalidomide on NK cells.	Lenalidomide	154-166	cereblon	Homo sapiens	49-53
34503111-8	2021	Notwithstanding, the mechanisms by which PIM kinases modulate the immune microenvironment and synergize with the immunomodulatory agents such as lenalidomide have not been deliberately depicted.	Lenalidomide	145-157	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	41-44
34341502-8	2021	Furthermore, treating the EOL-1 human eosinophilic cell line with lenalidomide yielded a dose-dependent decrease in Aiolos.	Lenalidomide	66-78	IKAROS family zinc finger 3	Homo sapiens	116-122
34455369-0	2021	Involvement of EZH2 inhibition in lenalidomide and pomalidomide-mediated growth suppression in HTLV-1-infected cells.	Lenalidomide	34-46	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	15-19
34455369-4	2021	In three of four tested HTLV-1-infected cell lines, the cells treated with lenalidomide or pomalidomide exhibited mild growth suppression without apoptosis, which was associated with decreased IRF4, c-Myc, and phosphorylated STAT3 levels as well as enhanced SOCS3 expression.	Lenalidomide	75-87	interferon regulatory factor 4	Homo sapiens	193-197
34455369-4	2021	In three of four tested HTLV-1-infected cell lines, the cells treated with lenalidomide or pomalidomide exhibited mild growth suppression without apoptosis, which was associated with decreased IRF4, c-Myc, and phosphorylated STAT3 levels as well as enhanced SOCS3 expression.	Lenalidomide	75-87	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	199-204
34455369-4	2021	In three of four tested HTLV-1-infected cell lines, the cells treated with lenalidomide or pomalidomide exhibited mild growth suppression without apoptosis, which was associated with decreased IRF4, c-Myc, and phosphorylated STAT3 levels as well as enhanced SOCS3 expression.	Lenalidomide	75-87	signal transducer and activator of transcription 3	Homo sapiens	225-230
34455369-4	2021	In three of four tested HTLV-1-infected cell lines, the cells treated with lenalidomide or pomalidomide exhibited mild growth suppression without apoptosis, which was associated with decreased IRF4, c-Myc, and phosphorylated STAT3 levels as well as enhanced SOCS3 expression.	Lenalidomide	75-87	suppressor of cytokine signaling 3	Homo sapiens	258-263
34680233-6	2021	We have found that lenalidomide-mediated degradation of IKZF1 leads to activation of the G protein-coupled receptor 68 (GPR68)/calcium/calpain pro-apoptotic pathway and inhibition of the regulator of calcineurin 1 (RCAN1)/calcineurin pro-survival pathway in MDS and acute myeloid leukemia (AML).	Lenalidomide	19-31	IKAROS family zinc finger 1	Homo sapiens	56-61
34680233-6	2021	We have found that lenalidomide-mediated degradation of IKZF1 leads to activation of the G protein-coupled receptor 68 (GPR68)/calcium/calpain pro-apoptotic pathway and inhibition of the regulator of calcineurin 1 (RCAN1)/calcineurin pro-survival pathway in MDS and acute myeloid leukemia (AML).	Lenalidomide	19-31	G protein-coupled receptor 68	Homo sapiens	89-118
34680233-6	2021	We have found that lenalidomide-mediated degradation of IKZF1 leads to activation of the G protein-coupled receptor 68 (GPR68)/calcium/calpain pro-apoptotic pathway and inhibition of the regulator of calcineurin 1 (RCAN1)/calcineurin pro-survival pathway in MDS and acute myeloid leukemia (AML).	Lenalidomide	19-31	G protein-coupled receptor 68	Homo sapiens	120-125
34680233-6	2021	We have found that lenalidomide-mediated degradation of IKZF1 leads to activation of the G protein-coupled receptor 68 (GPR68)/calcium/calpain pro-apoptotic pathway and inhibition of the regulator of calcineurin 1 (RCAN1)/calcineurin pro-survival pathway in MDS and acute myeloid leukemia (AML).	Lenalidomide	19-31	regulator of calcineurin 1	Homo sapiens	187-213
34680233-6	2021	We have found that lenalidomide-mediated degradation of IKZF1 leads to activation of the G protein-coupled receptor 68 (GPR68)/calcium/calpain pro-apoptotic pathway and inhibition of the regulator of calcineurin 1 (RCAN1)/calcineurin pro-survival pathway in MDS and acute myeloid leukemia (AML).	Lenalidomide	19-31	regulator of calcineurin 1	Homo sapiens	215-220
34583995-9	2021	Notably, USP15 is highly expressed in IMiD-resistant cells, and depletion of USP15 sensitizes these cells to lenalidomide.	Lenalidomide	109-121	ubiquitin specific peptidase 15	Homo sapiens	9-14
34583995-9	2021	Notably, USP15 is highly expressed in IMiD-resistant cells, and depletion of USP15 sensitizes these cells to lenalidomide.	Lenalidomide	109-121	ubiquitin specific peptidase 15	Homo sapiens	77-82
34503175-0	2021	miR-22 Modulates Lenalidomide Activity by Counteracting MYC Addiction in Multiple Myeloma.	Lenalidomide	17-29	microRNA 22	Homo sapiens	0-6
34503175-8	2021	Interestingly, we found that IMiD lenalidomide increases miR-22 expression by reducing MYC repression and, most importantly, that the combination of lenalidomide with miR-22 mimics results in a synergistic direct and NK-mediated cytotoxic activity.	Lenalidomide	34-46	microRNA 22	Homo sapiens	57-63
34503175-8	2021	Interestingly, we found that IMiD lenalidomide increases miR-22 expression by reducing MYC repression and, most importantly, that the combination of lenalidomide with miR-22 mimics results in a synergistic direct and NK-mediated cytotoxic activity.	Lenalidomide	34-46	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	87-90
34503175-8	2021	Interestingly, we found that IMiD lenalidomide increases miR-22 expression by reducing MYC repression and, most importantly, that the combination of lenalidomide with miR-22 mimics results in a synergistic direct and NK-mediated cytotoxic activity.	Lenalidomide	149-161	microRNA 22	Homo sapiens	57-63
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	140-152	microRNA 22	Homo sapiens	65-71
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	140-152	microRNA 22	Homo sapiens	186-192
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	140-152	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	201-204
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	304-316	microRNA 22	Homo sapiens	65-71
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	304-316	microRNA 22	Homo sapiens	186-192
34503175-9	2021	Conclusions: Taken together, our findings indicate that: (1) low miR-22 expression could represent a potential predictive biomarker of poor lenalidomide response in MM patients; and (2) miR-22 reduces MYC oncogenic activity, thus triggering a novel synthetic lethality loop, which sensitizes MM cells to lenalidomide.	Lenalidomide	304-316	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	201-204
34733611-4	2021	These peculiar mechanisms of action make TCL an attractive target for lenalidomide.	Lenalidomide	70-82	ras homolog family member J	Homo sapiens	41-44
34733611-5	2021	We have identified five clinical trials in which lenalidomide monotherapy was investigated to treat TCL, including cutaneous TCL (CTCL) and adult T-cell lymphoma/leukemia (ATLL).	Lenalidomide	49-61	ras homolog family member J	Homo sapiens	100-103
34733611-5	2021	We have identified five clinical trials in which lenalidomide monotherapy was investigated to treat TCL, including cutaneous TCL (CTCL) and adult T-cell lymphoma/leukemia (ATLL).	Lenalidomide	49-61	ras homolog family member J	Homo sapiens	125-128
34733611-11	2021	In conclusion, lenalidomide could represent a suitable treatment option for relapsed/refractory TCL, especially for neoplasms with a T-follicular helper origin, such as angioimmunoblastic TCL.	Lenalidomide	15-27	ras homolog family member J	Homo sapiens	96-99
34680570-0	2021	Lenalidomide and Pomalidomide Improve Function and Induce FcgammaRI/CD64 in Multiple Myeloma Neutrophils.	Lenalidomide	0-12	Fc gamma receptor Ia	Homo sapiens	58-67
34680570-0	2021	Lenalidomide and Pomalidomide Improve Function and Induce FcgammaRI/CD64 in Multiple Myeloma Neutrophils.	Lenalidomide	0-12	Fc gamma receptor Ia	Homo sapiens	68-72
34680570-10	2021	Similarly, in NDMM patients, lenalidomide but not bortezomib upregulated FcgammaRI/CD64 expression, improving phagocytic activity and oxidative bursta as tested in vitro.	Lenalidomide	29-41	Fc gamma receptor Ia	Homo sapiens	73-82
34680570-10	2021	Similarly, in NDMM patients, lenalidomide but not bortezomib upregulated FcgammaRI/CD64 expression, improving phagocytic activity and oxidative bursta as tested in vitro.	Lenalidomide	29-41	Fc gamma receptor Ia	Homo sapiens	83-87
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.	Lenalidomide	28-40	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.	Lenalidomide	28-40	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.	Lenalidomide	28-40	interleukin 6	Rattus norvegicus	148-152
34552051-6	2021	Lenalidomide refractoriness at first relapse was associated with inferior PFS2 (8.1 (95% CI: 6.4, 9.9) months vs. 19.9 (95% CI: 9.7, 30.2; p = 0.002) months in nonrefractory patients).	Lenalidomide	0-12	GINS complex subunit 2	Homo sapiens	74-78
34262292-14	2021	Chidamide enhanced the effect of lenalidomide-induced degradation of IKZF1 and IKZF3 by elevating H2O2.	Lenalidomide	33-45	IKAROS family zinc finger 1	Mus musculus	69-74
34316334-2	2021	Cereblon (CRBN)-targeting immunomodulatory agents (IMiDs ) lenalidomide (LEN) and pomalidomide (POM) play a central role in combination regimens due to their pleiotropic antitumor/immunomodulatory mechanisms that synergize with many anti-myeloma approved or developmental agents.	Lenalidomide	59-71	cereblon	Homo sapiens	10-14
34316334-2	2021	Cereblon (CRBN)-targeting immunomodulatory agents (IMiDs ) lenalidomide (LEN) and pomalidomide (POM) play a central role in combination regimens due to their pleiotropic antitumor/immunomodulatory mechanisms that synergize with many anti-myeloma approved or developmental agents.	Lenalidomide	73-76	cereblon	Homo sapiens	10-14
34405005-10	2021	Our results also suggested that lenalidomide might relieve relapsed lymphoma with mutations in NFKBIA 202C>T (p.Q68*) and NFKBIE 433A>T (p.K145*) by targeting NF-Kappa B signaling.	Lenalidomide	32-44	NFKB inhibitor epsilon	Homo sapiens	122-128
34405005-10	2021	Our results also suggested that lenalidomide might relieve relapsed lymphoma with mutations in NFKBIA 202C>T (p.Q68*) and NFKBIE 433A>T (p.K145*) by targeting NF-Kappa B signaling.	Lenalidomide	32-44	nuclear factor kappa B subunit 1	Homo sapiens	159-169
34262292-14	2021	Chidamide enhanced the effect of lenalidomide-induced degradation of IKZF1 and IKZF3 by elevating H2O2.	Lenalidomide	33-45	IKAROS family zinc finger 3	Mus musculus	79-84
34395218-16	2021	However, the NMDAR antagonist MK-801 (0.01 mg/kg, i.p) significantly reversed the anticonvulsive effects of lenalidomide (10 mg/kg).	Lenalidomide	108-120	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	13-18
34395218-17	2021	Conclusions: Our study demonstrated a role for the NMDAR/NO pathway in the anticonvulsive effects of lenalidomide on the PTZ-induced clonic seizures in mice.	Lenalidomide	101-113	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	51-56
34168051-4	2021	The sensitizing effect of IKZF1 loss-of-function was then validated and leveraged for combination treatment with lenalidomide.	Lenalidomide	113-125	IKAROS family zinc finger 1	Homo sapiens	26-31
34168051-7	2021	Treating cells with tazemetostat and lenalidomide, an immunomodulatory drug that selectively degrades Ikaros and Aiolos, phenocopied the effects of the CRISPR/Cas9 screen.	Lenalidomide	37-49	IKAROS family zinc finger 1	Homo sapiens	102-108
34168051-7	2021	Treating cells with tazemetostat and lenalidomide, an immunomodulatory drug that selectively degrades Ikaros and Aiolos, phenocopied the effects of the CRISPR/Cas9 screen.	Lenalidomide	37-49	IKAROS family zinc finger 3	Homo sapiens	113-119
34168051-11	2021	Gene expression of key immune response factors such as IRF7 and DDX58 were induced in cells treated with lenalidomide and tazemetostat, with a concomitant increase of H3K27 acetylation at their promoters.	Lenalidomide	105-117	interferon regulatory factor 7	Homo sapiens	55-59
34168051-11	2021	Gene expression of key immune response factors such as IRF7 and DDX58 were induced in cells treated with lenalidomide and tazemetostat, with a concomitant increase of H3K27 acetylation at their promoters.	Lenalidomide	105-117	DExD/H-box helicase 58	Homo sapiens	64-69
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.	Lenalidomide	206-218	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.	Lenalidomide	206-218	cereblon	Homo sapiens	42-46
34117218-2	2021	We found that lenalidomide (LEN), a representative of immunomodulatory drugs (IMiDs), which have been long used for the treatment of multiple myeloma, specifically induced accumulation of Ik6 with the disappearance of functional isoforms within 24 h (i.e., abrupt and complete shut-down of the IKZF1 activity) in Ik6-positive Ph+ALL cells in a neddylation-dependent manner.	Lenalidomide	14-26	IKAROS family zinc finger 1	Homo sapiens	294-299
34117218-2	2021	We found that lenalidomide (LEN), a representative of immunomodulatory drugs (IMiDs), which have been long used for the treatment of multiple myeloma, specifically induced accumulation of Ik6 with the disappearance of functional isoforms within 24 h (i.e., abrupt and complete shut-down of the IKZF1 activity) in Ik6-positive Ph+ALL cells in a neddylation-dependent manner.	Lenalidomide	28-31	IKAROS family zinc finger 1	Homo sapiens	294-299
34088671-4	2021	RNA sequencing of MM patient samples shows nearly universal ERK pathway activation at relapse on lenalidomide maintenance therapy, confirming its clinical relevance.	Lenalidomide	97-109	mitogen-activated protein kinase 1	Homo sapiens	60-63
35359004-0	2022	SIRPalpha+ macrophages are increased in patients with FL who progress or relapse after frontline lenalidomide and rituximab.	Lenalidomide	97-109	signal regulatory protein alpha	Homo sapiens	0-9
35583604-1	2022	PURPOSE: Cereblon (CRBN), a substrate receptor of the E3 ubiquitin ligase complex CRL4CRBN, is the target of the small molecules lenalidomide (Len) and avadomide (Ava).	Lenalidomide	129-141	cereblon	Homo sapiens	19-23
35467582-0	2022	Combination Therapy of an Antibody Specific for Transferrin Receptor 1 (ch128.1/IgG1) With Bortezomib or Lenalidomide Results in Increased Survival in an In Vivo Model of Human Multiple Myeloma: A Brief Communication.	Lenalidomide	105-117	transferrin receptor	Homo sapiens	48-70
35467582-0	2022	Combination Therapy of an Antibody Specific for Transferrin Receptor 1 (ch128.1/IgG1) With Bortezomib or Lenalidomide Results in Increased Survival in an In Vivo Model of Human Multiple Myeloma: A Brief Communication.	Lenalidomide	105-117	LOC105243590	Mus musculus	80-84
35583604-1	2022	PURPOSE: Cereblon (CRBN), a substrate receptor of the E3 ubiquitin ligase complex CRL4CRBN, is the target of the small molecules lenalidomide (Len) and avadomide (Ava).	Lenalidomide	129-141	interleukin 17 receptor B	Homo sapiens	82-90
35583604-1	2022	PURPOSE: Cereblon (CRBN), a substrate receptor of the E3 ubiquitin ligase complex CRL4CRBN, is the target of the small molecules lenalidomide (Len) and avadomide (Ava).	Lenalidomide	143-146	cereblon	Homo sapiens	19-23
35583604-1	2022	PURPOSE: Cereblon (CRBN), a substrate receptor of the E3 ubiquitin ligase complex CRL4CRBN, is the target of the small molecules lenalidomide (Len) and avadomide (Ava).	Lenalidomide	143-146	interleukin 17 receptor B	Homo sapiens	82-90
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.	Lenalidomide	103-115	ribosomal protein L34	Homo sapiens	177-204
35586751-7	2022	Moreover, we speculate that lenalidomide improves cognitive function by regulating intracranial inflammation via multiple pathways, not only by TNF-alpha blocking.	Lenalidomide	28-40	tumor necrosis factor	Homo sapiens	144-153
35512188-0	2022	Lenalidomide promotes the development of TP53-mutated therapy-related myeloid neoplasms.	Lenalidomide	0-12	tumor protein p53	Homo sapiens	41-45
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.	Lenalidomide	207-219	tumor protein p53	Homo sapiens	102-106
35512188-4	2022	We demonstrated experimentally that lenalidomide treatment provides a selective advantage to Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) in vitro and in vivo, the effect of which was specific to Trp53-mutant HSPCs and was not observed in HSPCs with other CH mutations.	Lenalidomide	36-48	tumor protein p53	Homo sapiens	93-98
35512188-4	2022	We demonstrated experimentally that lenalidomide treatment provides a selective advantage to Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) in vitro and in vivo, the effect of which was specific to Trp53-mutant HSPCs and was not observed in HSPCs with other CH mutations.	Lenalidomide	36-48	tumor protein p53	Homo sapiens	212-217
35512188-6	2022	These findings highlight the role of lenalidomide treatment in promoting TP53-mutated t-MNs and offer a potential alternative strategy to mitigate the risk of t-MN development.	Lenalidomide	37-49	tumor protein p53	Homo sapiens	73-77
35064823-1	2022	PURPOSE: This study sought to compare the efficacy of prophylactic long-acting and standard granulocyte colony-stimulating factor (G-CSF) on febrile neutropenia, early infections, and treatment delay in patients with newly diagnosed multiple myeloma (MM) receiving the therapeutic regimen of bortezomib, lenalidomide, and dexamethasone (VRd).	Lenalidomide	304-316	colony stimulating factor 3	Homo sapiens	131-136
34979567-0	2022	SORT1/LAMP2-mediated Extracellular Vesicle Secretion and Cell Adhesion Are Linked to Lenalidomide Resistance in Multiple Myeloma.	Lenalidomide	85-97	sortilin 1	Homo sapiens	0-5
34979567-0	2022	SORT1/LAMP2-mediated Extracellular Vesicle Secretion and Cell Adhesion Are Linked to Lenalidomide Resistance in Multiple Myeloma.	Lenalidomide	85-97	lysosomal associated membrane protein 2	Homo sapiens	6-11
34979567-8	2022	Together, our findings reveal a novel mechanism of lenalidomide resistance in MM mediated by EV secretion and cell adhesion via SORT1 and LAMP2.	Lenalidomide	51-63	sortilin 1	Homo sapiens	128-133
34979567-8	2022	Together, our findings reveal a novel mechanism of lenalidomide resistance in MM mediated by EV secretion and cell adhesion via SORT1 and LAMP2.	Lenalidomide	51-63	lysosomal associated membrane protein 2	Homo sapiens	138-143
35380709-8	2022	RSK2 or CREB1 inhibition increased CRBN levels and were synergic with lenalidomide in inducing cell death, especially in CD56-expressing MM cells.	Lenalidomide	70-82	ribosomal protein S6 kinase A3	Homo sapiens	0-4
35380709-8	2022	RSK2 or CREB1 inhibition increased CRBN levels and were synergic with lenalidomide in inducing cell death, especially in CD56-expressing MM cells.	Lenalidomide	70-82	cAMP responsive element binding protein 1	Homo sapiens	8-13
35380709-8	2022	RSK2 or CREB1 inhibition increased CRBN levels and were synergic with lenalidomide in inducing cell death, especially in CD56-expressing MM cells.	Lenalidomide	70-82	cereblon	Homo sapiens	35-39
35380709-8	2022	RSK2 or CREB1 inhibition increased CRBN levels and were synergic with lenalidomide in inducing cell death, especially in CD56-expressing MM cells.	Lenalidomide	70-82	neural cell adhesion molecule 1	Homo sapiens	121-125
35433994-7	2022	In order to understand the possible mechanisms of lenalidomide in CAR-T therapy, CAR-T copies of peripheral blood were regularly detected by quantitative real-time polymerase chain reaction, and an in vitro test was also conducted.	Lenalidomide	50-62	CXADR pseudogene 1	Homo sapiens	66-69
35089607-1	2022	In the phase 3 APOLLO trial, daratumumab in combination with pomalidomide and dexamethasone (D-Pd) significantly reduced the rate of disease progression or death by 37% relative to Pd alone in patients with relapsed/refractory multiple myeloma (RRMM) who had received >=1 prior line of therapy including lenalidomide and a proteasome inhibitor.	Lenalidomide	304-316	dihydropyrimidine dehydrogenase	Homo sapiens	93-97
35194739-0	2022	Integrin beta5 and beta7 expression in lenalidomide-resistant multiple myeloma cells.	Lenalidomide	39-51	integrin subunit beta 5	Homo sapiens	0-14
35194739-0	2022	Integrin beta5 and beta7 expression in lenalidomide-resistant multiple myeloma cells.	Lenalidomide	39-51	immunoglobulin kappa variable 2D-24 (non-functional)	Homo sapiens	19-24
35338347-6	2022	Overexpression of IRF4 and c-Myc is a major mechanism of Len resistance.	Lenalidomide	57-60	interferon regulatory factor 4	Homo sapiens	18-22
35338347-6	2022	Overexpression of IRF4 and c-Myc is a major mechanism of Len resistance.	Lenalidomide	57-60	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-32
35321428-3	2022	Bortezomib and lenalidomide activate caspase-8 and promote the apoptosis of myeloma cells.	Lenalidomide	15-27	caspase 8	Homo sapiens	37-46
35321428-4	2022	However, caspase-8 inhibition potentiated the antiproliferative effect of lenalidomide and bortezomib in myeloma cells, suggesting that caspase-8 could regulate proliferation and apoptosis in the opposite pathway.	Lenalidomide	74-86	caspase 8	Homo sapiens	136-145
35433994-7	2022	In order to understand the possible mechanisms of lenalidomide in CAR-T therapy, CAR-T copies of peripheral blood were regularly detected by quantitative real-time polymerase chain reaction, and an in vitro test was also conducted.	Lenalidomide	50-62	CXADR pseudogene 1	Homo sapiens	81-84
35433994-9	2022	Furthermore, one case responding to CAR-T therapy initially but suffering a relapse shortly achieved complete remission again after lenalidomide exposure, with an increase in the number of CAR-T copies detected.	Lenalidomide	132-144	CXADR pseudogene 1	Homo sapiens	36-39
35433994-10	2022	The in vitro test showed that lenalidomide could delay the exhaustion of CAR-T cells.	Lenalidomide	30-42	CXADR pseudogene 1	Homo sapiens	73-76
35433994-12	2022	We confirmed that lenalidomide maintenance can improve patients" OS, and the delayed exhaustion of CAR-T cells may contribute to this OS benefit.	Lenalidomide	18-30	CXADR pseudogene 1	Homo sapiens	99-102
35197447-0	2022	Proteomic profiling reveals CDK6 upregulation as a targetable resistance mechanism for lenalidomide in multiple myeloma.	Lenalidomide	87-99	cyclin dependent kinase 6	Homo sapiens	28-32
35092513-6	2022	CDK9 inhibitors were able to induce dose-dependent cytotoxicity in Doxorubicin-resistant, Lenalidomide-resistant and Bortezomib-resistant cell lines.	Lenalidomide	90-102	cyclin dependent kinase 9	Homo sapiens	0-4
35092513-9	2022	Synergistic effects between CDK9 inhibitors and either Venetoclax, Bortezomib, Lenalidomide or Erlotinib have been proven and are awaiting verification in clinical trials.	Lenalidomide	79-91	cyclin dependent kinase 9	Homo sapiens	28-32
34768284-0	2022	MCT1 is a Predictive Marker for Lenalidomide Maintenance Therapy in Multiple Myeloma.	Lenalidomide	32-44	solute carrier family 16 member 1	Homo sapiens	0-4
34768284-4	2022	Patients with high gene expression levels of MCT1 showed significantly reduced PFS (31.9 vs. 48.2 months in MCT1high vs. MCT1low, P=.03) and OS (75.9 months vs. not reached (NR) months in MCT1high vs. MCT1low; P=.001) in case of lenalidomide maintenance, whereas MCT1 expression had no significant impact on PFS or OS in patients with bortezomib maintenance.	Lenalidomide	229-241	solute carrier family 16 member 1	Homo sapiens	45-49
34768284-6	2022	Functional validation showed that MCT1 overexpression in human MM cell lines significantly reduced efficacy of lenalidomide, while no change was observed upon bortezomib treatment, both in vitro and in an MM xenograft model.	Lenalidomide	111-123	solute carrier family 16 member 1	Homo sapiens	34-38
34768284-7	2022	Together, we establish MCT1-expression as a predictive marker for response to lenalidomide-based maintenance treatment.	Lenalidomide	78-90	solute carrier family 16 member 1	Homo sapiens	23-27
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.	Lenalidomide	25-37	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.	Lenalidomide	25-37	interleukin 17 receptor B	Homo sapiens	156-160
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.	Lenalidomide	39-42	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.	Lenalidomide	39-42	interleukin 17 receptor B	Homo sapiens	156-160
34978798-5	2022	eIF3i is directly labeled by pLen and forms a ternary complex with CRBN in the presence of Len across several epithelial cell lines but is itself not ubiquitylated or degraded.	Lenalidomide	91-94	eukaryotic translation initiation factor 3 subunit I	Homo sapiens	0-5
34978798-5	2022	eIF3i is directly labeled by pLen and forms a ternary complex with CRBN in the presence of Len across several epithelial cell lines but is itself not ubiquitylated or degraded.	Lenalidomide	91-94	cereblon	Homo sapiens	67-71