PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 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. Panobinostat 13-25 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 166-171 28193631-6 2017 Here, we show that several other human NPC1 mutant fibroblast cell lines can also be corrected by vorinostat or panobinostat and that treatment with vorinostat extends the lifetime of the NPC1I1061T protein. Panobinostat 112-124 NPC intracellular cholesterol transporter 1 Homo sapiens 39-43 27226420-9 2017 Both cytochrome p450 (CYP) 3A4 and non-CYP mechanisms govern the clearance of panobinostat. Panobinostat 78-90 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 5-20 27226420-9 2017 Both cytochrome p450 (CYP) 3A4 and non-CYP mechanisms govern the clearance of panobinostat. Panobinostat 78-90 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 22-25 27226420-9 2017 Both cytochrome p450 (CYP) 3A4 and non-CYP mechanisms govern the clearance of panobinostat. Panobinostat 78-90 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 39-42 27226420-10 2017 CYP3A4-related drug-drug interactions with panobinostat have been documented with ketoconazole (inhibitor) and dexamethasone (inducer). Panobinostat 43-55 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 0-6 28147319-4 2017 This means that co-treatment with mevastatin and LBH589 activated LKB1/AMPK signaling and subsequently inhibited mTOR. Panobinostat 49-55 serine/threonine kinase 11 Mus musculus 66-70 28147319-4 2017 This means that co-treatment with mevastatin and LBH589 activated LKB1/AMPK signaling and subsequently inhibited mTOR. Panobinostat 49-55 mechanistic target of rapamycin kinase Mus musculus 113-117 28019030-4 2017 STUDY DESIGN AND METHODS: Quantitative polymerase chain reactions were carried out for the ABO transcripts in erythroid-lineage K562 and epithelial-lineage KATOIII cells after incubation with HDACIs, such as sodium butyrate, panobinostat, vorinostat, and sodium valproate. Panobinostat 225-237 ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase Homo sapiens 91-94 27935859-4 2017 We found that pan- HDACIs (vorinostat and panobinostat) inhibited the migration of CTCL cells and downregulated CCR6. Panobinostat 42-54 TSPY like 2 Homo sapiens 83-87 27935859-4 2017 We found that pan- HDACIs (vorinostat and panobinostat) inhibited the migration of CTCL cells and downregulated CCR6. Panobinostat 42-54 chemokine (C-C motif) receptor 6 Mus musculus 112-116 27738323-6 2016 Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. Panobinostat 87-99 caspase 8 Homo sapiens 16-25 27802904-9 2016 In addition, panobinostat also showed synergistic effect with topoisomerase inhibitors mediated by increased activation of caspase-3/7 activity compared to that in cells treated with panobinostat alone. Panobinostat 13-25 caspase 3 Homo sapiens 123-132 27802904-9 2016 In addition, panobinostat also showed synergistic effect with topoisomerase inhibitors mediated by increased activation of caspase-3/7 activity compared to that in cells treated with panobinostat alone. Panobinostat 183-195 caspase 3 Homo sapiens 123-132 27738323-6 2016 Addition of the caspase-8 inhibitor z-IETD-FMK abolished the Sp1 reduction not only by panobinostat alone but also by its combination with bortezomib, suggesting caspase-8-mediated Sp1 degradation. Panobinostat 87-99 caspase 8 Homo sapiens 162-171 27738323-9 2016 Collectively, caspase-8-mediated post-translational Sp1 degradation appears to be among major mechanisms for synergistic anti-MM effects of panobinostat and proteasome inhibitors in combination. Panobinostat 140-152 caspase 8 Homo sapiens 14-23 27245095-4 2016 Our patient developed inoperable progressive lung metastases and was treated with the HDAC inhibitor panobinostat. Panobinostat 101-113 histone deacetylase 9 Homo sapiens 86-90 27554046-8 2016 Panobinostat inhibited MM cell growth by degrading protein phosphatase 3 catalytic subunit alpha (PPP3CA), a catalytic subunit of calcineurin. Panobinostat 0-12 protein phosphatase 3 catalytic subunit alpha Homo sapiens 51-96 27554046-8 2016 Panobinostat inhibited MM cell growth by degrading protein phosphatase 3 catalytic subunit alpha (PPP3CA), a catalytic subunit of calcineurin. Panobinostat 0-12 protein phosphatase 3 catalytic subunit alpha Homo sapiens 98-104 27279362-8 2016 Chromatin immunoprecipitation assay confirmed an enhanced binding of HDAC3 to the sGCbeta1 proximal promoter, which could be reversed by panobinostat (LBH-589) treatment. Panobinostat 137-149 histone deacetylase 3 Homo sapiens 69-74 26640144-6 2016 Knockdown of HMGA2, or suppressing HMGA2 expression with the histone deacetylase inhibitor LBH589, inhibits epithelial-mesenchymal plasticity and stemness activities in vitro and markedly reduces tumor growth and metastasis in vivo through successful targeting of EMT and mesenchymal-like tumor cells. Panobinostat 91-97 high mobility group AT-hook 2 Homo sapiens 35-40 27239721-4 2016 Till date, four drugs, namely Vorinostat (SAHA), Romidepsin (FK-228), Belinostat (PXD-101) and Panobinostat (LBH-589) have been granted FDA approval for cancer and several HDAC inhibitors are currently in various phases of clinical trials, either as monotherapy and/or in combination with existing/novel anticancer agents. Panobinostat 95-107 histone deacetylase 9 Homo sapiens 172-176 26640144-7 2016 Importantly, LBH589 treatment in combination with castration prevents mCRPC development and significantly prolongs survival following castration by enhancing p53 and androgen receptor acetylation and in turn sensitizing castration-resistant mesenchymal-like tumor cells to androgen deprivation therapy. Panobinostat 13-19 tumor protein p53 Homo sapiens 158-161 26727990-7 2016 In this study, we have found that vorinostat and panobinostat activate P-TEFb in resting primary CD4(+) T cells through induction of CDK9 T-loop phosphorylation. Panobinostat 49-61 CD4 molecule Homo sapiens 97-100 27261467-15 2016 CONCLUSION: The HDAC inhibitor panobinostat has a high stable disease rate and reasonable PFS in low-grade NET, but has a low response rate. Panobinostat 31-43 histone deacetylase 9 Homo sapiens 16-20 27058414-8 2016 Map1LC3B and Beclin1 were significantly over-expressed in HepG2 xenografts in nude mice treated with panobinostat for 4 weeks. Panobinostat 101-113 microtubule-associated protein 1 light chain 3 beta Mus musculus 0-8 27058414-8 2016 Map1LC3B and Beclin1 were significantly over-expressed in HepG2 xenografts in nude mice treated with panobinostat for 4 weeks. Panobinostat 101-113 beclin 1, autophagy related Mus musculus 13-20 26733615-0 2016 The Bromodomain Inhibitor JQ1 and the Histone Deacetylase Inhibitor Panobinostat Synergistically Reduce N-Myc Expression and Induce Anticancer Effects. Panobinostat 68-80 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 104-109 27699258-0 2016 Histone deacetylase inhibitor panobinostat induces calcineurin degradation in multiple myeloma. Panobinostat 30-42 histone deacetylase 9 Homo sapiens 0-19 27699258-2 2016 Addition of panobinostat, a histone deacetylase (HDAC) inhibitor, to bortezomib and dexamethasone improved progression-free survival (PFS) in relapsed and refractory MM patients. Panobinostat 12-24 histone deacetylase 9 Homo sapiens 28-47 27699258-2 2016 Addition of panobinostat, a histone deacetylase (HDAC) inhibitor, to bortezomib and dexamethasone improved progression-free survival (PFS) in relapsed and refractory MM patients. Panobinostat 12-24 histone deacetylase 9 Homo sapiens 49-53 27166836-11 2016 In conclusion, panobinostat enhanced the cytotoxicity of ponatinib towards IM-resistant CML cells including those with T315I-mutated BCR-ABL. Panobinostat 15-27 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 133-140 26914605-0 2016 Long term, continuous exposure to panobinostat induces terminal differentiation and long term survival in the TH-MYCN neuroblastoma mouse model. Panobinostat 34-46 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 113-117 26914605-7 2016 Continuous treatment of tumor bearing TH-MYCN transgenic mice with panobinostat for nine weeks led to a significant improvement in survival as compared with mice treated with panobinostat for a three-week period. Panobinostat 67-79 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 41-45 25589513-13 2016 The HDAC inhibitor, panobinostat and the potent HDAC inhibitor, ITF-B, also decreased ex vivo C16.0+MSU-induced IL-1beta production. Panobinostat 20-32 histone deacetylase 9 Homo sapiens 4-8 25589513-13 2016 The HDAC inhibitor, panobinostat and the potent HDAC inhibitor, ITF-B, also decreased ex vivo C16.0+MSU-induced IL-1beta production. Panobinostat 20-32 interleukin 1 beta Homo sapiens 112-120 26727990-11 2016 We conclude that the ability of vorinostat and panobinostat to induce latent HIV is, in part, likely due to the ability of the broad-spectrum HDACis to upregulate P-TEFb through increased CDK9 T-loop phosphorylation. Panobinostat 47-59 cyclin dependent kinase 9 Homo sapiens 188-192 26727990-7 2016 In this study, we have found that vorinostat and panobinostat activate P-TEFb in resting primary CD4(+) T cells through induction of CDK9 T-loop phosphorylation. Panobinostat 49-61 cyclin dependent kinase 9 Homo sapiens 133-137 26727990-10 2016 Vorinostat and panobinostat treatment of cells harboring latent HIV increased CDK9 T-loop phosphorylation and reactivation of latent virus, whereas tacedinaline and romidepsin failed to induce T-loop phosphorylation or reactivate latent virus. Panobinostat 15-27 cyclin dependent kinase 9 Homo sapiens 78-82 26675484-0 2015 The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells. Panobinostat 23-35 histone deacetylase 9 Homo sapiens 8-12 26498249-6 2015 Inhibition of multiple HDAC by the general inhibitors panobinostat or trichostatin provided protection against LPS-induced transendothelial hyperpermeability, acetylated and suppressed Hsp90 chaperone function, and attenuated RhoA activity and signaling crucial to endothelial barrier function. Panobinostat 54-66 heat shock protein, 3 Mus musculus 185-190 26498249-6 2015 Inhibition of multiple HDAC by the general inhibitors panobinostat or trichostatin provided protection against LPS-induced transendothelial hyperpermeability, acetylated and suppressed Hsp90 chaperone function, and attenuated RhoA activity and signaling crucial to endothelial barrier function. Panobinostat 54-66 ras homolog family member A Mus musculus 226-230 26447190-2 2015 Vorinostat, romidepsin, belinostat, and panobinostat are Food and Drug Administration-approved for hematological malignancies and inhibit class II and/or class I HDACs, including HDAC1, 2, 3, and 6. Panobinostat 40-52 histone deacetylase 1 Mus musculus 179-197 26848406-14 2015 Treatment of THP-1 cells (represents M5-subtype) with HDAC inhibitors AR-42, Panobinostat, or Decitabine showed miR-199b expression was significantly elevated upon AR-42 and Panobinostat treatment. Panobinostat 77-89 microRNA 199b Homo sapiens 112-120 26675484-0 2015 The pan-HDAC inhibitor panobinostat acts as a sensitizer for erlotinib activity in EGFR-mutated and -wildtype non-small cell lung cancer cells. Panobinostat 23-35 epidermal growth factor receptor Homo sapiens 83-87 25904215-10 2015 Treatment of HCC1937 cells with LBH589 and salinomycin had a potent synergistic effect inhibiting TNBC cell proliferation, ALDH1-positive cells, and mammosphere growth. Panobinostat 32-38 aldehyde dehydrogenase 1 family member A1 Homo sapiens 123-128 26202945-11 2015 An increased significant expression of CTGF was only seen after 24 h treatment with 0.1 microM panobinostat in HepG2 cells and Hep3B cells, whereas after 72 h treatment CTGF expression clearly decreased. Panobinostat 95-107 cellular communication network factor 2 Homo sapiens 39-43 26162688-3 2015 Here, we demonstrate the efficacy of the potent histone deacetylase (HDAC) inhibitors, panobinostat and vorinostat, as agents that inhibit RMS tumor growth in vivo, induce apoptosis, and inhibit invasion of RD and Rh30 RMS cell lines. Panobinostat 87-99 histone deacetylase 9 Homo sapiens 48-67 26162688-3 2015 Here, we demonstrate the efficacy of the potent histone deacetylase (HDAC) inhibitors, panobinostat and vorinostat, as agents that inhibit RMS tumor growth in vivo, induce apoptosis, and inhibit invasion of RD and Rh30 RMS cell lines. Panobinostat 87-99 histone deacetylase 9 Homo sapiens 69-73 26176219-0 2015 Molecular Mechanism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells. Panobinostat 87-93 adenosine deaminase 2 Homo sapiens 73-76 26176219-0 2015 Molecular Mechanism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells. Panobinostat 95-107 adenosine deaminase 2 Homo sapiens 73-76 26169416-0 2015 Ex Vivo Bioactivity and HIV-1 Latency Reversal by Ingenol Dibenzoate and Panobinostat in Resting CD4(+) T Cells from Aviremic Patients. Panobinostat 73-85 CD4 molecule Homo sapiens 97-100 25944617-0 2015 The predictive value of ERCC1 and p53 for the effect of panobinostat and cisplatin combination treatment in NSCLC. Panobinostat 56-68 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 24-29 25944617-0 2015 The predictive value of ERCC1 and p53 for the effect of panobinostat and cisplatin combination treatment in NSCLC. Panobinostat 56-68 tumor protein p53 Homo sapiens 34-37 25944617-5 2015 Our study found that panobinostat, an HDAC inhibitor, increased the cisplatin sensitivity of several NSCLC cell lines with low ERCC1 expression but not those with high ERCC1 expression or gain-of-function (GOF) p53 mutation despite of ERCC1 expression level. Panobinostat 21-33 ERCC excision repair 1, endonuclease non-catalytic subunit Homo sapiens 127-132 25904215-11 2015 In xenograft mouse models treated with LBH589 and salinomycin, the drug combination effectively and synergistically inhibited tumor growth of ALDH1-positive cells. Panobinostat 39-45 aldehyde dehydrogenase family 1, subfamily A1 Mus musculus 142-147 25482131-8 2015 Co-treatment with the pan-histone deacetylase inhibitor panobinostat and BC synergistically induced apoptosis of cultured and primary AML BPCs, including those expressing FLT3-ITD, as well as further significantly improved the survival of immune-depleted mice engrafted with primary AML BPCs. Panobinostat 56-68 FMS-like tyrosine kinase 3 Mus musculus 171-175 25993039-16 2015 LBH589 increased LDH and phospho-p70S6K consumption. Panobinostat 0-6 ribosomal protein S6 kinase B1 Homo sapiens 33-39 25236537-5 2015 A histone deacetylase inhibitor, panobinostat, significantly increased MIRLET7 expression and reduced variant 1 of HMGA2 mRNA expression, but not variant 2, in both U937 cells and PMF-derived CD34(+) cells. Panobinostat 33-45 high mobility group AT-hook 2 Homo sapiens 115-120 25737447-6 2015 Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31). Panobinostat 53-65 microRNA 31 Homo sapiens 123-133 25737447-6 2015 Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31). Panobinostat 53-65 microRNA 31 Homo sapiens 127-133 25737447-6 2015 Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31). Panobinostat 67-73 microRNA 31 Homo sapiens 123-133 25737447-6 2015 Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31). Panobinostat 67-73 microRNA 31 Homo sapiens 127-133 25636517-3 2015 In our study, we observed that IL-6 induced the resistance of CLL cells to pan-histone deacetylase (HDAC) inhibitors vorinostat (SAHA) and panobinostat (LBH589). Panobinostat 139-151 interleukin 6 Homo sapiens 31-35 25636517-3 2015 In our study, we observed that IL-6 induced the resistance of CLL cells to pan-histone deacetylase (HDAC) inhibitors vorinostat (SAHA) and panobinostat (LBH589). Panobinostat 153-159 interleukin 6 Homo sapiens 31-35 25636517-4 2015 Furthermore, low concentrations of SAHA and LBH589 enhanced the activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway induced by IL-6 in CLL cells. Panobinostat 44-50 signal transducer and activator of transcription 3 Homo sapiens 82-132 25636517-4 2015 Furthermore, low concentrations of SAHA and LBH589 enhanced the activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway induced by IL-6 in CLL cells. Panobinostat 44-50 signal transducer and activator of transcription 3 Homo sapiens 134-139 25636517-4 2015 Furthermore, low concentrations of SAHA and LBH589 enhanced the activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway induced by IL-6 in CLL cells. Panobinostat 44-50 interleukin 6 Homo sapiens 170-174 25636517-10 2015 Moreover, WP1066 reversed the resistance of CLL cells to SAHA and LBH589 induced by either IL-6 or co-culture with BMSCs. Panobinostat 66-72 interleukin 6 Homo sapiens 91-95 25458954-3 2015 We have previously demonstrated that treatment with the pan-histone deacetylase inhibitor panobinostat (LBH589) can cause down-regulation of CHK1. Panobinostat 90-102 checkpoint kinase 1 Homo sapiens 141-145 25514379-8 2015 LBH589 can eliminate C/EBPe and the mitochondrial apoptosis regulator B-cell lymphoma (BCL)-xL in immature and differentiated NB4 cells. Panobinostat 0-6 CCAAT enhancer binding protein epsilon Homo sapiens 21-27 25305451-6 2015 Differences after treatment with SAHA/RTx or LBH589/RTx in a sensitive and resistant culture were increased acetylated-H3, caspase-3/7 and prolonged DNA damage repair gammaH2AX/53BP1 foci. Panobinostat 45-51 caspase 3 Homo sapiens 123-132 25458954-3 2015 We have previously demonstrated that treatment with the pan-histone deacetylase inhibitor panobinostat (LBH589) can cause down-regulation of CHK1. Panobinostat 104-110 checkpoint kinase 1 Homo sapiens 141-145 25236537-5 2015 A histone deacetylase inhibitor, panobinostat, significantly increased MIRLET7 expression and reduced variant 1 of HMGA2 mRNA expression, but not variant 2, in both U937 cells and PMF-derived CD34(+) cells. Panobinostat 33-45 CD34 molecule Homo sapiens 192-196 26696749-5 2015 Histone deacetylase (HDAC) inhibitors (e.g., panobinostat) are actively under investigation as potential latency reversing agents in HIV eradication studies. Panobinostat 45-57 histone deacetylase 9 Homo sapiens 0-19 26696749-5 2015 Histone deacetylase (HDAC) inhibitors (e.g., panobinostat) are actively under investigation as potential latency reversing agents in HIV eradication studies. Panobinostat 45-57 histone deacetylase 9 Homo sapiens 21-25 25500581-4 2014 We explored the strategy of augmenting CRC cell death by inhibiting all survival pathways induced by the pro-apoptotic agent LBH589, a histone deacetylase inhibitor: AKT, JAK/STAT, and ERK signaling. Panobinostat 125-131 AKT serine/threonine kinase 1 Homo sapiens 166-169 25308916-9 2015 MK-1775 treatment in SK-N-BE(2) cells induced increased levels of p-CHK1(S345) , which could be decreased by the addition of panobinostat. Panobinostat 125-137 checkpoint kinase 1 Homo sapiens 68-72 24810497-3 2014 We previously showed the pan-deacetylase inhibitor LBH589 induces CDH1 expression in TNBC cells, suggesting regulation of EMT. Panobinostat 51-57 cadherin 1 Homo sapiens 66-70 25674239-20 2014 Furthermore, panobinostat inhibits Sirt1 pathway when present, and celecoxib inhibits NF-kappaB pathway activation independent of COX2. Panobinostat 13-25 sirtuin 1 Homo sapiens 35-40 25409711-8 2014 Similar results were obtained with anaplastic thyroid carcinoma cells expressing or not HMGA1 proteins, treated with doxorubicin or the HDAC inhibitor LBH589. Panobinostat 151-157 histone deacetylase 9 Homo sapiens 136-140 25568669-2 2014 We study the efficacy of SAHA/RTx and LBH589/RTx when manipulating Bcl-2 family proteins using the Bcl-2 inhibitor Obatoclax in patient-derived glioblastoma stem-like cell (GSC) cultures. Panobinostat 38-44 BCL2 apoptosis regulator Homo sapiens 67-72 25176354-2 2014 Inhibition of histone deacetylase (HDAC) 6 by the HDAC inhibitor panobinostat hinders the refolding of unfolded proteins by increasing the acetylation of heat shock protein 90. Panobinostat 65-77 histone deacetylase 9 Homo sapiens 14-33 25176354-2 2014 Inhibition of histone deacetylase (HDAC) 6 by the HDAC inhibitor panobinostat hinders the refolding of unfolded proteins by increasing the acetylation of heat shock protein 90. Panobinostat 65-77 histone deacetylase 9 Homo sapiens 35-39 25176354-2 2014 Inhibition of histone deacetylase (HDAC) 6 by the HDAC inhibitor panobinostat hinders the refolding of unfolded proteins by increasing the acetylation of heat shock protein 90. Panobinostat 65-77 histone deacetylase 9 Homo sapiens 50-54 25176354-11 2014 Enhanced acetylation of the HDAC6 substrate alpha-tubulin was consistent with the suppression of HDAC6 activity by panobinostat, and the combination was shown to induce ER stress and ubiquitinated protein accumulation synergistically. Panobinostat 115-127 histone deacetylase 6 Homo sapiens 28-33 25176354-11 2014 Enhanced acetylation of the HDAC6 substrate alpha-tubulin was consistent with the suppression of HDAC6 activity by panobinostat, and the combination was shown to induce ER stress and ubiquitinated protein accumulation synergistically. Panobinostat 115-127 tubulin alpha 1b Homo sapiens 44-57 25176354-11 2014 Enhanced acetylation of the HDAC6 substrate alpha-tubulin was consistent with the suppression of HDAC6 activity by panobinostat, and the combination was shown to induce ER stress and ubiquitinated protein accumulation synergistically. Panobinostat 115-127 histone deacetylase 6 Homo sapiens 97-102 25105535-0 2014 Immune regulatory effects of panobinostat in patients with Hodgkin lymphoma through modulation of serum cytokine levels and T-cell PD1 expression. Panobinostat 29-41 programmed cell death 1 Homo sapiens 131-134 24810497-12 2014 These effects of LBH589 were mediated in part by inhibition of ZEB, as overexpression of ZEB1 or ZEB2 mitigated the effects of LBH589 on MDA-MB-231 EMT-associated gene expression, migration, invasion, CDH1 expression, and tumorigenesis. Panobinostat 17-23 zinc finger E-box binding homeobox 2 Homo sapiens 97-101 24810497-12 2014 These effects of LBH589 were mediated in part by inhibition of ZEB, as overexpression of ZEB1 or ZEB2 mitigated the effects of LBH589 on MDA-MB-231 EMT-associated gene expression, migration, invasion, CDH1 expression, and tumorigenesis. Panobinostat 17-23 cadherin 1 Homo sapiens 201-205 23822537-0 2014 Early thymus and activation-regulated chemokine (TARC) reduction and response following panobinostat treatment in patients with relapsed/refractory Hodgkin lymphoma following autologous stem cell transplant. Panobinostat 88-100 C-C motif chemokine ligand 17 Homo sapiens 6-47 24597570-0 2014 Progress of HDAC inhibitor panobinostat in the treatment of cancer. Panobinostat 27-39 histone deacetylase 9 Homo sapiens 12-16 24597570-4 2014 Among these drug candidates, the pan-HDAC inhibitor, panobinostat demonstrated high therapeutic potential as monotherapy and combined therapy in both preclinical models and clinical cancer patients. Panobinostat 53-65 histone deacetylase 9 Homo sapiens 37-41 25016802-5 2014 We found that panobinostat suppresses expression of MLL protein through modulation of its stability as well as Hsp90 inhibitor. Panobinostat 14-26 lysine methyltransferase 2A Homo sapiens 52-55 24435446-2 2014 Here, we demonstrate the sensitizing effects of the histone hyperacetylation-inducing pan-histone deacetylase (HDAC) inhibitor panobinostat on human acute myelogenous leukemia (AML) blast progenitor cells (BPC) to the BET protein antagonist JQ1. Panobinostat 127-139 histone deacetylase 9 Homo sapiens 111-115 24435446-2 2014 Here, we demonstrate the sensitizing effects of the histone hyperacetylation-inducing pan-histone deacetylase (HDAC) inhibitor panobinostat on human acute myelogenous leukemia (AML) blast progenitor cells (BPC) to the BET protein antagonist JQ1. Panobinostat 127-139 delta/notch like EGF repeat containing Homo sapiens 218-221 24435446-5 2014 Cotreatment with JQ1 and the HDAC inhibitor panobinostat synergistically induced apoptosis of the AML BPCs, but not of normal CD34(+) hematopoietic progenitor cells. Panobinostat 44-56 histone deacetylase 9 Homo sapiens 29-33 23822537-0 2014 Early thymus and activation-regulated chemokine (TARC) reduction and response following panobinostat treatment in patients with relapsed/refractory Hodgkin lymphoma following autologous stem cell transplant. Panobinostat 88-100 C-C motif chemokine ligand 17 Homo sapiens 49-53 24491799-6 2014 Conversely, treatment with the histone deacetylase inhibitor panobinostat reversed this switch, in a manner associated with tumor suppression in Cbp(pc-/-);Pten(pc+/-) mice. Panobinostat 61-73 CREB binding protein Mus musculus 145-148 24491799-6 2014 Conversely, treatment with the histone deacetylase inhibitor panobinostat reversed this switch, in a manner associated with tumor suppression in Cbp(pc-/-);Pten(pc+/-) mice. Panobinostat 61-73 phosphatase and tensin homolog Mus musculus 156-160 24429877-0 2014 A phase I, pharmacokinetic, and pharmacodynamic study of panobinostat, an HDAC inhibitor, combined with erlotinib in patients with advanced aerodigestive tract tumors. Panobinostat 57-69 histone deacetylase 9 Homo sapiens 74-78 24429877-1 2014 PURPOSE: Panobinostat, a histone deacetylase (HDAC) inhibitor, enhances antiproliferative activity in non-small cell lung cancer (NSCLC) cell lines when combined with erlotinib. Panobinostat 9-21 histone deacetylase 9 Homo sapiens 25-44 24429877-1 2014 PURPOSE: Panobinostat, a histone deacetylase (HDAC) inhibitor, enhances antiproliferative activity in non-small cell lung cancer (NSCLC) cell lines when combined with erlotinib. Panobinostat 9-21 histone deacetylase 9 Homo sapiens 46-50 24434430-7 2014 Pharmacologically active concentrations of panobinostat and IM were achieved as evidenced by histone H3 acetylation in blood mononuclear cells in vivo and inhibition of the IM-resistant KIT (D816) mutation in vitro. Panobinostat 43-55 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 186-189 24366407-4 2014 We report that the pan-histone deacetylase inhibitor LBH589, a potent anti-proliferative agent, induced E-cadherin expression on cell membranes of MDA-MB-231 cells (TNBC), determining a reduction of cell invasion and migration. Panobinostat 53-59 cadherin 1 Homo sapiens 104-114 24311721-6 2014 The epigenetic modifier drugs, panobinostat and azacitidine, increased CD33 expression in some cell lines and augmented AMG 330-induced cytotoxicity. Panobinostat 31-43 CD33 molecule Homo sapiens 71-75 24075958-0 2014 MYB down-regulation enhances sensitivity of U937 myeloid leukemia cells to the histone deacetylase inhibitor LBH589 in vitro and in vivo. Panobinostat 109-115 MYB proto-oncogene, transcription factor Homo sapiens 0-3 24075958-2 2014 MYB knockdown inhibited proliferation and induced apoptosis in U937 and K562 cells in vitro, and also sensitized both to the pro-apoptotic effect of LBH589. Panobinostat 149-155 MYB proto-oncogene, transcription factor Homo sapiens 0-3 24297862-0 2014 Reducing TNF receptor 2+ regulatory T cells via the combined action of azacitidine and the HDAC inhibitor, panobinostat for clinical benefit in acute myeloid leukemia patients. Panobinostat 107-119 tumor necrosis factor Homo sapiens 9-12 24297862-0 2014 Reducing TNF receptor 2+ regulatory T cells via the combined action of azacitidine and the HDAC inhibitor, panobinostat for clinical benefit in acute myeloid leukemia patients. Panobinostat 107-119 histone deacetylase 9 Homo sapiens 91-95 24297862-8 2014 Furthermore, we demonstrate that the level of TNFR2(+) Tregs in the peripheral blood and the bone marrow of patients are decreased in vivo after exposure to panobinostat and azacitidine. Panobinostat 157-169 TNF receptor superfamily member 1B Homo sapiens 46-51 24297862-11 2014 CONCLUSIONS: Our study provides for the first time, in vivo validation of the ability of panobinostat in combination with azacitidine to suppress prevalent TNFR2(+) Tregs, resulting in clinical benefits within patients with AML. Panobinostat 89-101 TNF receptor superfamily member 1B Homo sapiens 156-161 24311721-6 2014 The epigenetic modifier drugs, panobinostat and azacitidine, increased CD33 expression in some cell lines and augmented AMG 330-induced cytotoxicity. Panobinostat 31-43 amelogenin X-linked Homo sapiens 120-123 24244429-8 2013 Our results establish a novel mechanism underlying the cooperative antileukemic activities of these drug combinations in which panobinostat suppresses expression of BRCA1, CHK1, and RAD51 to enhance cytarabine and daunorubicin sensitivities in AML cells. Panobinostat 127-139 breast cancer 1, early onset Mus musculus 165-170 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 nuclear factor kappa B subunit 1 Homo sapiens 179-188 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 microRNA 146a Homo sapiens 196-204 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 interleukin 1 beta Homo sapiens 240-248 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 RELA proto-oncogene, NF-kB subunit Homo sapiens 269-272 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 interleukin 6 Homo sapiens 303-307 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 histone deacetylase 9 Homo sapiens 0-4 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 nuclear factor kappa B subunit 1 Homo sapiens 179-188 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 microRNA 146a Homo sapiens 196-204 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 interleukin 1 beta Homo sapiens 240-248 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 RELA proto-oncogene, NF-kB subunit Homo sapiens 269-272 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 interleukin 6 Homo sapiens 303-307 24301913-3 2013 We aimed to determine the efficacy of panobinostat, alone and in combination with cisplatin, on cell survival and mRNA expression of FOXO3A, CCND1, and CASP9 genes in both mesothelioma and healthy mesothelial cell lines. Panobinostat 38-50 forkhead box O3 Homo sapiens 133-139 24301913-3 2013 We aimed to determine the efficacy of panobinostat, alone and in combination with cisplatin, on cell survival and mRNA expression of FOXO3A, CCND1, and CASP9 genes in both mesothelioma and healthy mesothelial cell lines. Panobinostat 38-50 cyclin D1 Homo sapiens 141-146 24301913-3 2013 We aimed to determine the efficacy of panobinostat, alone and in combination with cisplatin, on cell survival and mRNA expression of FOXO3A, CCND1, and CASP9 genes in both mesothelioma and healthy mesothelial cell lines. Panobinostat 38-50 caspase 9 Homo sapiens 152-157 23888956-5 2014 Treatment with the histone deacetylase inhibitor (HDACi) LBH589 induced a profound upregulation of PR mRNA. Panobinostat 57-63 progesterone receptor Homo sapiens 99-101 23888956-7 2014 LBH589 promoted a dose-dependent increase in PR protein levels, with an obvious increase with 10 nM LBH589. Panobinostat 0-6 progesterone receptor Homo sapiens 45-47 23888956-7 2014 LBH589 promoted a dose-dependent increase in PR protein levels, with an obvious increase with 10 nM LBH589. Panobinostat 100-106 progesterone receptor Homo sapiens 45-47 23979523-6 2014 PTPN6 gene suppression was reversed by 5-aza-deoxycytidine (5-Aza), a DNA methyltransferase inhibitor, and the histone deacetylase inhibitor (HDACi) LBH589. Panobinostat 149-155 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 0-5 23979523-7 2014 LBH589 and 5-Aza in combination inhibited DLBCL survival and PTPN6 hypermethylation at CpG2. Panobinostat 0-6 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 61-66 23979523-9 2014 3-Deazaneplanocin A, a histone methyltransferase inhibitor, decreased the H3K27me3 mark, whereas HDACi LBH589 increased the H3K9Ac mark within P2 resulting in re-expression of PTPN6. Panobinostat 103-109 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 176-181 24278143-5 2013 In co-culture experiments of lymphocytes with HL cells, LBH589 suppressed the IFNgamma-release but increased the TNFalpha secretion. Panobinostat 56-62 tumor necrosis factor Homo sapiens 113-121 24244429-8 2013 Our results establish a novel mechanism underlying the cooperative antileukemic activities of these drug combinations in which panobinostat suppresses expression of BRCA1, CHK1, and RAD51 to enhance cytarabine and daunorubicin sensitivities in AML cells. Panobinostat 127-139 checkpoint kinase 1 Mus musculus 172-176 24244429-8 2013 Our results establish a novel mechanism underlying the cooperative antileukemic activities of these drug combinations in which panobinostat suppresses expression of BRCA1, CHK1, and RAD51 to enhance cytarabine and daunorubicin sensitivities in AML cells. Panobinostat 127-139 RAD51 recombinase Mus musculus 182-187 24093956-0 2013 LBH589 Inhibits proliferation and metastasis of hepatocellular carcinoma via inhibition of gankyrin/STAT3/Akt pathway. Panobinostat 0-6 proteasome 26S subunit, non-ATPase 10 Homo sapiens 91-99 24157872-5 2013 In the present report, we found a potent synergistic antiproliferative effect of panobinostat/ZOL treatment in three PCa and three MM cell lines as well as in a PCa ZOL-resistant subline, independently of p53/KRAS status, androgen dependency, or the schedule of administration. Panobinostat 81-93 KRAS proto-oncogene, GTPase Homo sapiens 209-213 24157872-9 2013 Finally, at the molecular level, the inhibition of basal and ZOL-induced activation of p38-MAPK by panobinostat in sensitive and ZOL-resistant cells and in tumor xenografts could explain, at least in part, the observed synergism. Panobinostat 99-111 mitogen-activated protein kinase 14 Homo sapiens 87-90 24093956-0 2013 LBH589 Inhibits proliferation and metastasis of hepatocellular carcinoma via inhibition of gankyrin/STAT3/Akt pathway. Panobinostat 0-6 signal transducer and activator of transcription 3 Homo sapiens 100-105 24093956-0 2013 LBH589 Inhibits proliferation and metastasis of hepatocellular carcinoma via inhibition of gankyrin/STAT3/Akt pathway. Panobinostat 0-6 AKT serine/threonine kinase 1 Homo sapiens 106-109 24093956-9 2013 LBH589 inhibited metastasis in vitro via down-regulation of N-cadherin, vimentin, TWIST1, VEGF and up-regulation of E-cadherin. Panobinostat 0-6 cadherin 2 Homo sapiens 60-70 24093956-9 2013 LBH589 inhibited metastasis in vitro via down-regulation of N-cadherin, vimentin, TWIST1, VEGF and up-regulation of E-cadherin. Panobinostat 0-6 vimentin Homo sapiens 72-80 24093956-9 2013 LBH589 inhibited metastasis in vitro via down-regulation of N-cadherin, vimentin, TWIST1, VEGF and up-regulation of E-cadherin. Panobinostat 0-6 twist family bHLH transcription factor 1 Homo sapiens 82-88 24093956-9 2013 LBH589 inhibited metastasis in vitro via down-regulation of N-cadherin, vimentin, TWIST1, VEGF and up-regulation of E-cadherin. Panobinostat 0-6 vascular endothelial growth factor A Homo sapiens 90-94 24093956-9 2013 LBH589 inhibited metastasis in vitro via down-regulation of N-cadherin, vimentin, TWIST1, VEGF and up-regulation of E-cadherin. Panobinostat 0-6 cadherin 1 Homo sapiens 116-126 24093956-11 2013 Ectopic expression of gankyrin attenuated the effects of LBH589, which indicates that gankyrin might play an important role in LBH589 mediated anticancer effects. Panobinostat 57-63 proteasome 26S subunit, non-ATPase 10 Homo sapiens 22-30 24093956-11 2013 Ectopic expression of gankyrin attenuated the effects of LBH589, which indicates that gankyrin might play an important role in LBH589 mediated anticancer effects. Panobinostat 57-63 proteasome 26S subunit, non-ATPase 10 Homo sapiens 86-94 24093956-13 2013 CONCLUSIONS: Our results suggested that LBH589 could inhibit HCC growth and metastasis through down-regulating gankyrin/STAT3/Akt pathway. Panobinostat 40-46 proteasome 26S subunit, non-ATPase 10 Homo sapiens 111-119 24093956-13 2013 CONCLUSIONS: Our results suggested that LBH589 could inhibit HCC growth and metastasis through down-regulating gankyrin/STAT3/Akt pathway. Panobinostat 40-46 signal transducer and activator of transcription 3 Homo sapiens 120-125 24093956-13 2013 CONCLUSIONS: Our results suggested that LBH589 could inhibit HCC growth and metastasis through down-regulating gankyrin/STAT3/Akt pathway. Panobinostat 40-46 AKT serine/threonine kinase 1 Homo sapiens 126-129 23877235-0 2013 The HDAC inhibitor, panobinostat, induces apoptosis by suppressing the expresssion of specificity protein 1 in oral squamous cell carcinoma. Panobinostat 20-32 histone deacetylase 9 Homo sapiens 4-8 24013574-2 2013 Panobinostat was shown to inhibit CYP2D6 activity in vitro; thus understanding the magnitude of the potential clinical inhibition of panobinostat on co-medications that are CYP2D6 substrates becomes important. Panobinostat 0-12 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 34-40 24013574-2 2013 Panobinostat was shown to inhibit CYP2D6 activity in vitro; thus understanding the magnitude of the potential clinical inhibition of panobinostat on co-medications that are CYP2D6 substrates becomes important. Panobinostat 0-12 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 173-179 24013574-2 2013 Panobinostat was shown to inhibit CYP2D6 activity in vitro; thus understanding the magnitude of the potential clinical inhibition of panobinostat on co-medications that are CYP2D6 substrates becomes important. Panobinostat 133-145 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 34-40 24013574-2 2013 Panobinostat was shown to inhibit CYP2D6 activity in vitro; thus understanding the magnitude of the potential clinical inhibition of panobinostat on co-medications that are CYP2D6 substrates becomes important. Panobinostat 133-145 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 173-179 24013574-3 2013 METHODS: This study evaluated the effects of co-administration of panobinostat with a sensitive CYP2D6 substrate, dextromethorphan (DM), in patients with advanced cancer who have functional CYP2D6 genes. Panobinostat 66-78 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 190-196 24013574-7 2013 These results indicated that panobinostat weakly inhibited a sensitive CYP2D6 substrate in cancer patients by increasing DM exposure by less than twofold. Panobinostat 29-41 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 71-77 24013574-8 2013 CONCLUSION: Safety monitoring of sensitive CYP2D6 substrates with narrow therapeutic index is recommended when co-administering with panobinostat in future clinical practice. Panobinostat 133-145 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 43-49 23877235-0 2013 The HDAC inhibitor, panobinostat, induces apoptosis by suppressing the expresssion of specificity protein 1 in oral squamous cell carcinoma. Panobinostat 20-32 Sp1 transcription factor Homo sapiens 86-107 23877235-2 2013 Panobinostat (LBH589) induces apoptosis through the regulation of specificity protein 1 (Sp1) in the oral squamous cell carcinoma (OSCC) cell lines, HN22 and HSC4. Panobinostat 14-20 Sp1 transcription factor Homo sapiens 66-87 23877235-7 2013 Treatment with LBH589 also induced the cleavage of caspase-3 and PARP in the HN22 and HSC4 cells. Panobinostat 15-21 caspase 3 Homo sapiens 51-60 23877235-7 2013 Treatment with LBH589 also induced the cleavage of caspase-3 and PARP in the HN22 and HSC4 cells. Panobinostat 15-21 poly(ADP-ribose) polymerase 1 Homo sapiens 65-69 24144737-9 2013 CONCLUSION: TSA and LBH589 can cause cell cycle arrest and induce apoptosis in OS-RC-2 cells, in which process P-JNK pathway plays an important role. Panobinostat 20-26 mitogen-activated protein kinase 8 Homo sapiens 113-116 24098799-9 2013 Furthermore, panobinostat treatment resulted in substantial down-regulation of CHK1 and its downstream pathway and abrogation of the G2 cell cycle checkpoint. Panobinostat 13-25 checkpoint kinase 1 Homo sapiens 79-83 23299388-7 2013 In contrast, panobinostat-induced acetyl-H3, acetyl-H4, and p21 persisted for 48 h after an initial 3 h exposure. Panobinostat 13-25 H3 histone pseudogene 16 Homo sapiens 60-63 23701016-4 2013 This study evaluated panobinostat, a pan-deacetylase inhibitor that depletes JAK2 V617F levels and JAK/STAT signalling in MPN cells, in patients with primary MF, post-essential thrombocythaemia MF, and post-polycythaemia vera MF. Panobinostat 21-33 Janus kinase 2 Homo sapiens 77-81 24023871-0 2013 The HDAC inhibitor LBH589 induces ERK-dependent prometaphase arrest in prostate cancer via HDAC6 inactivation and down-regulation. Panobinostat 19-25 mitogen-activated protein kinase 1 Homo sapiens 34-37 24023871-0 2013 The HDAC inhibitor LBH589 induces ERK-dependent prometaphase arrest in prostate cancer via HDAC6 inactivation and down-regulation. Panobinostat 19-25 histone deacetylase 6 Homo sapiens 91-96 24023871-6 2013 Mechanistically, LBH589 inhibited HDAC6 activity, caused its dissociation from protein phosphatase PP1alpha, and increased 14-3-3zeta acetylation. Panobinostat 17-23 histone deacetylase 6 Homo sapiens 34-39 24023871-8 2013 Enhanced ERK activity by LBH589 further down-regulated HDAC6 protein levels and sustained ERK activation by free-forward regulation. Panobinostat 25-31 mitogen-activated protein kinase 1 Homo sapiens 9-12 24023871-8 2013 Enhanced ERK activity by LBH589 further down-regulated HDAC6 protein levels and sustained ERK activation by free-forward regulation. Panobinostat 25-31 histone deacetylase 6 Homo sapiens 55-60 24023871-8 2013 Enhanced ERK activity by LBH589 further down-regulated HDAC6 protein levels and sustained ERK activation by free-forward regulation. Panobinostat 25-31 mitogen-activated protein kinase 1 Homo sapiens 90-93 23744355-4 2013 Cotreatment with the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) or panobinostat (LBH589) and the BRAF inhibitor PLX4720 activated the caspase cascade, but caspases appeared dispensable for killing, in that inhibition of caspases did not invariably block induction of cell death. Panobinostat 92-98 histone deacetylase 9 Homo sapiens 21-25 23160924-4 2013 LBH589 treatment also reduced the level of NF-kappaB1 which is overexpressed when AI resistance develops. Panobinostat 0-6 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 43-53 23681230-9 2013 In addition, the binding of NF-kappaB/STAT3 complexes to the GADD45G promoter is inhibited following panobinostat, SRT501 or resveratrol treatment. Panobinostat 101-113 nuclear factor kappa B subunit 1 Homo sapiens 28-37 23681230-9 2013 In addition, the binding of NF-kappaB/STAT3 complexes to the GADD45G promoter is inhibited following panobinostat, SRT501 or resveratrol treatment. Panobinostat 101-113 signal transducer and activator of transcription 3 Homo sapiens 38-43 23681230-9 2013 In addition, the binding of NF-kappaB/STAT3 complexes to the GADD45G promoter is inhibited following panobinostat, SRT501 or resveratrol treatment. Panobinostat 101-113 growth arrest and DNA damage inducible gamma Homo sapiens 61-68 23330839-8 2013 We conclude that panobinostat is a well-tolerated, clinically active treatment for MF patients, regardless of JAK2 V617F status, and most effective when given at low doses over long periods of time. Panobinostat 17-29 Janus kinase 2 Homo sapiens 110-114 23519125-11 2013 Interestingly, although the other HDAC inhibitors, such as SAHA and panobinostat, exhibited activity as potent as entinostat to induce growth inhibition and apoptosis in erbB2-overexpressing breast cancer cells, they had no significant effects on the three miRNAs. Panobinostat 68-80 erb-b2 receptor tyrosine kinase 2 Homo sapiens 170-175 23519125-12 2013 Instead, both SAHA- and panobinostat-decreased erbB2/erbB3 expression correlated with the reduction of their mRNA levels. Panobinostat 24-36 erb-b2 receptor tyrosine kinase 2 Homo sapiens 47-52 23519125-12 2013 Instead, both SAHA- and panobinostat-decreased erbB2/erbB3 expression correlated with the reduction of their mRNA levels. Panobinostat 24-36 erb-b2 receptor tyrosine kinase 3 Homo sapiens 53-58 22995071-0 2013 Low dose histone deacetylase inhibitor, LBH589, potentiates anticancer effect of docetaxel in epithelial ovarian cancer via PI3K/Akt pathway in vitro. Panobinostat 40-46 AKT serine/threonine kinase 1 Homo sapiens 129-132 23160924-10 2013 In all, our findings strongly support further investigation of LBH589 as a novel therapeutic strategy for patients with AI-resistant breast cancer, in part by suppressing the NF-kappaB1 pathway. Panobinostat 63-69 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 175-185 22863538-0 2012 Synergistic effect of panobinostat and bortezomib on chemoresistant acute myelogenous leukemia cells via AKT and NF-kappaB pathways. Panobinostat 22-34 AKT serine/threonine kinase 1 Homo sapiens 105-108 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 121-125 23257272-1 2012 Here, we report the case of a patient, who showed an antitumour response to a new combination therapy of sorafenib and the histon deacetylase inhibitor panobinostat (LBH-589). Panobinostat 152-164 LBH regulator of WNT signaling pathway Homo sapiens 166-169 23011180-3 2012 The role of the tumor suppressor death-associated protein kinase (DAPK) in LBH589-induced cytotoxicity has not been investigated to date. Panobinostat 75-81 death associated protein kinase 1 Homo sapiens 33-64 23011180-3 2012 The role of the tumor suppressor death-associated protein kinase (DAPK) in LBH589-induced cytotoxicity has not been investigated to date. Panobinostat 75-81 death associated protein kinase 1 Homo sapiens 66-70 23011180-5 2012 LBH589 inhibited cell proliferation, reduced the long-term survival, and up-regulated and activated DAPK in colorectal cancer cells. Panobinostat 0-6 death associated protein kinase 1 Homo sapiens 100-104 23011180-6 2012 Moreover, LBH589 significantly suppressed the growth of colon tumor xenografts and in accordance with the in vitro studies, increased DAPK levels were detected immunohistochemically. Panobinostat 10-16 death associated protein kinase 1 Homo sapiens 134-138 23011180-8 2012 LBH589-induced autophagy seems to be predominantly caused by DAPK protein interactions than by its kinase activity. Panobinostat 0-6 death associated protein kinase 1 Homo sapiens 61-65 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 127-132 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 cyclin D1 Homo sapiens 148-157 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 F-box protein 32 Homo sapiens 207-213 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 cyclin dependent kinase inhibitor 2A Homo sapiens 215-218 22988056-14 2012 Panobinostat, a histone deacetylase inhibitor, induced apoptosis of LCR B cells and CD138+ cells. Panobinostat 0-12 syndecan 1 Homo sapiens 84-89 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 H3 histone pseudogene 16 Homo sapiens 220-223 24026482-7 2013 Furthermore, we show a significant loss of E2F1 recruitment to the promoters of these genes in response to panobinostat treatment. Panobinostat 107-119 E2F transcription factor 1 Homo sapiens 43-47 22932665-8 2012 Furthermore, as compared with treatment with each agent alone, cotreatment with DZNep and PS caused greater depletion of EZH2, SUZ12, 3MeK27H3, and Cyclin D1 levels, whereas it induced greater expression of FBXO32, p16, p21, and p27. Panobinostat 90-92 interferon alpha inducible protein 27 Homo sapiens 229-232 22932665-9 2012 Combined treatment with DZNep and PS synergistically induced apoptosis of cultured and primary MCL cells while relatively sparing normal CD34 + cells. Panobinostat 34-36 CD34 molecule Homo sapiens 137-141 22864948-14 2012 Thus, CYP-mediated drug-drug interactions with panobinostat are predicted to be minor. Panobinostat 47-59 peptidylprolyl isomerase G Homo sapiens 6-9 22942377-0 2012 Breakdown of the FLT3-ITD/STAT5 axis and synergistic apoptosis induction by the histone deacetylase inhibitor panobinostat and FLT3-specific inhibitors. Panobinostat 110-122 fms related receptor tyrosine kinase 3 Homo sapiens 17-21 22942377-10 2012 Immunoblot analyses show that LBH589 + TKI induce apoptosis via degradation of FLT3-ITD and its prosurvival target STAT5. Panobinostat 30-36 fms related receptor tyrosine kinase 3 Homo sapiens 79-83 22942377-10 2012 Immunoblot analyses show that LBH589 + TKI induce apoptosis via degradation of FLT3-ITD and its prosurvival target STAT5. Panobinostat 30-36 signal transducer and activator of transcription 5A Homo sapiens 115-120 23232026-3 2012 Treatment with BEZ235 or PS inhibited cell cycle progression with induction of the cell cycle inhibitory proteins, p21waf1 and p27kip1. Panobinostat 25-27 cyclin dependent kinase inhibitor 1B Homo sapiens 127-134 23232026-4 2012 BEZ235 and PS also dose dependently induced loss of cell viability of the cultured PDAC cells, associated with depletion of phosphorylated (p) AKT, as well as of the TORC1 substrates 4EBP1 and p70S6 kinase. Panobinostat 11-13 AKT serine/threonine kinase 1 Homo sapiens 143-146 23232026-4 2012 BEZ235 and PS also dose dependently induced loss of cell viability of the cultured PDAC cells, associated with depletion of phosphorylated (p) AKT, as well as of the TORC1 substrates 4EBP1 and p70S6 kinase. Panobinostat 11-13 CREB regulated transcription coactivator 1 Homo sapiens 166-171 23232026-4 2012 BEZ235 and PS also dose dependently induced loss of cell viability of the cultured PDAC cells, associated with depletion of phosphorylated (p) AKT, as well as of the TORC1 substrates 4EBP1 and p70S6 kinase. Panobinostat 11-13 eukaryotic translation initiation factor 4E binding protein 1 Homo sapiens 183-188 23232026-5 2012 While inhibiting p-AKT, treatment with PS induced the levels of the pro-apoptotic proteins BIM and BAK. Panobinostat 39-41 AKT serine/threonine kinase 1 Homo sapiens 19-22 23232026-9 2012 Furthermore, co-treatment with BEZ235 and PS more effectively blocked tumor growth of primary PDAC heterotransplants (possessing K-RAS mutation and AKT2 amplification) subcutaneously implanted in the nude mice than each agent alone. Panobinostat 42-44 Kirsten rat sarcoma viral oncogene homolog Mus musculus 129-134 23232026-9 2012 Furthermore, co-treatment with BEZ235 and PS more effectively blocked tumor growth of primary PDAC heterotransplants (possessing K-RAS mutation and AKT2 amplification) subcutaneously implanted in the nude mice than each agent alone. Panobinostat 42-44 thymoma viral proto-oncogene 2 Mus musculus 148-152 23232026-10 2012 These findings demonstrate superior activity and support further in vivo evaluation of combined treatment with BEZ235 and PS against PDAC that possess heightened activity of RAS-RAF-ERK1/2 and PI3K-AKT-mTOR pathways. Panobinostat 122-124 AKT serine/threonine kinase 1 Homo sapiens 198-201 23232026-10 2012 These findings demonstrate superior activity and support further in vivo evaluation of combined treatment with BEZ235 and PS against PDAC that possess heightened activity of RAS-RAF-ERK1/2 and PI3K-AKT-mTOR pathways. Panobinostat 122-124 mechanistic target of rapamycin kinase Homo sapiens 202-206 22683924-3 2012 We here investigate whether HMGA2 (High Mobility Group AT-2 hook), a nuclear non-histone transcriptional co-factor with known oncogenic properties, can be influenced by the novel pan-deacetylase inhibitor panobinostat (LBH589) in human hepatocellular carcinoma models. Panobinostat 219-225 high mobility group AT-hook 2 Homo sapiens 28-33 23114131-5 2012 Western blot analysis showed that the histone H4 acetylation level was enhanced in concentration-dependent manner after MM1R cells were treated with different concentrations of LBH589 for 24 h. It is concluded that the LBH589 can inhibit the proliferation of MM1R cells, block the cell cycle, induce cell apoptosis, moreover LBH589 combined with Bor has synergistic effect on MM1R cells. Panobinostat 219-225 LBH regulator of WNT signaling pathway Homo sapiens 177-180 22465428-0 2012 Pan-histone deacetylase inhibitor panobinostat sensitizes gastric cancer cells to anthracyclines via induction of CITED2. Panobinostat 34-46 histone deacetylase 9 Homo sapiens 4-23 22744359-0 2012 Phase I study of bevacizumab, everolimus, and panobinostat (LBH-589) in advanced solid tumors. Panobinostat 46-58 LBH regulator of WNT signaling pathway Homo sapiens 60-63 22465428-13 2012 CONCLUSIONS: The HDAC inhibitor LBH589 can overcome the resistance of mouse gastric cancer cells to anthracyclines by inducing expression of CITED2. Panobinostat 32-38 histone deacetylase 9 Homo sapiens 17-21 22698484-7 2012 Accelerated GVHD in the recipients treated with LBH589 was associated with elevated Th1 cytokines in recipient serum, enhanced CXCR3 expression on donor T cells, and T cell infiltration in the liver. Panobinostat 48-54 negative elongation factor complex member C/D Homo sapiens 84-87 22698484-7 2012 Accelerated GVHD in the recipients treated with LBH589 was associated with elevated Th1 cytokines in recipient serum, enhanced CXCR3 expression on donor T cells, and T cell infiltration in the liver. Panobinostat 48-54 C-X-C motif chemokine receptor 3 Homo sapiens 127-132 22465428-0 2012 Pan-histone deacetylase inhibitor panobinostat sensitizes gastric cancer cells to anthracyclines via induction of CITED2. Panobinostat 34-46 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 114-120 22465428-13 2012 CONCLUSIONS: The HDAC inhibitor LBH589 can overcome the resistance of mouse gastric cancer cells to anthracyclines by inducing expression of CITED2. Panobinostat 32-38 Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2 Mus musculus 141-147 22465428-3 2012 METHODS: Gastric cancer cell lines were incubated with the HDAC inhibitor LBH589 (Panobinostat, Novartis, Germany); levels of proliferation, apoptosis, histone acetylation, and gene expression were determined. Panobinostat 74-80 histone deacetylase 9 Homo sapiens 59-63 22465428-11 2012 In CEA/Tag mice, LBH589 induced tumor-cell expression of CITED2 and increased the efficacy of anthracycline to reduce tumor growth. Panobinostat 17-23 carcinoembryonic antigen gene family Mus musculus 3-6 22465428-11 2012 In CEA/Tag mice, LBH589 induced tumor-cell expression of CITED2 and increased the efficacy of anthracycline to reduce tumor growth. Panobinostat 17-23 Cbp/p300-interacting transactivator, with Glu/Asp-rich carboxy-terminal domain, 2 Mus musculus 57-63 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 31-43 E1A binding protein p300 Homo sapiens 63-67 22322234-0 2012 Combination therapy for hepatocellular carcinoma: additive preclinical efficacy of the HDAC inhibitor panobinostat with sorafenib. Panobinostat 102-114 histone deacetylase 9 Homo sapiens 87-91 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 45-51 signal transducer and activator of transcription 3 Homo sapiens 77-82 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 31-43 signal transducer and activator of transcription 3 Homo sapiens 77-82 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 45-51 signal transducer and activator of transcription 3 Homo sapiens 136-141 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 31-43 signal transducer and activator of transcription 3 Homo sapiens 136-141 22116549-4 2012 Inhibition of HDAC activity by panobinostat (LBH589) increased p300-mediated STAT3(Lys685) acetylation with increased nuclear export of STAT3 to the cytoplasm. Panobinostat 45-51 E1A binding protein p300 Homo sapiens 63-67 22074700-0 2012 LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism. Panobinostat 9-21 LBH regulator of WNT signaling pathway Homo sapiens 0-3 22344701-2 2012 Under catalysis of recombinant human CYP3A4 and CYP2D6 coexpressed with human cytochrome P450 reductase in Escherichia coli JM109, five metabolites of panobinostat were produced via whole-cell biotransformation. Panobinostat 151-163 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 22344701-2 2012 Under catalysis of recombinant human CYP3A4 and CYP2D6 coexpressed with human cytochrome P450 reductase in Escherichia coli JM109, five metabolites of panobinostat were produced via whole-cell biotransformation. Panobinostat 151-163 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 48-54 22408261-4 2012 Paradoxically, panobinostat inhibited LKB1 and AMP-activated protein kinase, leading to activation of mammalian target of rapamycin (mTOR) that promotes survival. Panobinostat 15-27 serine/threonine kinase 11 Homo sapiens 38-42 22408261-4 2012 Paradoxically, panobinostat inhibited LKB1 and AMP-activated protein kinase, leading to activation of mammalian target of rapamycin (mTOR) that promotes survival. Panobinostat 15-27 mechanistic target of rapamycin kinase Homo sapiens 102-131 22408261-4 2012 Paradoxically, panobinostat inhibited LKB1 and AMP-activated protein kinase, leading to activation of mammalian target of rapamycin (mTOR) that promotes survival. Panobinostat 15-27 mechanistic target of rapamycin kinase Homo sapiens 133-137 22408261-5 2012 Combining panobinostat with the mTOR inhibitor everolimus (RAD001) inhibited panobinostat-induced mTOR activation and enhanced panobinostat antiproliferative effects. Panobinostat 10-22 mechanistic target of rapamycin kinase Homo sapiens 98-102 22408261-5 2012 Combining panobinostat with the mTOR inhibitor everolimus (RAD001) inhibited panobinostat-induced mTOR activation and enhanced panobinostat antiproliferative effects. Panobinostat 77-89 mechanistic target of rapamycin kinase Homo sapiens 32-36 22408261-5 2012 Combining panobinostat with the mTOR inhibitor everolimus (RAD001) inhibited panobinostat-induced mTOR activation and enhanced panobinostat antiproliferative effects. Panobinostat 77-89 mechanistic target of rapamycin kinase Homo sapiens 98-102 22408261-6 2012 Collectively, our data demonstrate that panobinostat is a potent deacetylase inhibitor against Hodgkin lymphoma-derived cell lines, and provide a mechanistic rationale for combining panobinostat with mTOR inhibitors for treating Hodgkin lymphoma patients. Panobinostat 40-52 mechanistic target of rapamycin kinase Homo sapiens 200-204 22392915-6 2012 RESULTS: In the human MM cell line RPMI8226, treatment with PPP and LBH589 in combination resulted in a five-fold increase of apoptosis, and an additive effect on the cleavage of the active forms of caspase-8 was observed as compared with the single drug treatments. Panobinostat 68-74 caspase 8 Homo sapiens 199-208 22074700-0 2012 LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism. Panobinostat 9-21 mitogen-activated protein kinase 8 Homo sapiens 80-84 22074700-0 2012 LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanism. Panobinostat 9-21 X-linked inhibitor of apoptosis Homo sapiens 89-93 23427335-2 2012 Six human breast cancer cell lines, both receptor rich and receptor poor, were studied.Panobinostat (LBH-589), a pan histone deacetylase inhibitor with a multitude of biological effects, exhibits time-dependent synergistic effects in breast cancer cell lines with docetaxel, doxorubicin, or gemcitabine in clinically relevant concentrations. Panobinostat 87-99 LBH regulator of WNT signaling pathway Homo sapiens 101-104 22367781-5 2012 Treatment with panobinostat also induced the accumulation and colocalization of p62 with LC3B-II in cytosolic foci as evidenced by immunofluorescent confocal microscopy. Panobinostat 15-27 nucleoporin 62 Homo sapiens 80-83 22367781-6 2012 Inhibition of panobinostat-induced autophagic flux by chloroquine markedly induced the accumulation of polyubiquitylated proteins and p62, caused synergistic cell death of MB-231 and SUM159PT cells, and inhibited mammosphere formation in MB-231 cells, compared with treatment with each agent alone. Panobinostat 14-26 nucleoporin 62 Homo sapiens 134-137 21400508-5 2012 Mechanistically, we showed that LBH589 not only affected the expression of p21 and cyclin D1, but markedly determined microtubule stabilization as evidenced by tubulin acetylation and increased tubulin polymerization. Panobinostat 32-38 cyclin dependent kinase inhibitor 1A Homo sapiens 75-78 21984064-2 2012 Panobinostat is a histone deacetylase inhibitor with anti-neoplastic and anti-angiogenic effects and may work synergistically with VEGF inhibitors. Panobinostat 0-12 vascular endothelial growth factor A Homo sapiens 131-135 22144178-0 2012 KLF9 is a novel transcriptional regulator of bortezomib- and LBH589-induced apoptosis in multiple myeloma cells. Panobinostat 61-67 Kruppel like factor 9 Homo sapiens 0-4 22144178-6 2012 Instead, KLF9 levels correlated with bortezomib-dependent inhibition of histone deacetylases (HDAC) and were increased by the HDAC inhibitor LBH589 (panobinostat). Panobinostat 141-147 Kruppel like factor 9 Homo sapiens 9-13 22144178-6 2012 Instead, KLF9 levels correlated with bortezomib-dependent inhibition of histone deacetylases (HDAC) and were increased by the HDAC inhibitor LBH589 (panobinostat). Panobinostat 141-147 histone deacetylase 9 Homo sapiens 126-130 22144178-6 2012 Instead, KLF9 levels correlated with bortezomib-dependent inhibition of histone deacetylases (HDAC) and were increased by the HDAC inhibitor LBH589 (panobinostat). Panobinostat 149-161 Kruppel like factor 9 Homo sapiens 9-13 22144178-6 2012 Instead, KLF9 levels correlated with bortezomib-dependent inhibition of histone deacetylases (HDAC) and were increased by the HDAC inhibitor LBH589 (panobinostat). Panobinostat 149-161 histone deacetylase 9 Homo sapiens 126-130 21400508-5 2012 Mechanistically, we showed that LBH589 not only affected the expression of p21 and cyclin D1, but markedly determined microtubule stabilization as evidenced by tubulin acetylation and increased tubulin polymerization. Panobinostat 32-38 cyclin D1 Homo sapiens 83-92 21772049-9 2011 Among the genes uniquely altered by the combination of panobinostat and decitabine were VHL, TCEB1, WT1, and DIRAS3. Panobinostat 55-67 elongin C Homo sapiens 93-98 22866542-4 2012 In this study, a computational analysis to detect the most deleterious nonsynonymous SNPs of KIT gene was performed and investigated its binding affinity to native and predicted mutant protein structure (D816V) with sunitinib and HDAC (Trichostatin A and Panobinostat) inhibitors was investigated. Panobinostat 255-267 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 93-96 22916295-5 2012 However, combination treatment of ING1 with either LBH589 or 5azaC did show synergy. Panobinostat 51-57 inhibitor of growth family, member 1 Mus musculus 34-38 21772049-9 2011 Among the genes uniquely altered by the combination of panobinostat and decitabine were VHL, TCEB1, WT1, and DIRAS3. Panobinostat 55-67 WT1 transcription factor Homo sapiens 100-103 21772049-9 2011 Among the genes uniquely altered by the combination of panobinostat and decitabine were VHL, TCEB1, WT1, and DIRAS3. Panobinostat 55-67 DIRAS family GTPase 3 Homo sapiens 109-115 21965751-0 2011 Low-dose combinations of LBH589 and TRAIL can overcome TRAIL-resistance in colon cancer cell lines. Panobinostat 25-31 TNF superfamily member 10 Homo sapiens 55-60 21965751-3 2011 RESULTS: It was found that TRAIL-induced cytotoxicity was enhanced by LBH589 cotreatment in the TRAIL-sensitive cell lines, and in the TRAIL-resistant HT29 cell line. Panobinostat 70-76 TNF superfamily member 10 Homo sapiens 27-32 21965751-3 2011 RESULTS: It was found that TRAIL-induced cytotoxicity was enhanced by LBH589 cotreatment in the TRAIL-sensitive cell lines, and in the TRAIL-resistant HT29 cell line. Panobinostat 70-76 TNF superfamily member 10 Homo sapiens 96-101 21965751-3 2011 RESULTS: It was found that TRAIL-induced cytotoxicity was enhanced by LBH589 cotreatment in the TRAIL-sensitive cell lines, and in the TRAIL-resistant HT29 cell line. Panobinostat 70-76 TNF superfamily member 10 Homo sapiens 96-101 21965751-6 2011 CONCLUSION: LBH589 enhances TRAIL-induced apoptosis in human colon cancer cell lines, especially those resistant to TRAIL-induced apoptosis. Panobinostat 12-18 TNF superfamily member 10 Homo sapiens 28-33 21965751-6 2011 CONCLUSION: LBH589 enhances TRAIL-induced apoptosis in human colon cancer cell lines, especially those resistant to TRAIL-induced apoptosis. Panobinostat 12-18 TNF superfamily member 10 Homo sapiens 116-121 21706316-0 2011 Effect of ketoconazole-mediated CYP3A4 inhibition on clinical pharmacokinetics of panobinostat (LBH589), an orally active histone deacetylase inhibitor. Panobinostat 82-94 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 32-38 20715169-0 2011 Antitumor activities and on-target toxicities mediated by a TRAIL receptor agonist following cotreatment with panobinostat. Panobinostat 110-122 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 60-65 21712146-1 2011 Our previous studies have demonstrated that osthole, a Chinese herbal compound, could be incorporated into the hydroxycinnamide scaffold of LBH-589, a potent HDAC inhibitor, as an effective hydrophobic cap; the resulting compounds showed significant potency against several HDAC isoforms. Panobinostat 140-147 histone deacetylase 9 Homo sapiens 158-162 21712146-1 2011 Our previous studies have demonstrated that osthole, a Chinese herbal compound, could be incorporated into the hydroxycinnamide scaffold of LBH-589, a potent HDAC inhibitor, as an effective hydrophobic cap; the resulting compounds showed significant potency against several HDAC isoforms. Panobinostat 140-147 histone deacetylase 9 Homo sapiens 274-278 21436030-7 2011 LBH589 (panobinostat) is an orally available HDAC inhibitor that crosses the blood-brain barrier and is currently in phase III clinical trials for several types of cancer. Panobinostat 0-6 histone deacetylase 9 Homo sapiens 45-49 21464044-0 2011 The dual EGFR/HER2 inhibitor lapatinib synergistically enhances the antitumor activity of the histone deacetylase inhibitor panobinostat in colorectal cancer models. Panobinostat 124-136 epidermal growth factor receptor Homo sapiens 9-13 21464044-0 2011 The dual EGFR/HER2 inhibitor lapatinib synergistically enhances the antitumor activity of the histone deacetylase inhibitor panobinostat in colorectal cancer models. Panobinostat 124-136 erb-b2 receptor tyrosine kinase 2 Homo sapiens 14-18 21464044-9 2011 Panobinostat treatment induced downregulation of EGFR, HER2, and HER3 mRNA and protein through transcriptional and posttranslational mechanisms. Panobinostat 0-12 epidermal growth factor receptor Homo sapiens 49-53 21464044-9 2011 Panobinostat treatment induced downregulation of EGFR, HER2, and HER3 mRNA and protein through transcriptional and posttranslational mechanisms. Panobinostat 0-12 erb-b2 receptor tyrosine kinase 2 Homo sapiens 55-59 21464044-9 2011 Panobinostat treatment induced downregulation of EGFR, HER2, and HER3 mRNA and protein through transcriptional and posttranslational mechanisms. Panobinostat 0-12 erb-b2 receptor tyrosine kinase 3 Homo sapiens 65-69 20213084-0 2010 The pan-DAC inhibitor LBH589 is a multi-functional agent in breast cancer cells: cytotoxic drug and inducer of sodium-iodide symporter (NIS). Panobinostat 22-28 arylacetamide deacetylase Homo sapiens 8-11 20810927-0 2010 Pan-histone deacetylase inhibitor panobinostat depletes CXCR4 levels and signaling and exerts synergistic antimyeloid activity in combination with CXCR4 antagonists. Panobinostat 34-46 C-X-C motif chemokine receptor 4 Homo sapiens 56-61 20810927-0 2010 Pan-histone deacetylase inhibitor panobinostat depletes CXCR4 levels and signaling and exerts synergistic antimyeloid activity in combination with CXCR4 antagonists. Panobinostat 34-46 C-X-C motif chemokine receptor 4 Homo sapiens 147-152 20810927-3 2010 Here, we demonstrate that treatment with the pan-histone deacetylase inhibitor panobinostat (PS) depleted the mRNA and protein levels of CXCR4 in the cultured and primary AML cells. Panobinostat 79-91 C-X-C motif chemokine receptor 4 Homo sapiens 137-142 20810927-4 2010 PS-induced acetylation of the heat shock protein (hsp) 90 reduced the chaperone association between CXCR4 and hsp90, directing CXCR4 to degradation by the 20S proteasome. Panobinostat 0-2 heat shock protein 90 alpha family class A member 1 Homo sapiens 30-57 20810927-4 2010 PS-induced acetylation of the heat shock protein (hsp) 90 reduced the chaperone association between CXCR4 and hsp90, directing CXCR4 to degradation by the 20S proteasome. Panobinostat 0-2 C-X-C motif chemokine receptor 4 Homo sapiens 100-105 20810927-4 2010 PS-induced acetylation of the heat shock protein (hsp) 90 reduced the chaperone association between CXCR4 and hsp90, directing CXCR4 to degradation by the 20S proteasome. Panobinostat 0-2 heat shock protein 90 alpha family class A member 1 Homo sapiens 110-115 20810927-4 2010 PS-induced acetylation of the heat shock protein (hsp) 90 reduced the chaperone association between CXCR4 and hsp90, directing CXCR4 to degradation by the 20S proteasome. Panobinostat 0-2 C-X-C motif chemokine receptor 4 Homo sapiens 127-132 20810927-7 2010 PS and FC-131 exerted more lethal effects on primary AML versus normal CD34(+) bone marrow progenitor cells. Panobinostat 0-2 CD34 molecule Homo sapiens 71-75 20810927-8 2010 These findings support the rationale to test the in vivo efficacy of PS in enhancing the lethal effects of CXCR4 antagonists against AML cells. Panobinostat 69-71 C-X-C motif chemokine receptor 4 Homo sapiens 107-112 21242994-0 2011 LBH589, a deacetylase inhibitor, induces apoptosis in adult T-cell leukemia/lymphoma cells via activation of a novel RAIDD-caspase-2 pathway. Panobinostat 0-6 CASP2 and RIPK1 domain containing adaptor with death domain Homo sapiens 117-122 21242994-0 2011 LBH589, a deacetylase inhibitor, induces apoptosis in adult T-cell leukemia/lymphoma cells via activation of a novel RAIDD-caspase-2 pathway. Panobinostat 0-6 caspase 2 Homo sapiens 123-132 21242994-8 2011 In conclusion, we showed that LBH589 is a strong inducer of apoptosis in ATLL cells and uncovered a novel apoptotic pathway initiated by activation of RAIDD. Panobinostat 30-36 CASP2 and RIPK1 domain containing adaptor with death domain Homo sapiens 151-156 21102427-4 2011 Exposure to LBH589 affected the surface molecule expression on immature and mature DCs, which was associated with DC maturation (CD83 ), antigen presentation (human leukocyte antigen-ABC ) and T-cell co-stimulation (CD40 and CD86 ). Panobinostat 12-18 CD83 molecule Homo sapiens 129-133 21102427-4 2011 Exposure to LBH589 affected the surface molecule expression on immature and mature DCs, which was associated with DC maturation (CD83 ), antigen presentation (human leukocyte antigen-ABC ) and T-cell co-stimulation (CD40 and CD86 ). Panobinostat 12-18 CD40 molecule Homo sapiens 216-220 21102427-4 2011 Exposure to LBH589 affected the surface molecule expression on immature and mature DCs, which was associated with DC maturation (CD83 ), antigen presentation (human leukocyte antigen-ABC ) and T-cell co-stimulation (CD40 and CD86 ). Panobinostat 12-18 CD86 molecule Homo sapiens 226-230 21102427-7 2011 LBH589 also significantly repressed the production of interleukin (IL)-6, IL-10, IL-12p70, IL-23 and tumor necrosis factor-alpha by Toll-like receptor (TLR)3 and TLR4-induced DC activation, indicating an important role of HDAC activity in immune regulation and inflammation. Panobinostat 0-6 interleukin 10 Homo sapiens 74-79 21102427-7 2011 LBH589 also significantly repressed the production of interleukin (IL)-6, IL-10, IL-12p70, IL-23 and tumor necrosis factor-alpha by Toll-like receptor (TLR)3 and TLR4-induced DC activation, indicating an important role of HDAC activity in immune regulation and inflammation. Panobinostat 0-6 interleukin 23 subunit alpha Homo sapiens 91-128 21102427-7 2011 LBH589 also significantly repressed the production of interleukin (IL)-6, IL-10, IL-12p70, IL-23 and tumor necrosis factor-alpha by Toll-like receptor (TLR)3 and TLR4-induced DC activation, indicating an important role of HDAC activity in immune regulation and inflammation. Panobinostat 0-6 toll like receptor 3 Homo sapiens 152-157 21102427-7 2011 LBH589 also significantly repressed the production of interleukin (IL)-6, IL-10, IL-12p70, IL-23 and tumor necrosis factor-alpha by Toll-like receptor (TLR)3 and TLR4-induced DC activation, indicating an important role of HDAC activity in immune regulation and inflammation. Panobinostat 0-6 toll like receptor 4 Homo sapiens 162-166 22087262-4 2011 Panobinostat/everolimus combination treatment resulted in significantly greater antitumor activity in mice bearing androgen sensitive Myc-CaP and castrate resistant Myc-CaP tumors compared to single treatments. Panobinostat 0-12 myelocytomatosis oncogene Mus musculus 134-137 22087262-5 2011 We identified that panobinostat/everolimus combination resulted in enhanced anti-tumor activity mediated by decreased tumor growth concurrent with augmentation of p21 and p27 expression and the attenuation of angiogenesis and tumor proliferation via androgen receptor, c-Myc and HIF-1alpha signaling. Panobinostat 19-31 cyclin-dependent kinase inhibitor 1A (P21) Mus musculus 163-166 22087262-5 2011 We identified that panobinostat/everolimus combination resulted in enhanced anti-tumor activity mediated by decreased tumor growth concurrent with augmentation of p21 and p27 expression and the attenuation of angiogenesis and tumor proliferation via androgen receptor, c-Myc and HIF-1alpha signaling. Panobinostat 19-31 cyclin-dependent kinase inhibitor 1B Mus musculus 171-174 22087262-5 2011 We identified that panobinostat/everolimus combination resulted in enhanced anti-tumor activity mediated by decreased tumor growth concurrent with augmentation of p21 and p27 expression and the attenuation of angiogenesis and tumor proliferation via androgen receptor, c-Myc and HIF-1alpha signaling. Panobinostat 19-31 androgen receptor Mus musculus 250-267 22087262-5 2011 We identified that panobinostat/everolimus combination resulted in enhanced anti-tumor activity mediated by decreased tumor growth concurrent with augmentation of p21 and p27 expression and the attenuation of angiogenesis and tumor proliferation via androgen receptor, c-Myc and HIF-1alpha signaling. Panobinostat 19-31 myelocytomatosis oncogene Mus musculus 271-274 22087262-5 2011 We identified that panobinostat/everolimus combination resulted in enhanced anti-tumor activity mediated by decreased tumor growth concurrent with augmentation of p21 and p27 expression and the attenuation of angiogenesis and tumor proliferation via androgen receptor, c-Myc and HIF-1alpha signaling. Panobinostat 19-31 hypoxia inducible factor 1, alpha subunit Mus musculus 279-289 21687633-7 2011 Our data indicate that depletion of MTDH in endometrial cancer cells resulted in sensitization of cells that were previously resistant in response to combinatorial treatment with TRAIL and the HDAC inhibitor LBH589. Panobinostat 208-214 metadherin Homo sapiens 36-40 21687633-7 2011 Our data indicate that depletion of MTDH in endometrial cancer cells resulted in sensitization of cells that were previously resistant in response to combinatorial treatment with TRAIL and the HDAC inhibitor LBH589. Panobinostat 208-214 histone deacetylase 9 Homo sapiens 193-197 21687633-10 2011 On the other hand, in MTDH depleted cells, inhibition of PDK1 and AKT phosphorylation along with increased Bim expression and XIAP degradation correlated with enhanced sensitivity to cell death in response to TRAIL and LBH589. Panobinostat 219-225 metadherin Homo sapiens 22-26 21687633-10 2011 On the other hand, in MTDH depleted cells, inhibition of PDK1 and AKT phosphorylation along with increased Bim expression and XIAP degradation correlated with enhanced sensitivity to cell death in response to TRAIL and LBH589. Panobinostat 219-225 pyruvate dehydrogenase kinase 1 Homo sapiens 57-61 21687633-10 2011 On the other hand, in MTDH depleted cells, inhibition of PDK1 and AKT phosphorylation along with increased Bim expression and XIAP degradation correlated with enhanced sensitivity to cell death in response to TRAIL and LBH589. Panobinostat 219-225 AKT serine/threonine kinase 1 Homo sapiens 66-69 20213084-4 2010 In the present study, we report for the first time that the pan-deacetylase (DAC) inhibitor LBH589 (panobinostat) significantly induced NIS, both as mRNA and as protein, through the increase of NIS promoter activity, with the final consequence of obtaining a significant up-take of iodide in MCF7, T47D, and MDA-MB231 breast cancer cells. Panobinostat 92-98 arylacetamide deacetylase Homo sapiens 77-80 20213084-4 2010 In the present study, we report for the first time that the pan-deacetylase (DAC) inhibitor LBH589 (panobinostat) significantly induced NIS, both as mRNA and as protein, through the increase of NIS promoter activity, with the final consequence of obtaining a significant up-take of iodide in MCF7, T47D, and MDA-MB231 breast cancer cells. Panobinostat 100-112 arylacetamide deacetylase Homo sapiens 77-80 20508617-5 2010 We report here that treatment of AML cells with the HDACi LBH589 induces the ubiquitin-conjugating enzyme UBCH8 and degradation of FLT3-ITD. Panobinostat 58-64 ubiquitin conjugating enzyme E2 L6 Homo sapiens 106-111 20647473-7 2010 Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells. Panobinostat 49-61 DNA damage inducible transcript 3 Homo sapiens 105-109 20647473-7 2010 Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells. Panobinostat 49-61 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 114-118 20647473-9 2010 CONCLUSION: These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib. Panobinostat 141-153 DNA damage inducible transcript 3 Homo sapiens 71-75 20127862-1 2010 Panobinostat (LBH589) is a highly potent deacetylase inhibitor that has demonstrated clinical efficacy in patients with advanced cutaneous T-cell lymphoma (CTCL). Panobinostat 0-12 TSPY like 2 Homo sapiens 156-160 20127862-1 2010 Panobinostat (LBH589) is a highly potent deacetylase inhibitor that has demonstrated clinical efficacy in patients with advanced cutaneous T-cell lymphoma (CTCL). Panobinostat 14-20 TSPY like 2 Homo sapiens 156-160 20127862-8 2010 Inhibition of Bcl-2 sensitized cells to the cytotoxic activity of panobinostat. Panobinostat 66-78 BCL2 apoptosis regulator Homo sapiens 14-19 20127862-10 2010 Interestingly, panobinostat could induce cytotoxicity in vorinostat-resistant CTCL cells by downregulating phosphorylated STAT3 and STAT5 proteins. Panobinostat 15-27 TSPY like 2 Homo sapiens 78-82 20127862-10 2010 Interestingly, panobinostat could induce cytotoxicity in vorinostat-resistant CTCL cells by downregulating phosphorylated STAT3 and STAT5 proteins. Panobinostat 15-27 signal transducer and activator of transcription 3 Homo sapiens 122-127 20127862-10 2010 Interestingly, panobinostat could induce cytotoxicity in vorinostat-resistant CTCL cells by downregulating phosphorylated STAT3 and STAT5 proteins. Panobinostat 15-27 signal transducer and activator of transcription 5A Homo sapiens 132-137 20508617-5 2010 We report here that treatment of AML cells with the HDACi LBH589 induces the ubiquitin-conjugating enzyme UBCH8 and degradation of FLT3-ITD. Panobinostat 58-64 fms related receptor tyrosine kinase 3 Homo sapiens 131-139 20634887-8 2010 The S-adenosylhomocysteine hydrolase inhibitor 3-Deazaneplanocin (DZNep) and the histone deacetylase inhibitor LBH589 (Panobinostat), reactivated the expression of genes repressed by H3K27me3, depleted cells from the PRC2 component EZH2 and induced apoptosis in human MM cell lines. Panobinostat 111-117 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 232-236 20534486-0 2010 The HDAC inhibitor LBH589 (panobinostat) is an inhibitory modulator of aromatase gene expression. Panobinostat 19-25 histone deacetylase 9 Homo sapiens 4-8 20534486-0 2010 The HDAC inhibitor LBH589 (panobinostat) is an inhibitory modulator of aromatase gene expression. Panobinostat 27-39 histone deacetylase 9 Homo sapiens 4-8 20534486-9 2010 LBH589 reduces the levels of C/EBPdelta, decreases the binding of C/EBPdelta, and increases the levels and binding of acetyl-histones to the promoters I.3/II. Panobinostat 0-6 CCAAT enhancer binding protein delta Homo sapiens 29-39 20534486-9 2010 LBH589 reduces the levels of C/EBPdelta, decreases the binding of C/EBPdelta, and increases the levels and binding of acetyl-histones to the promoters I.3/II. Panobinostat 0-6 CCAAT enhancer binding protein delta Homo sapiens 66-76 20028416-9 2010 These data show impressive synergistic action of the novel HSP90 inhibitor NVP-AUY922 with melphalan, doxorubicin, NVP-LBH589, and SAHA in multiple myeloma and build the frame work for clinical trials. Panobinostat 119-125 heat shock protein 90 alpha family class A member 1 Homo sapiens 59-64 20217089-11 2010 Since preclinical studies suggest a dose-dependent effect of panobinostat on PSA expression, and other phase I data demonstrate that intravenous panobinostat produces higher peak concentrations (>20- to 30-fold) and area under the curve (3.5x-5x), a decision was made to focus the development of panobinostat on the intravenous formulation to treat CRPC. Panobinostat 145-157 kallikrein related peptidase 3 Homo sapiens 77-80 20442774-0 2010 c-FLIP degradation mediates sensitization of pancreatic cancer cells to TRAIL-induced apoptosis by the histone deacetylase inhibitor LBH589. Panobinostat 133-139 CASP8 and FADD like apoptosis regulator Homo sapiens 0-6 20442774-0 2010 c-FLIP degradation mediates sensitization of pancreatic cancer cells to TRAIL-induced apoptosis by the histone deacetylase inhibitor LBH589. Panobinostat 133-139 TNF superfamily member 10 Homo sapiens 72-77 20442774-4 2010 In this study, we have shown that the histone deacetylase inhibitor LBH589 can synergize with TRAIL to augment apoptosis even in TRAIL-resistant cells. Panobinostat 68-74 TNF superfamily member 10 Homo sapiens 94-99 20442774-4 2010 In this study, we have shown that the histone deacetylase inhibitor LBH589 can synergize with TRAIL to augment apoptosis even in TRAIL-resistant cells. Panobinostat 68-74 TNF superfamily member 10 Homo sapiens 129-134 20442774-7 2010 Moreover, LBH589 decreased c-FLIP stability and the presence of the proteasome inhibitor MG132 prevented c-FLIP from reduction by LBH589. Panobinostat 10-16 CASP8 and FADD like apoptosis regulator Homo sapiens 27-33 20442774-7 2010 Moreover, LBH589 decreased c-FLIP stability and the presence of the proteasome inhibitor MG132 prevented c-FLIP from reduction by LBH589. Panobinostat 130-136 CASP8 and FADD like apoptosis regulator Homo sapiens 105-111 20442774-9 2010 These data thus indicate that LBH589 promotes ubiqutin/proteasome-mediated degradation of c-FLIP, leading to downregulation of c-FLIP. Panobinostat 30-36 CASP8 and FADD like apoptosis regulator Homo sapiens 90-96 20442774-9 2010 These data thus indicate that LBH589 promotes ubiqutin/proteasome-mediated degradation of c-FLIP, leading to downregulation of c-FLIP. Panobinostat 30-36 CASP8 and FADD like apoptosis regulator Homo sapiens 127-133 20442774-10 2010 Collectively, LBH589 induces c-FLIP degradation and accordingly sensitizes pancreatic cancer cells to TRAIL-induced apoptosis, highlighting a novel therapeutic regimen against pancreatic cancer. Panobinostat 14-20 CASP8 and FADD like apoptosis regulator Homo sapiens 29-35 20442774-10 2010 Collectively, LBH589 induces c-FLIP degradation and accordingly sensitizes pancreatic cancer cells to TRAIL-induced apoptosis, highlighting a novel therapeutic regimen against pancreatic cancer. Panobinostat 14-20 TNF superfamily member 10 Homo sapiens 102-107 20371724-0 2010 Treatment with panobinostat induces glucose-regulated protein 78 acetylation and endoplasmic reticulum stress in breast cancer cells. Panobinostat 15-27 heat shock protein family A (Hsp70) member 5 Homo sapiens 36-64 20371724-6 2010 Treatment with panobinostat increased the levels of phosphorylated-eukaryotic translation initiation factor (p-eIF2alpha), ATF4, and CAAT/enhancer binding protein homologous protein (CHOP). Panobinostat 15-27 DNA damage inducible transcript 3 Homo sapiens 183-187 20371724-6 2010 Treatment with panobinostat increased the levels of phosphorylated-eukaryotic translation initiation factor (p-eIF2alpha), ATF4, and CAAT/enhancer binding protein homologous protein (CHOP). Panobinostat 15-27 activating transcription factor 4 Homo sapiens 123-127 20371724-8 2010 Knockdown of GRP78 sensitized MCF-7 cells to bortezomib and panobinostat-induced UPR and cell death. Panobinostat 60-72 heat shock protein family A (Hsp70) member 5 Homo sapiens 13-18 20371724-9 2010 These findings indicate that enforced acetylation and decreased binding of GRP78 to PERK is mechanistically linked to panobinostat-induced UPR and cell death of breast cancer cells. Panobinostat 118-130 heat shock protein family A (Hsp70) member 5 Homo sapiens 75-80 20086250-5 2010 Treatment of cells with the histone deacetylase inhibitor LBH589 resulted in a clear up-regulation in the expression of Bim. Panobinostat 58-64 BCL2 like 11 Homo sapiens 120-123 20371724-9 2010 These findings indicate that enforced acetylation and decreased binding of GRP78 to PERK is mechanistically linked to panobinostat-induced UPR and cell death of breast cancer cells. Panobinostat 118-130 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 84-88 20039095-3 2010 Based on this observation, this study was designed to investigate the cellular effects of curcumin combination with the pan-HDAC inhibitors, vorinostat and panobinostat, which induce hyperacetylation of Hsp90, resulting in inhibition of its chaperone function. Panobinostat 156-168 heat shock protein 90 alpha family class A member 1 Homo sapiens 203-208 20043870-6 2010 We discovered that two HDAC inhibitors belonging to the hydroxamate group, namely TSA and LBH589, are the most efficient inducers of TAp63 expression. Panobinostat 90-96 histone deacetylase 9 Homo sapiens 23-27 19790234-5 2010 RESULTS: Within 16 hr of treatment of AI-cells with low concentrations of the histone deacetylase inhibitor LBH589, a shift of cytoplasmic Puralpha restored the nuclear levels and the binding of Puralpha to the ARS. Panobinostat 108-114 purine rich element binding protein A Homo sapiens 139-147 19790234-5 2010 RESULTS: Within 16 hr of treatment of AI-cells with low concentrations of the histone deacetylase inhibitor LBH589, a shift of cytoplasmic Puralpha restored the nuclear levels and the binding of Puralpha to the ARS. Panobinostat 108-114 purine rich element binding protein A Homo sapiens 195-203 19790234-5 2010 RESULTS: Within 16 hr of treatment of AI-cells with low concentrations of the histone deacetylase inhibitor LBH589, a shift of cytoplasmic Puralpha restored the nuclear levels and the binding of Puralpha to the ARS. Panobinostat 108-114 RIEG2 Homo sapiens 211-214 19790234-8 2010 Most notably, treatment of bicalutamide-resistant AI-cells with 10 nM LBH589 combined with 12.5 microM bicalutamide synergistically inhibited cell growth and induced a fivefold higher level of caspase 3/7 activation than observed in AD-cells. Panobinostat 70-76 caspase 3 Homo sapiens 193-202 19790234-9 2010 CONCLUSIONS: Low-dose LBH589 restores Puralpha binding to ARS and down-regulates AR transcription. Panobinostat 22-28 purine rich element binding protein A Homo sapiens 38-46 19790234-9 2010 CONCLUSIONS: Low-dose LBH589 restores Puralpha binding to ARS and down-regulates AR transcription. Panobinostat 22-28 RIEG2 Homo sapiens 58-61 19790234-9 2010 CONCLUSIONS: Low-dose LBH589 restores Puralpha binding to ARS and down-regulates AR transcription. Panobinostat 22-28 androgen receptor Homo sapiens 58-60 20208142-3 2010 HepG2 (p53wt) and Hep3B (p53null) responded to panobinostat treatment with a reduction of cell proliferation and a significant increase in apoptotic cell death at low micromolar concentrations. Panobinostat 47-59 tumor protein p53 Homo sapiens 7-10 20208142-3 2010 HepG2 (p53wt) and Hep3B (p53null) responded to panobinostat treatment with a reduction of cell proliferation and a significant increase in apoptotic cell death at low micromolar concentrations. Panobinostat 47-59 tumor protein p53 Homo sapiens 25-28 19828702-0 2009 Cotreatment with panobinostat and JAK2 inhibitor TG101209 attenuates JAK2V617F levels and signaling and exerts synergistic cytotoxic effects against human myeloproliferative neoplastic cells. Panobinostat 17-29 Janus kinase 2 Homo sapiens 69-73 19828702-5 2009 Treatment with PS also disrupted the chaperone association of JAK2V617F with hsp90, promoting proteasomal degradation of JAK2V617F. Panobinostat 15-17 heat shock protein 90 alpha family class A member 1 Homo sapiens 77-82 19828702-9 2009 Cotreatment with TG101209 and PS exerted greater cytotoxicity against primary CD34(+) MPN cells than normal CD34(+) HPCs. Panobinostat 30-32 CD34 molecule Homo sapiens 78-82 19828702-9 2009 Cotreatment with TG101209 and PS exerted greater cytotoxicity against primary CD34(+) MPN cells than normal CD34(+) HPCs. Panobinostat 30-32 CD34 molecule Homo sapiens 108-112 19706776-6 2009 KIT activity, expression, and activation of downstream pathways were strongly inhibited by several HDACI (SAHA, LBH589, VPA, trichostatin A, and NaButyrate). Panobinostat 112-118 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 0-3 19638619-7 2009 Furthermore, compared with treatment with each agent alone, cotreatment with DZNep and the pan-histone deacetylase inhibitor panobinostat caused more depletion of EZH2, induced more apoptosis of AML, but not normal CD34(+) bone marrow progenitor cells, and significantly improved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia. Panobinostat 125-137 enhancer of zeste 2 polycomb repressive complex 2 subunit Mus musculus 163-167 19638619-7 2009 Furthermore, compared with treatment with each agent alone, cotreatment with DZNep and the pan-histone deacetylase inhibitor panobinostat caused more depletion of EZH2, induced more apoptosis of AML, but not normal CD34(+) bone marrow progenitor cells, and significantly improved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia. Panobinostat 125-137 CD34 antigen Mus musculus 215-219 19584083-11 2009 Notably, LBH589 also induces SMN2 expression in SMA fibroblasts inert to VPA, in human neural stem cells and in the spinal cord of SMN2-transgenic mice. Panobinostat 9-15 survival of motor neuron 2, centromeric Homo sapiens 29-33 19584083-11 2009 Notably, LBH589 also induces SMN2 expression in SMA fibroblasts inert to VPA, in human neural stem cells and in the spinal cord of SMN2-transgenic mice. Panobinostat 9-15 survival of motor neuron 2, centromeric Homo sapiens 131-135 19706776-7 2009 SAHA and LBH589 induced apoptosis in KIT-positive GIST, and strong synergism with imatinib was observed at low concentrations of SAHA and LBH589. Panobinostat 9-15 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 37-40 19509169-2 2009 DNA methyltransferase (DNMT) inhibitors such as 5-aza-2"-deoxycytidine or 5-azacytidine have been approved in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML), whereas the histone deacetylase inhibitors (HDIs) including vorinostat, romidepsin, panobinostat, belinostat, and entinostat have been shown to be active in cutaneous and peripheral T-cell lymphoma. Panobinostat 263-275 DNA methyltransferase 1 Homo sapiens 0-21 19344997-0 2009 Development of the pan-DAC inhibitor panobinostat (LBH589): successes and challenges. Panobinostat 37-49 arylacetamide deacetylase Homo sapiens 23-26 19344997-0 2009 Development of the pan-DAC inhibitor panobinostat (LBH589): successes and challenges. Panobinostat 51-57 arylacetamide deacetylase Homo sapiens 23-26 19344997-2 2009 The HDAC inhibitor, panobinostat (LBH589, Novartis Pharmaceuticals), achieves potent inhibition of all HDAC enzymes implicated in cancer and has demonstrated potent anti-tumor activity in preclinical models and promising clinical efficacy in cancer patients. Panobinostat 20-32 histone deacetylase 9 Homo sapiens 4-8 19344997-2 2009 The HDAC inhibitor, panobinostat (LBH589, Novartis Pharmaceuticals), achieves potent inhibition of all HDAC enzymes implicated in cancer and has demonstrated potent anti-tumor activity in preclinical models and promising clinical efficacy in cancer patients. Panobinostat 20-32 histone deacetylase 9 Homo sapiens 103-107 19344997-2 2009 The HDAC inhibitor, panobinostat (LBH589, Novartis Pharmaceuticals), achieves potent inhibition of all HDAC enzymes implicated in cancer and has demonstrated potent anti-tumor activity in preclinical models and promising clinical efficacy in cancer patients. Panobinostat 34-40 histone deacetylase 9 Homo sapiens 4-8 19344997-2 2009 The HDAC inhibitor, panobinostat (LBH589, Novartis Pharmaceuticals), achieves potent inhibition of all HDAC enzymes implicated in cancer and has demonstrated potent anti-tumor activity in preclinical models and promising clinical efficacy in cancer patients. Panobinostat 34-40 histone deacetylase 9 Homo sapiens 103-107 19402126-4 2009 As with other human cancer cell lines, LBH589 causes up-regulation of p21, G2/M cell cycle arrest, and cell death of human HNSCC cell lines, as measured using flow cytometry and cDNA microarrays. Panobinostat 39-45 H3 histone pseudogene 16 Homo sapiens 70-73 19329208-10 2009 LBH589 led acetylation of histone H3 and HSP90. Panobinostat 0-6 heat shock protein 90 alpha family class A member 1 Homo sapiens 41-46 19509169-2 2009 DNA methyltransferase (DNMT) inhibitors such as 5-aza-2"-deoxycytidine or 5-azacytidine have been approved in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML), whereas the histone deacetylase inhibitors (HDIs) including vorinostat, romidepsin, panobinostat, belinostat, and entinostat have been shown to be active in cutaneous and peripheral T-cell lymphoma. Panobinostat 263-275 DNA methyltransferase 1 Homo sapiens 23-27 19176386-3 2009 Here, we show that histone deacetylase (HDAC) inhibitors, including SAHA (vorinostat) and LBH589, which are currently being tested in clinic, could be such a therapy. Panobinostat 90-96 histone deacetylase 9 Homo sapiens 19-38 19322073-1 2009 Histone deacetylase (HDAC) inhibitors such as vorinostat (suberoylanilide hydroxamic acid), valproic acid, romidepsin (FK-228), and LBH589 comprise a relatively new class of potent anticancer agents. Panobinostat 132-138 histone deacetylase 9 Homo sapiens 0-19 19322073-4 2009 This acquired resistance also associates with cross-resistance to the hydroxamate-class (LBH589 and JNJ26481585) and to the aliphatic acid-class (valproic acid) HDAC inhibitors but not to the benzamide-class (MGCD0103) and the cyclic peptide-class (romidepsin) HDAC inhibitors. Panobinostat 89-95 histone deacetylase 9 Homo sapiens 261-265 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 62-68 DNA methyltransferase 1 Homo sapiens 89-94 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 62-68 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 99-103 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 62-68 DNA methyltransferase 1 Homo sapiens 148-153 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 62-68 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 159-163 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 62-68 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 189-193 19279403-3 2009 Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2. Panobinostat 70-82 heat shock protein 90 alpha family class A member 1 Homo sapiens 30-35 19279403-3 2009 Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2. Panobinostat 70-82 DNA methyltransferase 1 Homo sapiens 154-159 19279403-3 2009 Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2. Panobinostat 70-82 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 164-168 19279403-3 2009 Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2. Panobinostat 70-82 DNA methyltransferase 1 Homo sapiens 216-221 19279403-3 2009 Similar to treatment with the hsp90 inhibitor 17-DMAG, treatment with panobinostat also inhibited the chaperone association of heat shock protein 90 with DNMT1 and EZH2, which promoted the proteasomal degradation of DNMT1 and EZH2. Panobinostat 70-82 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 226-230 19279403-4 2009 Unlike treatment with the DNA methyltransferase inhibitor decitabine, which demethylates JunB promoter DNA, panobinostat treatment mediated chromatin alterations in the JunB promoter. Panobinostat 108-120 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 169-173 19279403-5 2009 Combined treatment with panobinostat and decitabine caused greater attenuation of DNMT1 and EZH2 levels than either agent alone, which was accompanied by more JunB de-repression and loss of clonogenic survival of K562 cells. Panobinostat 24-36 DNA methyltransferase 1 Homo sapiens 82-87 19279403-5 2009 Combined treatment with panobinostat and decitabine caused greater attenuation of DNMT1 and EZH2 levels than either agent alone, which was accompanied by more JunB de-repression and loss of clonogenic survival of K562 cells. Panobinostat 24-36 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 92-96 19279403-5 2009 Combined treatment with panobinostat and decitabine caused greater attenuation of DNMT1 and EZH2 levels than either agent alone, which was accompanied by more JunB de-repression and loss of clonogenic survival of K562 cells. Panobinostat 24-36 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 159-163 19279403-7 2009 Collectively, these findings indicate that co-treatment with panobinostat and decitabine targets multiple epigenetic mechanisms to de-repress JunB and exerts antileukemia activity against human acute myeloid leukemia cells. Panobinostat 61-73 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 142-146 19188154-0 2009 Dual degradation of aurora A and B kinases by the histone deacetylase inhibitor LBH589 induces G2-M arrest and apoptosis of renal cancer cells. Panobinostat 80-86 aurora kinase A Homo sapiens 20-28 19188154-4 2009 RESULTS: HDACI LBH589 induced degradation of both Aurora A and B kinases through a proteasome-mediated pathway by targeting HDAC3 and HDAC6. Panobinostat 15-21 aurora kinase A Homo sapiens 50-58 19188154-4 2009 RESULTS: HDACI LBH589 induced degradation of both Aurora A and B kinases through a proteasome-mediated pathway by targeting HDAC3 and HDAC6. Panobinostat 15-21 histone deacetylase 3 Homo sapiens 124-129 19188154-4 2009 RESULTS: HDACI LBH589 induced degradation of both Aurora A and B kinases through a proteasome-mediated pathway by targeting HDAC3 and HDAC6. Panobinostat 15-21 histone deacetylase 6 Homo sapiens 134-139 19188154-5 2009 The dual degradation of Aurora A and B kinases mediated by LBH589 resulted in inducing G2-M arrest and apoptosis of renal cancer cell lines and our results also showed that LBH589 potently inhibited renal cancer cell growth in vitro and suppressed tumor formation in vivo. Panobinostat 59-65 aurora kinase A Homo sapiens 24-32 19279403-0 2009 Panobinostat treatment depletes EZH2 and DNMT1 levels and enhances decitabine mediated de-repression of JunB and loss of survival of human acute leukemia cells. Panobinostat 0-12 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 32-36 19279403-0 2009 Panobinostat treatment depletes EZH2 and DNMT1 levels and enhances decitabine mediated de-repression of JunB and loss of survival of human acute leukemia cells. Panobinostat 0-12 DNA methyltransferase 1 Homo sapiens 41-46 19279403-0 2009 Panobinostat treatment depletes EZH2 and DNMT1 levels and enhances decitabine mediated de-repression of JunB and loss of survival of human acute leukemia cells. Panobinostat 0-12 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 104-108 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 48-60 DNA methyltransferase 1 Homo sapiens 89-94 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 48-60 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 99-103 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 48-60 DNA methyltransferase 1 Homo sapiens 148-153 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 48-60 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 159-163 19279403-2 2009 Here, we determined that the pan-HDAC inhibitor panobinostat (LBH589) treatment depletes DNMT1 and EZH2 protein levels, disrupts the interaction of DNMT1 with EZH2, as well as de-represses JunB in human acute leukemia cells. Panobinostat 48-60 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 189-193 19074726-4 2009 Here, we demonstrate that treatment with panobinostat rapidly inhibits the in vitro and intracellular activity, as well as the mRNA and protein levels of HDAC7, and induces expression and translocation of Nur77 to the mitochondria. Panobinostat 41-53 histone deacetylase 7 Homo sapiens 154-159 19074726-4 2009 Here, we demonstrate that treatment with panobinostat rapidly inhibits the in vitro and intracellular activity, as well as the mRNA and protein levels of HDAC7, and induces expression and translocation of Nur77 to the mitochondria. Panobinostat 41-53 nuclear receptor subfamily 4 group A member 1 Homo sapiens 205-210 19176386-3 2009 Here, we show that histone deacetylase (HDAC) inhibitors, including SAHA (vorinostat) and LBH589, which are currently being tested in clinic, could be such a therapy. Panobinostat 90-96 histone deacetylase 9 Homo sapiens 40-44 19179889-0 2009 A histone deacetylase inhibitor LBH589 downregulates XIAP in mesothelioma cell lines which is likely responsible for increased apoptosis with TRAIL. Panobinostat 32-38 X-linked inhibitor of apoptosis Homo sapiens 53-57 19179889-0 2009 A histone deacetylase inhibitor LBH589 downregulates XIAP in mesothelioma cell lines which is likely responsible for increased apoptosis with TRAIL. Panobinostat 32-38 TNF superfamily member 10 Homo sapiens 142-147 19179889-8 2009 LBH589 and TRAIL appeared to induce higher levels of caspase 3 and 7 and this appeared to be closely related to ability of LBH589 to degrade XIAP. Panobinostat 0-6 X-linked inhibitor of apoptosis Homo sapiens 141-145 19179889-10 2009 CONCLUSIONS: In mesothelioma cell lines, LBH589 increases the sensitivity to TRAIL. Panobinostat 41-47 TNF superfamily member 10 Homo sapiens 77-82 18424067-6 2008 HDAC inhibitors, under clinical evaluation in the treatment of NSCLC patients, are pivanex, CI-994, vorinostat, and LBH589. Panobinostat 116-122 histone deacetylase 9 Homo sapiens 0-4 18628465-2 2008 Herein, we report the safety and activity of the histone deacetylase inhibitor panobinostat (LBH589) in cutaneous T-cell lymphoma (CTCL) and identify genes commonly regulated by panobinostat. Panobinostat 79-91 TSPY like 2 Homo sapiens 131-135 18628465-2 2008 Herein, we report the safety and activity of the histone deacetylase inhibitor panobinostat (LBH589) in cutaneous T-cell lymphoma (CTCL) and identify genes commonly regulated by panobinostat. Panobinostat 93-99 TSPY like 2 Homo sapiens 131-135 18628465-3 2008 EXPERIMENTAL DESIGN: Panobinostat was administered orally to patients with CTCL on Monday, Wednesday, and Friday of each week on a 28-day cycle. Panobinostat 21-33 TSPY like 2 Homo sapiens 75-79 18349321-4 2008 LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Panobinostat 0-6 FA complementation group G Homo sapiens 109-114 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 53-65 histone deacetylase 9 Homo sapiens 38-42 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 53-65 heat shock protein 90 alpha family class A member 1 Homo sapiens 94-104 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 53-65 matrix metallopeptidase 2 Homo sapiens 141-146 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 67-73 histone deacetylase 9 Homo sapiens 38-42 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 67-73 heat shock protein 90 alpha family class A member 1 Homo sapiens 94-104 18559531-6 2008 Notably, after treatment with the pan-HDAC inhibitor panobinostat (LBH589), the extracellular hsp90alpha was hyperacetylated and it bound to MMP-2, which was associated with increased in vitro tumor cell invasiveness. Panobinostat 67-73 matrix metallopeptidase 2 Homo sapiens 141-146 18519793-3 2008 Thus, we hypothesized that combination treatment of rapamycin and the HDAC inhibitor LBH589 has greater antiangiogenic and antitumor activity compared with single agents. Panobinostat 85-91 histone deacetylase 9 Homo sapiens 70-74 18519793-8 2008 LBH589 decreased both constitutively expressed and rapamycin-induced phosphorylated Akt levels in PC3 and C2 cell lines. Panobinostat 0-6 AKT serine/threonine kinase 1 Homo sapiens 84-87 18519793-8 2008 LBH589 decreased both constitutively expressed and rapamycin-induced phosphorylated Akt levels in PC3 and C2 cell lines. Panobinostat 0-6 keratin 6A Homo sapiens 98-101 18445700-4 2008 In U251 cells, bortezomib alone or in combination with LBH589 decreased Raf-1 levels and suppressed Akt and Erk activation. Panobinostat 55-61 Raf-1 proto-oncogene, serine/threonine kinase Homo sapiens 72-77 18445700-4 2008 In U251 cells, bortezomib alone or in combination with LBH589 decreased Raf-1 levels and suppressed Akt and Erk activation. Panobinostat 55-61 AKT serine/threonine kinase 1 Homo sapiens 100-103 18445700-4 2008 In U251 cells, bortezomib alone or in combination with LBH589 decreased Raf-1 levels and suppressed Akt and Erk activation. Panobinostat 55-61 mitogen-activated protein kinase 1 Homo sapiens 108-111 18445700-5 2008 LBH589 or bortezomib alone increased expression of the cell cycle regulators p21 and p27. Panobinostat 0-6 H3 histone pseudogene 16 Homo sapiens 77-80 18445700-5 2008 LBH589 or bortezomib alone increased expression of the cell cycle regulators p21 and p27. Panobinostat 0-6 interferon alpha inducible protein 27 Homo sapiens 85-88 18445700-7 2008 Synergistic induction of apoptosis after exposure to LBH589 and bortezomib was partially mediated by Bax translocation from the cytosol to the mitochondria resulting from Bax conformational changes. Panobinostat 53-59 BCL2 associated X, apoptosis regulator Homo sapiens 101-104 18445700-7 2008 Synergistic induction of apoptosis after exposure to LBH589 and bortezomib was partially mediated by Bax translocation from the cytosol to the mitochondria resulting from Bax conformational changes. Panobinostat 53-59 BCL2 associated X, apoptosis regulator Homo sapiens 171-174 18445700-8 2008 Bax translocation precedes cytochrome c release and apoptosis, and selective down-regulation of Bax using siRNA significantly mitigates the cytotoxicity of LBH589 and bortezomib. Panobinostat 156-162 BCL2 associated X, apoptosis regulator Homo sapiens 0-3 18445700-8 2008 Bax translocation precedes cytochrome c release and apoptosis, and selective down-regulation of Bax using siRNA significantly mitigates the cytotoxicity of LBH589 and bortezomib. Panobinostat 156-162 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 18349321-4 2008 LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Panobinostat 0-6 growth arrest and DNA damage inducible alpha Homo sapiens 124-131 18349321-4 2008 LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Panobinostat 0-6 forkhead box O3 Homo sapiens 116-122 18349321-4 2008 LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Panobinostat 0-6 growth arrest and DNA damage inducible beta Homo sapiens 133-140 18349321-4 2008 LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Panobinostat 0-6 growth arrest and DNA damage inducible gamma Homo sapiens 146-153 18483358-8 2008 Treatment of CD9-nonexpressing 5T33MMvt cells with the clinically relevant histone deacetylase inhibitor LBH589 resulted in a significant increase in CD9 expression. Panobinostat 105-111 CD9 antigen Mus musculus 13-16 18483358-8 2008 Treatment of CD9-nonexpressing 5T33MMvt cells with the clinically relevant histone deacetylase inhibitor LBH589 resulted in a significant increase in CD9 expression. Panobinostat 105-111 CD9 antigen Mus musculus 150-153 18349321-5 2008 The most dramatically expressed gene (up to 45-fold induction) observed after treatment with LBH589 is GADD45G. Panobinostat 93-99 growth arrest and DNA damage inducible gamma Homo sapiens 103-110 18349321-7 2008 Furthermore, treatment with LBH589 was active against cultured primary Ph(-) ALL cells, including those from a relapsed patient, inducing loss of cell viability (up to 70%) and induction of GADD45G mRNA expression (up to 35-fold). Panobinostat 28-34 growth arrest and DNA damage inducible gamma Homo sapiens 190-197 18505931-5 2008 Deletion of the NH(2)-terminal 120 amino acids of DNMT1 diminishes LBH589-induced ubiquitination, indicating that this domain is essential for its proteasomal degradation. Panobinostat 67-73 DNA methyltransferase 1 Homo sapiens 50-55 18505931-7 2008 Treatment with LBH589 induces hyperacetylation of Hsp90, thereby inhibiting the association of DNMT1 with Hsp90 and promoting ubiquitination of DNMT1. Panobinostat 15-21 heat shock protein 90 alpha family class A member 1 Homo sapiens 50-55 18505931-7 2008 Treatment with LBH589 induces hyperacetylation of Hsp90, thereby inhibiting the association of DNMT1 with Hsp90 and promoting ubiquitination of DNMT1. Panobinostat 15-21 DNA methyltransferase 1 Homo sapiens 95-100 18505931-7 2008 Treatment with LBH589 induces hyperacetylation of Hsp90, thereby inhibiting the association of DNMT1 with Hsp90 and promoting ubiquitination of DNMT1. Panobinostat 15-21 heat shock protein 90 alpha family class A member 1 Homo sapiens 106-111 18505931-7 2008 Treatment with LBH589 induces hyperacetylation of Hsp90, thereby inhibiting the association of DNMT1 with Hsp90 and promoting ubiquitination of DNMT1. Panobinostat 15-21 DNA methyltransferase 1 Homo sapiens 144-149 17455259-3 2007 In biochemical assays using recombinant HDAC1, 3, 6 and 8 isoenzymes, SAHA and LAQ824/LBH589 behave as quite unselective HDAC inhibitors. Panobinostat 86-92 histone deacetylase 1 Homo sapiens 40-45 18505931-3 2008 Here, we show that the HDAC inhibitor LBH589 down-regulates DNA methyltransferase 1 (DNMT1) protein expression in the nucleus of human breast cancer cells. Panobinostat 38-44 histone deacetylase 9 Homo sapiens 23-27 18505931-3 2008 Here, we show that the HDAC inhibitor LBH589 down-regulates DNA methyltransferase 1 (DNMT1) protein expression in the nucleus of human breast cancer cells. Panobinostat 38-44 DNA methyltransferase 1 Homo sapiens 60-83 18505931-3 2008 Here, we show that the HDAC inhibitor LBH589 down-regulates DNA methyltransferase 1 (DNMT1) protein expression in the nucleus of human breast cancer cells. Panobinostat 38-44 DNA methyltransferase 1 Homo sapiens 85-90 17455259-3 2007 In biochemical assays using recombinant HDAC1, 3, 6 and 8 isoenzymes, SAHA and LAQ824/LBH589 behave as quite unselective HDAC inhibitors. Panobinostat 86-92 histone deacetylase 9 Homo sapiens 40-44 17699868-2 2007 By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90. Panobinostat 93-99 histone deacetylase 6 Homo sapiens 14-19 17876048-0 2007 Effect of the histone deacetylase inhibitor LBH589 against epidermal growth factor receptor-dependent human lung cancer cells. Panobinostat 44-50 epidermal growth factor receptor Homo sapiens 59-91 17876048-6 2007 LBH589 resulted in increased acetylation of Hsp90 and reduced association of Hsp90 with EGFR, Akt, and STAT3. Panobinostat 0-6 heat shock protein 90 alpha family class A member 1 Homo sapiens 44-49 17876048-6 2007 LBH589 resulted in increased acetylation of Hsp90 and reduced association of Hsp90 with EGFR, Akt, and STAT3. Panobinostat 0-6 heat shock protein 90 alpha family class A member 1 Homo sapiens 77-82 17876048-6 2007 LBH589 resulted in increased acetylation of Hsp90 and reduced association of Hsp90 with EGFR, Akt, and STAT3. Panobinostat 0-6 epidermal growth factor receptor Homo sapiens 88-92 17876048-6 2007 LBH589 resulted in increased acetylation of Hsp90 and reduced association of Hsp90 with EGFR, Akt, and STAT3. Panobinostat 0-6 AKT serine/threonine kinase 1 Homo sapiens 94-97 17876048-6 2007 LBH589 resulted in increased acetylation of Hsp90 and reduced association of Hsp90 with EGFR, Akt, and STAT3. Panobinostat 0-6 signal transducer and activator of transcription 3 Homo sapiens 103-108 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 0-6 epidermal growth factor receptor Homo sapiens 93-97 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 0-6 epidermal growth factor receptor Homo sapiens 124-128 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 0-6 signal transducer and activator of transcription 3 Homo sapiens 130-135 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 0-6 AKT serine/threonine kinase 1 Homo sapiens 141-144 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 204-210 epidermal growth factor receptor Homo sapiens 93-97 17876048-7 2007 LBH589 selectively depleted proteins important in signaling cascades in cell lines harboring EGFR kinase mutations, such as EGFR, STAT3, and Akt, and these cells underwent apoptosis following exposure to LBH589. Panobinostat 204-210 epidermal growth factor receptor Homo sapiens 124-128 17876048-11 2007 Treatment of cells with erlotinib and LBH589 resulted in synergistic effects on lung cancer cells dependent on EGFR for growth and/or survival. Panobinostat 38-44 epidermal growth factor receptor Homo sapiens 111-115 17699868-2 2007 By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90. Panobinostat 93-99 histone deacetylase 6 Homo sapiens 148-153 17699868-2 2007 By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90. Panobinostat 93-99 heat shock protein 90 alpha family class A member 1 Homo sapiens 183-188 16537804-0 2006 Combined effects of novel tyrosine kinase inhibitor AMN107 and histone deacetylase inhibitor LBH589 against Bcr-Abl-expressing human leukemia cells. Panobinostat 93-99 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 108-115 17317822-7 2007 Inhibition of either MAPK and/or Akt enhanced LBH589-induced apoptosis. Panobinostat 46-52 AKT serine/threonine kinase 1 Homo sapiens 33-36 17317822-8 2007 In contrast, constitutively active MAPK or Akt attenuated LBH589 or LBH589 + AEE788-induced apoptosis. Panobinostat 58-64 AKT serine/threonine kinase 1 Homo sapiens 43-46 17317822-8 2007 In contrast, constitutively active MAPK or Akt attenuated LBH589 or LBH589 + AEE788-induced apoptosis. Panobinostat 68-74 AKT serine/threonine kinase 1 Homo sapiens 43-46 17172825-0 2007 Histone deacetylase inhibitor LBH589 reactivates silenced estrogen receptor alpha (ER) gene expression without loss of DNA hypermethylation. Panobinostat 30-36 estrogen receptor 1 Homo sapiens 58-81 17172825-7 2007 By chromatin immunoprecipitation analysis, LBH treatment released DNMT1, HDAC1, and the H3 lysine 9 (H3-K9) methyltransferase SUV39H 1 from the ER promoter. Panobinostat 43-46 DNA methyltransferase 1 Homo sapiens 66-71 17172825-7 2007 By chromatin immunoprecipitation analysis, LBH treatment released DNMT1, HDAC1, and the H3 lysine 9 (H3-K9) methyltransferase SUV39H 1 from the ER promoter. Panobinostat 43-46 histone deacetylase 1 Homo sapiens 73-78 17172825-7 2007 By chromatin immunoprecipitation analysis, LBH treatment released DNMT1, HDAC1, and the H3 lysine 9 (H3-K9) methyltransferase SUV39H 1 from the ER promoter. Panobinostat 43-46 SUV39H1 histone lysine methyltransferase Homo sapiens 126-134 17172412-3 2006 In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells. Panobinostat 104-110 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 152-156 17172412-3 2006 In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells. Panobinostat 104-110 SUZ12 polycomb repressive complex 2 subunit Homo sapiens 158-163 17172412-3 2006 In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells. Panobinostat 104-110 embryonic ectoderm development Homo sapiens 169-172 17145876-0 2006 Histone deacetylase (HDAC) inhibitor LBH589 increases duration of gamma-H2AX foci and confines HDAC4 to the cytoplasm in irradiated non-small cell lung cancer. Panobinostat 37-43 histone deacetylase 4 Homo sapiens 95-100 17145876-7 2006 In contrast, treatment with LBH589 followed by irradiation resulted in HDAC4 confinement to the cytoplasm, indicating that HDAC inhibition affects the nuclear localization of HDAC4. Panobinostat 28-34 histone deacetylase 4 Homo sapiens 71-76 17145876-7 2006 In contrast, treatment with LBH589 followed by irradiation resulted in HDAC4 confinement to the cytoplasm, indicating that HDAC inhibition affects the nuclear localization of HDAC4. Panobinostat 28-34 histone deacetylase 4 Homo sapiens 175-180 16728695-2 2006 LBH589 is a novel hydroxamic acid derivative that at low nanomolar concentrations induces apoptosis in MM cells resistant to conventional therapies via caspase activation and poly-(ADP-ribose) polymerase (PARP) cleavage. Panobinostat 0-6 poly(ADP-ribose) polymerase 1 Homo sapiens 175-203 16728695-2 2006 LBH589 is a novel hydroxamic acid derivative that at low nanomolar concentrations induces apoptosis in MM cells resistant to conventional therapies via caspase activation and poly-(ADP-ribose) polymerase (PARP) cleavage. Panobinostat 0-6 poly(ADP-ribose) polymerase 1 Homo sapiens 205-209 16537804-2 2006 Treatment with the histone deacetylase inhibitor LBH589 (Novartis) depletes Bcr-Abl levels. Panobinostat 49-55 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 76-83 15514006-0 2005 Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. Panobinostat 49-55 fms related receptor tyrosine kinase 3 Homo sapiens 173-178 15937340-1 2005 The hydroxamic acid (HAA) analogue pan-histone deacetylase (HDAC) inhibitors (HDIs) LAQ824 and LBH589 have been shown to induce acetylation and inhibit the ATP binding and chaperone function of heat shock protein (HSP) 90. Panobinostat 95-101 heat shock protein 90 alpha family class A member 1 Homo sapiens 194-221 16740717-8 2006 LBH589 favored apoptosome formation by inducing cytochrome c release, Apaf-1 up-regulation, and caspase-9 cleavage. Panobinostat 0-6 cytochrome c, somatic Homo sapiens 48-60 16740717-8 2006 LBH589 favored apoptosome formation by inducing cytochrome c release, Apaf-1 up-regulation, and caspase-9 cleavage. Panobinostat 0-6 apoptotic peptidase activating factor 1 Homo sapiens 70-76 16740717-8 2006 LBH589 favored apoptosome formation by inducing cytochrome c release, Apaf-1 up-regulation, and caspase-9 cleavage. Panobinostat 0-6 caspase 9 Homo sapiens 96-105 15514006-1 2005 Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. Panobinostat 26-32 heat shock protein 90 alpha family class A member 1 Homo sapiens 153-174 15514006-1 2005 Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. Panobinostat 26-32 heat shock protein 90 alpha family class A member 1 Homo sapiens 176-181 15514006-1 2005 Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. Panobinostat 26-32 H3 histone pseudogene 16 Homo sapiens 194-197 15514006-1 2005 Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3. Panobinostat 26-32 fms related receptor tyrosine kinase 3 Homo sapiens 416-421 15514006-3 2005 In K562 cells, exposure to LBH589 attenuated Bcr-Abl, p-AKT, and p-ERK1/2. Panobinostat 27-33 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 45-52 33806487-6 2021 Panobinostat dose-dependently decreased expression of an anti-apoptotic protein, Mcl-1, concomitant with increasing acetylation of histone H4. Panobinostat 0-12 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 81-86 34592353-5 2022 We demonstrated that intranuclear acetylation of lys9 of histone H3 (Ac-H3K9) were increased, while that of both mRNA and protein of HDAC1, HDAC3, and HDAC4 were decreased when the treating concentration of panobinostat increased. Panobinostat 207-219 histone deacetylase 3 Homo sapiens 140-145 34592353-5 2022 We demonstrated that intranuclear acetylation of lys9 of histone H3 (Ac-H3K9) were increased, while that of both mRNA and protein of HDAC1, HDAC3, and HDAC4 were decreased when the treating concentration of panobinostat increased. Panobinostat 207-219 histone deacetylase 4 Homo sapiens 151-156 34592353-8 2022 Further, we combined panobinostat with Ad-hepaCAM, which resulted in significantly increased antitumor activity and significant attenuation of the proliferation-associated genes CCND1 and PCNA compared to each single treatment. Panobinostat 21-33 hepatic and glial cell adhesion molecule Homo sapiens 42-49 34592353-8 2022 Further, we combined panobinostat with Ad-hepaCAM, which resulted in significantly increased antitumor activity and significant attenuation of the proliferation-associated genes CCND1 and PCNA compared to each single treatment. Panobinostat 21-33 cyclin D1 Homo sapiens 178-183 34592353-8 2022 Further, we combined panobinostat with Ad-hepaCAM, which resulted in significantly increased antitumor activity and significant attenuation of the proliferation-associated genes CCND1 and PCNA compared to each single treatment. Panobinostat 21-33 proliferating cell nuclear antigen Homo sapiens 188-192 34592353-9 2022 In conclusion, panobinostat may enhance the acetylation of lys9 of histone 3 and reverse the hepaCAM expression through its inhibitory effect on HDACs activity in PCa LNCaP and DU145 cells; Ad-hepaCAM combined with panobinostat may synergistically inhibit the growth of LNCaP and DU145 cells, via a potential mechanism associated with the down-regulation of the expression of CCND1 and PCNA. Panobinostat 15-27 hepatic and glial cell adhesion molecule Homo sapiens 93-100 34592353-9 2022 In conclusion, panobinostat may enhance the acetylation of lys9 of histone 3 and reverse the hepaCAM expression through its inhibitory effect on HDACs activity in PCa LNCaP and DU145 cells; Ad-hepaCAM combined with panobinostat may synergistically inhibit the growth of LNCaP and DU145 cells, via a potential mechanism associated with the down-regulation of the expression of CCND1 and PCNA. Panobinostat 15-27 hepatic and glial cell adhesion molecule Homo sapiens 193-200 34592353-9 2022 In conclusion, panobinostat may enhance the acetylation of lys9 of histone 3 and reverse the hepaCAM expression through its inhibitory effect on HDACs activity in PCa LNCaP and DU145 cells; Ad-hepaCAM combined with panobinostat may synergistically inhibit the growth of LNCaP and DU145 cells, via a potential mechanism associated with the down-regulation of the expression of CCND1 and PCNA. Panobinostat 15-27 cyclin D1 Homo sapiens 376-381 34592353-9 2022 In conclusion, panobinostat may enhance the acetylation of lys9 of histone 3 and reverse the hepaCAM expression through its inhibitory effect on HDACs activity in PCa LNCaP and DU145 cells; Ad-hepaCAM combined with panobinostat may synergistically inhibit the growth of LNCaP and DU145 cells, via a potential mechanism associated with the down-regulation of the expression of CCND1 and PCNA. Panobinostat 15-27 proliferating cell nuclear antigen Homo sapiens 386-390 33806487-6 2021 Panobinostat dose-dependently decreased expression of an anti-apoptotic protein, Mcl-1, concomitant with increasing acetylation of histone H4. Panobinostat 0-12 H4 clustered histone 6 Homo sapiens 131-141 34726962-3 2022 The administration of the deacetylase inhibitors (DACi) panobinostat, trichostatin A and SAHA affected the cell viability of H295R monolayer and spheroids and induced the over-expression of H19 and autophagy transcripts. Panobinostat 56-68 H19 imprinted maternally expressed transcript Homo sapiens 190-193 34592353-0 2022 Panobinostat reverses HepaCAM gene expression and suppresses proliferation by increasing histone acetylation in prostate cancer. Panobinostat 0-12 hepatic and glial cell adhesion molecule Homo sapiens 22-29 34592353-4 2022 In this study, we investigated the effect of panobinostat, the broad-spectrum histone deacetylases inhibitor, on PCa LNCaP and DU145 cell growth, and observed re-expression of hepaCAM when treated with panobinostat. Panobinostat 202-214 hepatic and glial cell adhesion molecule Homo sapiens 176-183 34592353-5 2022 We demonstrated that intranuclear acetylation of lys9 of histone H3 (Ac-H3K9) were increased, while that of both mRNA and protein of HDAC1, HDAC3, and HDAC4 were decreased when the treating concentration of panobinostat increased. Panobinostat 207-219 histone deacetylase 1 Homo sapiens 133-138 34259396-0 2021 Zap-Pano: a Photocaged pro-drug of the KDAC inhibitor panobinostat. Panobinostat 54-66 zinc finger CCCH-type containing, antiviral 1 Homo sapiens 0-3 34259396-1 2021 We report the synthesis and biological evaluation of a light-activated (caged) pro-drug of the KDAC inhibitor panobinostat (Zap-Pano). Panobinostat 110-122 zinc finger CCCH-type containing, antiviral 1 Homo sapiens 124-127 34792282-7 2021 Importantly, SNAI2 expression levels in part determine sensitivity to the cancer drugs dasatinib and panobinostat. Panobinostat 101-113 snail family transcriptional repressor 2 Homo sapiens 13-18 34792282-9 2021 We elucidated how epigenetic silencing of SNAI2 controls the dynamic changes of SNAI2 expression that are essential for tumor initiation and progression, and discovered that restoring SNAI2 expression by treatment with panobinostat enhances dasatinib sensitivity, indicating a new therapeutic strategy for prostate cancer. Panobinostat 219-231 snail family transcriptional repressor 2 Homo sapiens 42-47 34792282-9 2021 We elucidated how epigenetic silencing of SNAI2 controls the dynamic changes of SNAI2 expression that are essential for tumor initiation and progression, and discovered that restoring SNAI2 expression by treatment with panobinostat enhances dasatinib sensitivity, indicating a new therapeutic strategy for prostate cancer. Panobinostat 219-231 snail family transcriptional repressor 2 Homo sapiens 80-85 34792282-9 2021 We elucidated how epigenetic silencing of SNAI2 controls the dynamic changes of SNAI2 expression that are essential for tumor initiation and progression, and discovered that restoring SNAI2 expression by treatment with panobinostat enhances dasatinib sensitivity, indicating a new therapeutic strategy for prostate cancer. Panobinostat 219-231 snail family transcriptional repressor 2 Homo sapiens 184-189 34464977-9 2021 Finally, combined LCL161/LBH589 treatment significantly increased survival compared to single-agent treatment in an immunocompetent 5TGM1 murine MM model. Panobinostat 25-31 transglutaminase 1, K polypeptide Mus musculus 133-137 34531855-0 2021 Synergistic Tumor Cytolysis by NK Cells in Combination With a Pan-HDAC Inhibitor, Panobinostat. Panobinostat 82-94 histone deacetylase 9 Homo sapiens 66-70 34485305-10 2021 Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat. Panobinostat 369-381 S100 calcium binding protein A1 Homo sapiens 36-40 34485305-10 2021 Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat. Panobinostat 369-381 S100 calcium binding protein A8 Homo sapiens 174-180 34485305-10 2021 Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat. Panobinostat 369-381 S100 calcium binding protein A9 Homo sapiens 182-188 34485305-10 2021 Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat. Panobinostat 369-381 S100 calcium binding protein A12 Homo sapiens 194-201 34384478-8 2021 Genes regulated by the male-specific factors SRY-Box Transcription Factor 9 (SOX9) and Doublesex and Mab-3-related Transcription factor 1 (DMRT1) were among the most upregulated genes in the ovaries of PB-exposed mice. Panobinostat 202-204 SRY (sex determining region Y)-box 9 Mus musculus 77-81 34384478-8 2021 Genes regulated by the male-specific factors SRY-Box Transcription Factor 9 (SOX9) and Doublesex and Mab-3-related Transcription factor 1 (DMRT1) were among the most upregulated genes in the ovaries of PB-exposed mice. Panobinostat 202-204 doublesex and mab-3 related transcription factor 1 Mus musculus 87-137 34384478-8 2021 Genes regulated by the male-specific factors SRY-Box Transcription Factor 9 (SOX9) and Doublesex and Mab-3-related Transcription factor 1 (DMRT1) were among the most upregulated genes in the ovaries of PB-exposed mice. Panobinostat 202-204 doublesex and mab-3 related transcription factor 1 Mus musculus 139-144 34384478-9 2021 In contrast, PB treatment led to decreases in the expression of genes regulated by the WNT4 pathway. Panobinostat 13-15 wingless-type MMTV integration site family, member 4 Mus musculus 87-91 34531855-4 2021 We showed that a pan-HDAC inhibitor, panobinostat, alone demonstrated anti-tumor and anti-proliferative activities on all tested tumors in vitro. Panobinostat 37-49 histone deacetylase 9 Homo sapiens 21-25 34531855-7 2021 Finally, panobinostat therapy led to better tumor control and synergized with anti-PD-L1 therapy. Panobinostat 9-21 CD274 molecule Homo sapiens 83-88 34281526-0 2021 Histone deacetylase inhibitor panobinostat induces antitumor activity in epithelioid sarcoma and rhabdoid tumor by growth factor receptor modulation. Panobinostat 30-42 histone deacetylase 9 Homo sapiens 0-19 34281526-5 2021 RESULTS: Pan-HDAC inhibitor panobinostat exhibited potent anti-proliferative activity at low nanomolar concentrations in A204 rhabdoid tumor, and VAESBJ/GRU1 epithelioid sarcoma cell lines, strongly induced apoptosis, and resulted in significant tumor growth inhibition in VAESBJ xenografts. Panobinostat 28-40 histone deacetylase 9 Homo sapiens 13-17 34888496-3 2021 However, bortezomib refractory disease is a major clinical concern, and the efficacy of the pan-histone deacetylase inhibitor (HDACi), panobinostat, in bortezomib refractory disease indicates that HDAC targeting is a viable strategy. Panobinostat 135-147 histone deacetylase 9 Homo sapiens 96-115 34204116-14 2021 Our results uncover epigenetic HDAC modulation using PB as a promising new therapeutic avenue in PanNET, linking cell-cycle modulation and pathways such as JAK2/STAT3 to epigenetic targeting. Panobinostat 53-55 Janus kinase 2 Homo sapiens 156-160 34204116-14 2021 Our results uncover epigenetic HDAC modulation using PB as a promising new therapeutic avenue in PanNET, linking cell-cycle modulation and pathways such as JAK2/STAT3 to epigenetic targeting. Panobinostat 53-55 signal transducer and activator of transcription 3 Homo sapiens 161-166 34073071-7 2021 Panobinostat induced the G2/M cell cycle arrest in SNU484 and SNU638 cells and subsequently decreased the G2/M phase regulatory-associated protein expression of p-Wee1, Myt1, and Cdc2. Panobinostat 0-12 WEE1 G2 checkpoint kinase Homo sapiens 163-167 34073071-7 2021 Panobinostat induced the G2/M cell cycle arrest in SNU484 and SNU638 cells and subsequently decreased the G2/M phase regulatory-associated protein expression of p-Wee1, Myt1, and Cdc2. Panobinostat 0-12 myelin transcription factor 1 Homo sapiens 169-173 34073071-7 2021 Panobinostat induced the G2/M cell cycle arrest in SNU484 and SNU638 cells and subsequently decreased the G2/M phase regulatory-associated protein expression of p-Wee1, Myt1, and Cdc2. Panobinostat 0-12 cyclin dependent kinase 1 Homo sapiens 179-183 34073071-8 2021 Furthermore, panobinostat significantly inhibited the metastasis of SNU484 and SNU638 cells by regulating the expression of MMP-9 and E-cadherin. Panobinostat 13-25 matrix metallopeptidase 9 Homo sapiens 124-129 34073071-8 2021 Furthermore, panobinostat significantly inhibited the metastasis of SNU484 and SNU638 cells by regulating the expression of MMP-9 and E-cadherin. Panobinostat 13-25 cadherin 1 Homo sapiens 134-144 34485908-8 2021 Results: Of all inhibitors tested, HDACi (panobinostat and romidepsin) showed the potential to increase the expression of ERbeta in GBM cells. Panobinostat 42-54 estrogen receptor 1 (alpha) Mus musculus 122-128 34888496-9 2021 Panobinostat was effective at inducing cell death in these lines and modulated HDAC expression in cell lines and patient samples. Panobinostat 0-12 histone deacetylase 9 Homo sapiens 79-83 35188042-3 2022 We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells. Panobinostat 79-91 BCL2 apoptosis regulator Homo sapiens 157-161 35575252-13 2022 In addition, Panobinostat might be a possible candidate drug to target LINC00313 in TGCT. Panobinostat 13-25 long intergenic non-protein coding RNA 313 Homo sapiens 71-80 35381875-6 2022 We go on to characterize a transcriptional program that is induced by the LTI6426/Pano combination, demonstrating a convergence of the two drugs on endoplasmic reticulum (ER) stress pathway effectors ATF3 (Activating Transcription Factor 3), DDIT3/CHOP (DNA Damage Inducible Transcript 3, a.k.a. Panobinostat 82-86 activating transcription factor 3 Mus musculus 200-204 35381875-6 2022 We go on to characterize a transcriptional program that is induced by the LTI6426/Pano combination, demonstrating a convergence of the two drugs on endoplasmic reticulum (ER) stress pathway effectors ATF3 (Activating Transcription Factor 3), DDIT3/CHOP (DNA Damage Inducible Transcript 3, a.k.a. Panobinostat 82-86 activating transcription factor 3 Mus musculus 206-239 35381875-6 2022 We go on to characterize a transcriptional program that is induced by the LTI6426/Pano combination, demonstrating a convergence of the two drugs on endoplasmic reticulum (ER) stress pathway effectors ATF3 (Activating Transcription Factor 3), DDIT3/CHOP (DNA Damage Inducible Transcript 3, a.k.a. Panobinostat 82-86 DNA-damage inducible transcript 3 Mus musculus 242-247 35381875-6 2022 We go on to characterize a transcriptional program that is induced by the LTI6426/Pano combination, demonstrating a convergence of the two drugs on endoplasmic reticulum (ER) stress pathway effectors ATF3 (Activating Transcription Factor 3), DDIT3/CHOP (DNA Damage Inducible Transcript 3, a.k.a. Panobinostat 82-86 DNA-damage inducible transcript 3 Mus musculus 248-252 35381875-6 2022 We go on to characterize a transcriptional program that is induced by the LTI6426/Pano combination, demonstrating a convergence of the two drugs on endoplasmic reticulum (ER) stress pathway effectors ATF3 (Activating Transcription Factor 3), DDIT3/CHOP (DNA Damage Inducible Transcript 3, a.k.a. Panobinostat 82-86 DNA-damage inducible transcript 3 Mus musculus 254-287 35192680-6 2022 Mechanistically, ectopic SIRT1 expression activated mitochondrial activity and sensitized ALL to panobinostat through activating mitochondria-related apoptosis pathway. Panobinostat 97-109 sirtuin 1 Homo sapiens 25-30 35192680-8 2022 Our data suggest that patients with higher SIRT1 expression in cancer cells might benefit from panobinostat treatment, supporting the implementation of combinatorial therapy with SIRT1 or mitochondrial activators to overcome panobinostat resistance. Panobinostat 95-107 sirtuin 1 Homo sapiens 43-48 35192680-8 2022 Our data suggest that patients with higher SIRT1 expression in cancer cells might benefit from panobinostat treatment, supporting the implementation of combinatorial therapy with SIRT1 or mitochondrial activators to overcome panobinostat resistance. Panobinostat 225-237 sirtuin 1 Homo sapiens 43-48 35188042-3 2022 We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells. Panobinostat 79-91 poly(ADP-ribose) polymerase 1 Homo sapiens 211-238 35159107-6 2022 In this study we show that the combination of low concentrations of panobinostat and Tegavivint have significant in vitro and in vivo anti-MM effects including in the context of proteasome inhibitor resistance, by targeting both aerobic glycolysis and mitochondrial respiration and the down-regulation of down-stream beta-catenin targets including myc, cyclinD1, and cyclinD2. Panobinostat 68-80 catenin beta 1 Homo sapiens 317-329 35159107-6 2022 In this study we show that the combination of low concentrations of panobinostat and Tegavivint have significant in vitro and in vivo anti-MM effects including in the context of proteasome inhibitor resistance, by targeting both aerobic glycolysis and mitochondrial respiration and the down-regulation of down-stream beta-catenin targets including myc, cyclinD1, and cyclinD2. Panobinostat 68-80 MYC proto-oncogene, bHLH transcription factor Homo sapiens 348-351 35159107-6 2022 In this study we show that the combination of low concentrations of panobinostat and Tegavivint have significant in vitro and in vivo anti-MM effects including in the context of proteasome inhibitor resistance, by targeting both aerobic glycolysis and mitochondrial respiration and the down-regulation of down-stream beta-catenin targets including myc, cyclinD1, and cyclinD2. Panobinostat 68-80 cyclin D1 Homo sapiens 353-361 35159107-6 2022 In this study we show that the combination of low concentrations of panobinostat and Tegavivint have significant in vitro and in vivo anti-MM effects including in the context of proteasome inhibitor resistance, by targeting both aerobic glycolysis and mitochondrial respiration and the down-regulation of down-stream beta-catenin targets including myc, cyclinD1, and cyclinD2. Panobinostat 68-80 cyclin D2 Homo sapiens 367-375 35188042-3 2022 We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells. Panobinostat 93-97 BCL2 apoptosis regulator Homo sapiens 157-161 35188042-3 2022 We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells. Panobinostat 93-97 poly(ADP-ribose) polymerase 1 Homo sapiens 211-238 35204163-4 2022 Hydroxamate-containing molecules, including anticancer drugs targeting histone deacetylase, vorinostat and panobinostat, significantly inhibited mushroom tyrosinase, with inhibitory constants in the submicromolar range. Panobinostat 107-119 tyrosinase Homo sapiens 154-164 35145418-6 2022 We show compounds Niclosamide, Panobinostat, and Candesartan Celexitil increased AQP5 abundance, and show that Niclosamide has favorable cellular toxicity profiles. Panobinostat 31-43 aquaporin 5 Homo sapiens 81-85 33904202-7 2021 The PBPK model predicted an area under the curve ratio (AUCR) of 1, and 1.8, for ruxolitinib and panobinostat, respectively in the presence of severe RIP. Panobinostat 97-109 receptor interacting serine/threonine kinase 1 Homo sapiens 150-153 35084211-6 2022 RESULTS: Interleukin (IL)-1beta inhibited the chondrogenic differentiation potential of SMSCs, while the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and panobinostat (LBH589), attenuated inhibition of IL-1beta-induced SMSC chondrogenesis. Panobinostat 165-177 interleukin 1 alpha Rattus norvegicus 213-221 35084211-8 2022 IL-6 (p < 0.001) and matrix metalloproteinase 13 (MMP13) (p = 0.006) were significantly upregulated after IL-1beta stimulation, while SAHA and LBH589 attenuated IL-6 and MMP13 expression, which was upregulated by IL-1beta in vitro. Panobinostat 143-149 matrix metallopeptidase 13 Rattus norvegicus 21-48 35084211-8 2022 IL-6 (p < 0.001) and matrix metalloproteinase 13 (MMP13) (p = 0.006) were significantly upregulated after IL-1beta stimulation, while SAHA and LBH589 attenuated IL-6 and MMP13 expression, which was upregulated by IL-1beta in vitro. Panobinostat 143-149 interleukin 6 Rattus norvegicus 161-165 35084211-8 2022 IL-6 (p < 0.001) and matrix metalloproteinase 13 (MMP13) (p = 0.006) were significantly upregulated after IL-1beta stimulation, while SAHA and LBH589 attenuated IL-6 and MMP13 expression, which was upregulated by IL-1beta in vitro. Panobinostat 143-149 matrix metallopeptidase 13 Rattus norvegicus 170-175 35084211-8 2022 IL-6 (p < 0.001) and matrix metalloproteinase 13 (MMP13) (p = 0.006) were significantly upregulated after IL-1beta stimulation, while SAHA and LBH589 attenuated IL-6 and MMP13 expression, which was upregulated by IL-1beta in vitro. Panobinostat 143-149 interleukin 1 alpha Rattus norvegicus 213-221 35084211-10 2022 CONCLUSION: HDAC inhibitors SAHA and LBH589 attenuated chondrogenesis inhibition of SMSC induced by IL-1beta in TMJ, and inhibition of IL-6/MMP13 pathway activation contributes to this biological progress. Panobinostat 37-43 histone deacetylase 9 Homo sapiens 12-16 35084211-10 2022 CONCLUSION: HDAC inhibitors SAHA and LBH589 attenuated chondrogenesis inhibition of SMSC induced by IL-1beta in TMJ, and inhibition of IL-6/MMP13 pathway activation contributes to this biological progress. Panobinostat 37-43 interleukin 1 alpha Rattus norvegicus 100-108 33994371-0 2021 Dual targeting of chromatin stability by the curaxin CBL0137 and histone deacetylase inhibitor panobinostat shows significant preclinical efficacy in neuroblastoma. Panobinostat 95-107 histone deacetylase 9 Homo sapiens 65-84 33994371-1 2021 Purpose: We investigated if targeting chromatin stability through a combination of the curaxin CBL0137 with the histone deacetylase (HDAC) inhibitor, panobinostat, constitutes an effective multimodal treatment for high-risk neuroblastoma.Experimental Design: The effects of the drug combination on cancer growth were examined in vitro and in animal models of MYCN-amplified neuroblastoma. Panobinostat 150-162 histone deacetylase 9 Homo sapiens 112-131 33994371-1 2021 Purpose: We investigated if targeting chromatin stability through a combination of the curaxin CBL0137 with the histone deacetylase (HDAC) inhibitor, panobinostat, constitutes an effective multimodal treatment for high-risk neuroblastoma.Experimental Design: The effects of the drug combination on cancer growth were examined in vitro and in animal models of MYCN-amplified neuroblastoma. Panobinostat 150-162 histone deacetylase 9 Homo sapiens 133-137 33501756-5 2021 Here, we proposed for the first time that the inhibitory effect of panobinostat was overshadowed, at least partially, through the aberrant activation of the PI3K/c-Myc axis. Panobinostat 67-79 MYC proto-oncogene, bHLH transcription factor Homo sapiens 162-167 33930758-3 2021 The in vitro effects of Panobinostat (LBH), a histone deacetylase inhibitor that exerts pleiotropic antitumor effects but induces autophagy, in combination with Chloroquine (CQ), an autophagy inhibitor that avoid this cell survival mechanism, were evaluated in 4 OC cell lines. Panobinostat 24-36 LBH regulator of WNT signaling pathway Homo sapiens 38-41 33852836-6 2021 Combined treatment of CBL0137 with the histone deacetylase inhibitor panobinostat leads to inhibition of the Rb/E2F1 pathway and induction of apoptosis. Panobinostat 69-81 E2F transcription factor 1 Homo sapiens 112-116 32945549-6 2021 The reduction in the proportion of CD127+ CD8+ T cells and CD4:CD8 ratio was significantly greater, after three and six cycles of panobinostat compared to pre-transplant, in non-responders when compared to responders. Panobinostat 130-142 interleukin 7 receptor Homo sapiens 35-40 32945549-6 2021 The reduction in the proportion of CD127+ CD8+ T cells and CD4:CD8 ratio was significantly greater, after three and six cycles of panobinostat compared to pre-transplant, in non-responders when compared to responders. Panobinostat 130-142 CD8a molecule Homo sapiens 42-45 32945549-6 2021 The reduction in the proportion of CD127+ CD8+ T cells and CD4:CD8 ratio was significantly greater, after three and six cycles of panobinostat compared to pre-transplant, in non-responders when compared to responders. Panobinostat 130-142 CD4 molecule Homo sapiens 59-62 32945549-6 2021 The reduction in the proportion of CD127+ CD8+ T cells and CD4:CD8 ratio was significantly greater, after three and six cycles of panobinostat compared to pre-transplant, in non-responders when compared to responders. Panobinostat 130-142 CD8a molecule Homo sapiens 63-66 33130903-3 2021 Investigations addressing DMG epigenetics have identified few promising drugs, including the HDAC inhibitor (HDACi) panobinostat. Panobinostat 116-128 histone deacetylase 9 Homo sapiens 93-97 33969806-5 2022 The companionship of the PI3K inhibitor with HDAC inhibitor also potentiated panobinostat-induced apoptotic cell death and enhanced the mRNA of Foxo3a and Foxo4. Panobinostat 77-89 forkhead box O3 Homo sapiens 144-150 33375520-5 2020 Two additional novel inhibitors of DNMT1 are the approved drugs glyburide and panobinostat. Panobinostat 78-90 DNA methyltransferase 1 Homo sapiens 35-40 33375520-6 2020 The DNMT1 enzymatic inhibitory activity of panobinostat, a known pan inhibitor of histone deacetylases, agrees with experimental reports of its ability to reduce DNMT1 activity in liver cancer cell lines. Panobinostat 43-55 DNA methyltransferase 1 Homo sapiens 4-9 33375520-6 2020 The DNMT1 enzymatic inhibitory activity of panobinostat, a known pan inhibitor of histone deacetylases, agrees with experimental reports of its ability to reduce DNMT1 activity in liver cancer cell lines. Panobinostat 43-55 DNA methyltransferase 1 Homo sapiens 162-167 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. Panobinostat 107-119 H3 histone pseudogene 16 Homo sapiens 45-48 33513156-8 2021 We tested the effects of two epigenetic modifiers, an EZH2 inhibitor, tazemetostat (EPZ6438) and a histone deacetylase inhibitor, panobinostat (LBH589) on SLFN11 expression in GCB-derived lymphoma cell lines. Panobinostat 130-142 schlafen family member 11 Homo sapiens 155-161 33513156-8 2021 We tested the effects of two epigenetic modifiers, an EZH2 inhibitor, tazemetostat (EPZ6438) and a histone deacetylase inhibitor, panobinostat (LBH589) on SLFN11 expression in GCB-derived lymphoma cell lines. Panobinostat 144-150 schlafen family member 11 Homo sapiens 155-161 32599665-6 2020 Mechanistically, the efficacy of panobinostat was linked to high expression of HDAC1 and HDAC2 in osteosarcoma, and silencing of HDAC1 and 2 greatly reduced osteosarcoma growth in vitro. Panobinostat 33-45 histone deacetylase 1 Homo sapiens 79-84 32599665-6 2020 Mechanistically, the efficacy of panobinostat was linked to high expression of HDAC1 and HDAC2 in osteosarcoma, and silencing of HDAC1 and 2 greatly reduced osteosarcoma growth in vitro. Panobinostat 33-45 histone deacetylase 2 Homo sapiens 89-94 33189849-3 2020 Some HDAC inhibitors such as the hydroxamic acid derivatives vorinostat or panobinostat were already approved for the treatment of hematologic cancer diseases, and are under intensive investigation for their use in solid tumors. Panobinostat 75-87 histone deacetylase 9 Homo sapiens 5-9 33969806-5 2022 The companionship of the PI3K inhibitor with HDAC inhibitor also potentiated panobinostat-induced apoptotic cell death and enhanced the mRNA of Foxo3a and Foxo4. Panobinostat 77-89 forkhead box O4 Homo sapiens 155-160 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. Panobinostat 107-119 dynactin subunit 6 Homo sapiens 50-53 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. Panobinostat 107-119 MYC proto-oncogene, bHLH transcription factor Homo sapiens 55-60 33969806-4 2022 Moreover, we found the altered expression of p21, p27, c-Myc, and CDK4 upon co-treatment of the cells with panobinostat and BKM120, which was associated with a substantial blockage of cell cycle progression at G2/M phase. Panobinostat 107-119 cyclin dependent kinase 4 Homo sapiens 66-70 32926125-9 2020 We then show how CD81-related signaling can be disrupted by treatment with the epigenetic drug combination of DNA hypomethylating agent azacitidine (aza) and histone deacetylase inhibitor panobinostat (pano), which we previously used to sensitize ALL cells to chemotherapy under conditions that promote BM microenvironment-induced chemoprotection. Panobinostat 188-200 CD81 molecule Homo sapiens 17-21 33023028-6 2020 However, the higher cytotoxicity of NK cells did not correlate with the induction of NKG2D-L. Of note, the expression of NKG2D-L and consequently NK cell-dependent killing could be induced upon LBH589 (LBH, panobinostat) or valproic acid (VPA) treatment irrespective of the SKI expression level but was significantly higher in pancreatic cancer cells upon genetic ablation of SKI. Panobinostat 194-200 killer cell lectin like receptor C1 Homo sapiens 121-125 33023028-6 2020 However, the higher cytotoxicity of NK cells did not correlate with the induction of NKG2D-L. Of note, the expression of NKG2D-L and consequently NK cell-dependent killing could be induced upon LBH589 (LBH, panobinostat) or valproic acid (VPA) treatment irrespective of the SKI expression level but was significantly higher in pancreatic cancer cells upon genetic ablation of SKI. Panobinostat 194-200 SKI proto-oncogene Homo sapiens 274-277 33023028-6 2020 However, the higher cytotoxicity of NK cells did not correlate with the induction of NKG2D-L. Of note, the expression of NKG2D-L and consequently NK cell-dependent killing could be induced upon LBH589 (LBH, panobinostat) or valproic acid (VPA) treatment irrespective of the SKI expression level but was significantly higher in pancreatic cancer cells upon genetic ablation of SKI. Panobinostat 194-200 SKI proto-oncogene Homo sapiens 376-379 33023028-6 2020 However, the higher cytotoxicity of NK cells did not correlate with the induction of NKG2D-L. Of note, the expression of NKG2D-L and consequently NK cell-dependent killing could be induced upon LBH589 (LBH, panobinostat) or valproic acid (VPA) treatment irrespective of the SKI expression level but was significantly higher in pancreatic cancer cells upon genetic ablation of SKI. Panobinostat 207-219 killer cell lectin like receptor C1 Homo sapiens 121-125 33023028-6 2020 However, the higher cytotoxicity of NK cells did not correlate with the induction of NKG2D-L. Of note, the expression of NKG2D-L and consequently NK cell-dependent killing could be induced upon LBH589 (LBH, panobinostat) or valproic acid (VPA) treatment irrespective of the SKI expression level but was significantly higher in pancreatic cancer cells upon genetic ablation of SKI. Panobinostat 207-219 LBH regulator of WNT signaling pathway Homo sapiens 194-197 33005729-6 2020 After treatment with LBH589 for indicated times, extracellular-regulated protein kinase (ERK), Akt, and c-Jun N-terminal kinase (JNK) signaling pathways in gammadeltaT cells were not activated. Panobinostat 21-27 mitogen-activated protein kinase 1 Homo sapiens 49-87 33005729-6 2020 After treatment with LBH589 for indicated times, extracellular-regulated protein kinase (ERK), Akt, and c-Jun N-terminal kinase (JNK) signaling pathways in gammadeltaT cells were not activated. Panobinostat 21-27 mitogen-activated protein kinase 1 Homo sapiens 89-92 33005729-6 2020 After treatment with LBH589 for indicated times, extracellular-regulated protein kinase (ERK), Akt, and c-Jun N-terminal kinase (JNK) signaling pathways in gammadeltaT cells were not activated. Panobinostat 21-27 AKT serine/threonine kinase 1 Homo sapiens 95-98 33005729-6 2020 After treatment with LBH589 for indicated times, extracellular-regulated protein kinase (ERK), Akt, and c-Jun N-terminal kinase (JNK) signaling pathways in gammadeltaT cells were not activated. Panobinostat 21-27 mitogen-activated protein kinase 8 Homo sapiens 104-127 33005729-6 2020 After treatment with LBH589 for indicated times, extracellular-regulated protein kinase (ERK), Akt, and c-Jun N-terminal kinase (JNK) signaling pathways in gammadeltaT cells were not activated. Panobinostat 21-27 mitogen-activated protein kinase 8 Homo sapiens 129-132 32315286-3 2020 By conducting a transcriptome analysis followed by chromatin immunoprecipitation (CHIP) sequencing coupled with a comprehensive metabolite analysis in GBM models, we unraveled that FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone-deacetylase (HDAC) inhibitors elicited metabolic reprogramming in concert with disruption of several Warburg-effect related super-enhancers. Panobinostat 202-214 histone deacetylase 9 Homo sapiens 255-274 32165429-7 2020 Treatment of DIPG cells with the AXL inhibitor BGB324 and the HDAC inhibitor panobinostat resulted in a decreased expression of mesenchymal and stem cell genes. Panobinostat 77-89 histone deacetylase 9 Homo sapiens 62-66 32315286-3 2020 By conducting a transcriptome analysis followed by chromatin immunoprecipitation (CHIP) sequencing coupled with a comprehensive metabolite analysis in GBM models, we unraveled that FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone-deacetylase (HDAC) inhibitors elicited metabolic reprogramming in concert with disruption of several Warburg-effect related super-enhancers. Panobinostat 202-214 histone deacetylase 9 Homo sapiens 276-280 32142770-4 2020 The favorable anti-leukemic effects of the inhibitor was further confirmed by cell cycle analysis, where we found that panobinostat prolonged the transition of the cells from G1 phase probably through c-Myc-mediated up-regulation of cyclin-dependent kinase inhibitors. Panobinostat 119-131 MYC proto-oncogene, bHLH transcription factor Homo sapiens 201-206 32517089-6 2020 Since therapeutic relevance is of key importance in HGSC research, for the first time, HAND2-AS1 upregulation was demonstrated to be one of the mechanisms through which HDAC inhibitor Panobinostat could be used in a strategy to increase HGSC cells" sensitivity to chemotherapeutic agents currently used in clinical trials. Panobinostat 184-196 heart and neural crest derivatives expressed 2 Homo sapiens 87-92 32517089-6 2020 Since therapeutic relevance is of key importance in HGSC research, for the first time, HAND2-AS1 upregulation was demonstrated to be one of the mechanisms through which HDAC inhibitor Panobinostat could be used in a strategy to increase HGSC cells" sensitivity to chemotherapeutic agents currently used in clinical trials. Panobinostat 184-196 prostaglandin D2 receptor Homo sapiens 93-96 32642294-13 2020 Histone deacetylase inhibitor (LBH589) and hypomethylating agent (5-aza-decitabine) restored functional PR expression at both the mRNA and protein levels and promoted marked cell death through induction of apoptosis in the presence of progesterone. Panobinostat 31-37 progesterone receptor Homo sapiens 104-106 32209637-6 2020 We also demonstrated that the FDA-approved HDAC inhibitor panobinostat and a MICA/B antibody acted synergistically to enhance MICA/B surface expression on tumor cells. Panobinostat 58-70 histone deacetylase 9 Homo sapiens 43-47 32142770-6 2020 Accordingly, we found that the inhibition of NF-kappaB pathway using bortezomib boosted the effect of panobinostat, indicating that panobinostat-induced apoptosis could be attenuated through the activation of the NF-kappaB pathway. Panobinostat 102-114 nuclear factor kappa B subunit 1 Homo sapiens 45-54 32142770-6 2020 Accordingly, we found that the inhibition of NF-kappaB pathway using bortezomib boosted the effect of panobinostat, indicating that panobinostat-induced apoptosis could be attenuated through the activation of the NF-kappaB pathway. Panobinostat 102-114 nuclear factor kappa B subunit 1 Homo sapiens 213-222 32142770-6 2020 Accordingly, we found that the inhibition of NF-kappaB pathway using bortezomib boosted the effect of panobinostat, indicating that panobinostat-induced apoptosis could be attenuated through the activation of the NF-kappaB pathway. Panobinostat 132-144 nuclear factor kappa B subunit 1 Homo sapiens 45-54 32142770-6 2020 Accordingly, we found that the inhibition of NF-kappaB pathway using bortezomib boosted the effect of panobinostat, indicating that panobinostat-induced apoptosis could be attenuated through the activation of the NF-kappaB pathway. Panobinostat 132-144 nuclear factor kappa B subunit 1 Homo sapiens 213-222 32119989-0 2020 Pan-HDAC inhibitor panobinostat, as a single agent or in combination with PI3K inhibitor, induces apoptosis in APL cells: An emerging approach to overcome MSC-induced resistance. Panobinostat 19-31 histone deacetylase 9 Homo sapiens 4-8 32119989-2 2020 Given to the prominent involvement of histone deacetylase (HDAC) enzymes in the formation of neoplastic nature of acute promyelocytic leukemia (APL), this study was aimed to evaluate the suppressive effect of pan-HDAC inhibitor panobinostat on both NB4 and primary APL patients cells, either in the context of mono- or co-culture with mesenchymal stem cells (MSC). Panobinostat 228-240 histone deacetylase 9 Homo sapiens 213-217 32119989-6 2020 Last but not least, we found that panobinostat combined with arsenic trioxide (ATO) prompted a synergistic effect and provided an improved therapeutic value in NB4; proposing that the abrogation of HDAC using panobinostat might be a befitting approach in APL, either as a single agent or in a combined-modal strategy. Panobinostat 34-46 histone deacetylase 9 Homo sapiens 198-202 32119989-6 2020 Last but not least, we found that panobinostat combined with arsenic trioxide (ATO) prompted a synergistic effect and provided an improved therapeutic value in NB4; proposing that the abrogation of HDAC using panobinostat might be a befitting approach in APL, either as a single agent or in a combined-modal strategy. Panobinostat 209-221 histone deacetylase 9 Homo sapiens 198-202 31999837-11 2020 Mechanistically, the combination of LBH589 and osimertinib enhanced the elevation of Bim in osimertinib-resistant cells. Panobinostat 36-42 BCL2-like 11 (apoptosis facilitator) Mus musculus 85-88 32365976-3 2020 We have demonstrated that the combination of TRAIL with doxorubicin, bortezomib, and panobinostat dramatically reduced the viability of TRAIL-resistant A549 and HT-29 cells. Panobinostat 85-97 TNF superfamily member 10 Homo sapiens 136-141 31390480-4 2020 First, the expression of BmApoLp-III could be upregulated when BmN cells were treated with the deacetylase inhibitor panobinostat (LBH589); similarly, the expression was downregulated when the cells were treated with the acetylase inhibitor C646. Panobinostat 117-129 apolipophorins Bombyx mori 25-36 31390480-4 2020 First, the expression of BmApoLp-III could be upregulated when BmN cells were treated with the deacetylase inhibitor panobinostat (LBH589); similarly, the expression was downregulated when the cells were treated with the acetylase inhibitor C646. Panobinostat 131-137 apolipophorins Bombyx mori 25-36 31390480-5 2020 Furthermore, the increase in acetylation by LBH589 could inhibit the degradation and improve the accumulation of BmApoLp-III in BmN cells treated with cycloheximide and MG132 respectively. Panobinostat 44-50 apolipophorins Bombyx mori 113-124 31390480-7 2020 Additionally, BmApoLp-III had an antiapoptosis function that increased after LBH589 treatment, which might have been due to the improved protein stability after acetylation. Panobinostat 77-83 apolipophorins Bombyx mori 14-25 31999837-0 2020 Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589). Panobinostat 186-198 epidermal growth factor receptor Mus musculus 34-66 31999837-0 2020 Overcoming acquired resistance of epidermal growth factor receptor-mutant non-small cell lung cancer cells to osimertinib by combining osimertinib with the histone deacetylase inhibitor panobinostat (LBH589). Panobinostat 200-206 epidermal growth factor receptor Mus musculus 34-66 32318119-0 2020 Design and synthesis of diazine-based panobinostat analogues for HDAC8 inhibition. Panobinostat 38-50 histone deacetylase 8 Homo sapiens 65-70 32318119-3 2020 By simply replacing the phenyl core of panobinostat with that of a diazine derivative, docking studies against HDAC2 and HDAC8 revealed that the four analogues exhibit inhibition activities comparable to that of panobinostat. Panobinostat 39-51 histone deacetylase 2 Homo sapiens 111-116 32318119-3 2020 By simply replacing the phenyl core of panobinostat with that of a diazine derivative, docking studies against HDAC2 and HDAC8 revealed that the four analogues exhibit inhibition activities comparable to that of panobinostat. Panobinostat 39-51 histone deacetylase 8 Homo sapiens 121-126 31811660-0 2020 Combined treatment with the histone deacetylase inhibitor LBH589 and a splice-switch antisense oligonucleotide enhances SMN2 splicing and SMN expression in Spinal Muscular Atrophy cells. Panobinostat 58-64 survival of motor neuron 2, centromeric Homo sapiens 120-124 31811660-5 2020 Herein, in vivo splicing assays indicated that the HDAC inhibitor LBH589 is particularly efficient in rescuing the SMN2 splicing defect in SMA fibroblasts and SMA type-I mice-derived neural stem cells. Panobinostat 66-72 glutamate receptor, metabotropic 7 Mus musculus 115-119 31811660-7 2020 Moreover chromatin immunoprecipitation analyses revealed that LBH589 treatment induces widespread H4 acetylation of the entire SMN2 locus and selectively favors the inclusion of the disease-linked exon 7 in SMN2 mature mRNA. Panobinostat 62-68 glutamate receptor, metabotropic 7 Mus musculus 127-131 31811660-7 2020 Moreover chromatin immunoprecipitation analyses revealed that LBH589 treatment induces widespread H4 acetylation of the entire SMN2 locus and selectively favors the inclusion of the disease-linked exon 7 in SMN2 mature mRNA. Panobinostat 62-68 glutamate receptor, metabotropic 7 Mus musculus 207-211 31811660-8 2020 The combined treatment of SMA cells with sub-optimal doses of LBH589 and of an antisense oligonucleotide that mimic Nusinersen (ASO_ISSN1) elicits additive effects on SMN2 splicing and SMN protein expression. Panobinostat 62-68 glutamate receptor, metabotropic 7 Mus musculus 167-171 32056234-0 2020 Combinatorial treatment for spinal muscular atrophy: An Editorial for "Combined treatment with the histone deacetylase inhibitor LBH589 and a splice-switch antisense oligonucleotide enhances SMN2 splicing and SMN expression in Spinal Muscular Atrophy cells" on page 264. Panobinostat 129-135 survival of motor neuron 2, centromeric Homo sapiens 191-195 32056234-0 2020 Combinatorial treatment for spinal muscular atrophy: An Editorial for "Combined treatment with the histone deacetylase inhibitor LBH589 and a splice-switch antisense oligonucleotide enhances SMN2 splicing and SMN expression in Spinal Muscular Atrophy cells" on page 264. Panobinostat 129-135 survival of motor neuron 1, telomeric Homo sapiens 191-194 32056234-11 2020 In addition, panobinostat increased exon 7 retention in the SMN2 mRNA. Panobinostat 13-25 survival of motor neuron 2, centromeric Homo sapiens 60-64 31999837-12 2020 Knockout of Bim in osimertinib-resistant cells substantially attenuated or abolished apoptosis enhanced by the LBH589 and osimertinib combination. Panobinostat 111-117 BCL2-like 11 (apoptosis facilitator) Mus musculus 12-15 31325448-0 2019 The mTOR inhibitor everolimus overcomes CXCR4-mediated resistance to histone deacetylase inhibitor panobinostat through inhibition of p21 and mitotic regulators. Panobinostat 99-111 mechanistic target of rapamycin kinase Homo sapiens 4-8 31801577-16 2019 Treatment of 5-azactidine and panobinostat restored CGRRF1 expression, supporting that the promoter of CGRRF1 is epigenetically modified in breast cancer. Panobinostat 30-42 cell growth regulator with ring finger domain 1 Homo sapiens 52-58 31801577-16 2019 Treatment of 5-azactidine and panobinostat restored CGRRF1 expression, supporting that the promoter of CGRRF1 is epigenetically modified in breast cancer. Panobinostat 30-42 cell growth regulator with ring finger domain 1 Homo sapiens 103-109 31801577-17 2019 Since 5-azactidine and panobinostat can increase CGRRF1 expression, they might be potential therapies for breast cancer treatment. Panobinostat 23-35 cell growth regulator with ring finger domain 1 Homo sapiens 49-55 31325448-0 2019 The mTOR inhibitor everolimus overcomes CXCR4-mediated resistance to histone deacetylase inhibitor panobinostat through inhibition of p21 and mitotic regulators. Panobinostat 99-111 C-X-C motif chemokine receptor 4 Homo sapiens 40-45 31325448-0 2019 The mTOR inhibitor everolimus overcomes CXCR4-mediated resistance to histone deacetylase inhibitor panobinostat through inhibition of p21 and mitotic regulators. Panobinostat 99-111 H3 histone pseudogene 16 Homo sapiens 134-137 31325448-3 2019 Sensitivity of MM cell lines and primary CD138+ cells from MM patients to panobinostat correlated with reduced expression of the chemokine receptor CXCR4, whereas overexpression of CXCR4 in MM cell lines increased their resistance to panobinostat. Panobinostat 74-86 syndecan 1 Homo sapiens 41-46 31325448-3 2019 Sensitivity of MM cell lines and primary CD138+ cells from MM patients to panobinostat correlated with reduced expression of the chemokine receptor CXCR4, whereas overexpression of CXCR4 in MM cell lines increased their resistance to panobinostat. Panobinostat 74-86 C-X-C motif chemokine receptor 4 Homo sapiens 148-153 31325448-3 2019 Sensitivity of MM cell lines and primary CD138+ cells from MM patients to panobinostat correlated with reduced expression of the chemokine receptor CXCR4, whereas overexpression of CXCR4 in MM cell lines increased their resistance to panobinostat. Panobinostat 234-246 C-X-C motif chemokine receptor 4 Homo sapiens 181-186 31325448-10 2019 Importantly, the combination of panobinostat with everolimus effectively targeted CXCR4-expressing resistant MM cells in vivo in the BM niche. Panobinostat 32-44 C-X-C motif chemokine receptor 4 Homo sapiens 82-87 31431326-7 2019 Based on our findings, the novel dual class I/HDAC6 inhibitors could serve as an option to overcome cisplatin resistance with fewer side effects in comparison to panobinostat. Panobinostat 162-174 histone deacetylase 6 Homo sapiens 46-51 31227503-2 2019 This study has used multiomics approaches and drug screens to identify the pan-HDAC inhibitor panobinostat as an effective strategy to limit MEK inhibitor resistance.Experimental Design: Mass spectrometry-based proteomics and RNA-Seq were used to identify the signaling pathways involved in the escape of uveal melanoma cells from MEK inhibitor therapy. Panobinostat 94-106 mitogen-activated protein kinase kinase 7 Homo sapiens 141-144 30846494-5 2019 Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines. Panobinostat 78-84 histone deacetylase 9 Homo sapiens 63-67 30846494-5 2019 Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines. Panobinostat 78-84 zinc fingers and homeoboxes 2 Homo sapiens 137-140 30846494-5 2019 Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines. Panobinostat 86-98 histone deacetylase 9 Homo sapiens 63-67 30846494-5 2019 Combining the MEK inhibitor AZD6244 (selumetinib) with the pan-HDAC inhibitor LBH589 (panobinostat) induced synergistic apoptosis in RAS/RAF mutated multiple myeloma cell lines. Panobinostat 86-98 zinc fingers and homeoboxes 2 Homo sapiens 137-140 30846494-8 2019 LBH589 dissociated BIM from MCL-1 and BCL-XL, which allowed it to bind BAX/BAK and thereby initiate apoptosis. Panobinostat 0-6 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 28-33 30846494-8 2019 LBH589 dissociated BIM from MCL-1 and BCL-XL, which allowed it to bind BAX/BAK and thereby initiate apoptosis. Panobinostat 0-6 BCL2 like 1 Homo sapiens 38-44 30846494-9 2019 The AZD6244/LBH589 combination was specifically active in cell lines with more BIM:MCL-1 complexes at baseline; resistant cell lines had more BIM:BCL-2 complexes. Panobinostat 12-18 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 83-88 31227503-2 2019 This study has used multiomics approaches and drug screens to identify the pan-HDAC inhibitor panobinostat as an effective strategy to limit MEK inhibitor resistance.Experimental Design: Mass spectrometry-based proteomics and RNA-Seq were used to identify the signaling pathways involved in the escape of uveal melanoma cells from MEK inhibitor therapy. Panobinostat 94-106 mitogen-activated protein kinase kinase 7 Homo sapiens 331-334 31330099-7 2019 We provide evidence that two prototypical, potent hydroxamic acid HDAC inhibitors that induce PGRN (panobinostat and trichostatin A) exhibit an initial fast-binding step followed by a second, slower step, referred to as mechanism B of slow binding, rather than simpler fast-on/fast-off binding kinetics. Panobinostat 100-112 histone deacetylase 9 Homo sapiens 66-70 31330099-7 2019 We provide evidence that two prototypical, potent hydroxamic acid HDAC inhibitors that induce PGRN (panobinostat and trichostatin A) exhibit an initial fast-binding step followed by a second, slower step, referred to as mechanism B of slow binding, rather than simpler fast-on/fast-off binding kinetics. Panobinostat 100-112 granulin precursor Homo sapiens 94-98 31152020-1 2019 PURPOSE: The histone deacetylase (HDAC) inhibitor panobinostat potentiates anthracycline and cytarabine cytotoxicity in acute myeloid leukemia (AML) cells. Panobinostat 50-62 histone deacetylase 9 Homo sapiens 13-32 31152020-1 2019 PURPOSE: The histone deacetylase (HDAC) inhibitor panobinostat potentiates anthracycline and cytarabine cytotoxicity in acute myeloid leukemia (AML) cells. Panobinostat 50-62 histone deacetylase 9 Homo sapiens 34-38 30954557-6 2019 Induction of ER stress and apoptosis by the p97 inhibitor CB-5083 was strongly enhanced in combination with the PI3Kalpha inhibitor BYL-719 or the HDAC inhibitor panobinostat suggesting potential therapeutic strategies to circumvent IXA resistance in MM. Panobinostat 162-174 melanotransferrin Homo sapiens 44-47 30515817-5 2019 IL-6 and IL-8 upregulation were blocked by broad-acting HDAC inhibitors SAHA and LBH589. Panobinostat 81-87 interleukin 6 Homo sapiens 0-4 30515817-5 2019 IL-6 and IL-8 upregulation were blocked by broad-acting HDAC inhibitors SAHA and LBH589. Panobinostat 81-87 C-X-C motif chemokine ligand 8 Homo sapiens 9-13 30880222-0 2019 Panobinostat (LBH589) inhibits Wnt/beta-catenin signaling pathway via upregulating APCL expression in breast cancer. Panobinostat 0-12 catenin beta 1 Homo sapiens 35-47 30880222-0 2019 Panobinostat (LBH589) inhibits Wnt/beta-catenin signaling pathway via upregulating APCL expression in breast cancer. Panobinostat 0-12 APC regulator of WNT signaling pathway 2 Homo sapiens 83-87 30880222-0 2019 Panobinostat (LBH589) inhibits Wnt/beta-catenin signaling pathway via upregulating APCL expression in breast cancer. Panobinostat 14-20 catenin beta 1 Homo sapiens 35-47 30880222-0 2019 Panobinostat (LBH589) inhibits Wnt/beta-catenin signaling pathway via upregulating APCL expression in breast cancer. Panobinostat 14-20 APC regulator of WNT signaling pathway 2 Homo sapiens 83-87 30880222-10 2019 We found that panobinostat inhibited beta-catenin expression by increasing its ubiquitylation and thus reducing its half-life. Panobinostat 14-26 catenin beta 1 Homo sapiens 37-49 31332289-7 2019 We identified Panobinostat, an FDA approved pan-HDAC inhibitor, could elevate and restore SOX7 expression in SOX7 silenced lung cancer cells. Panobinostat 14-26 SRY-box transcription factor 7 Homo sapiens 90-94 31332289-7 2019 We identified Panobinostat, an FDA approved pan-HDAC inhibitor, could elevate and restore SOX7 expression in SOX7 silenced lung cancer cells. Panobinostat 14-26 SRY-box transcription factor 7 Homo sapiens 109-113 31346162-6 2019 Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Panobinostat 102-114 jumonji domain containing 6 Mus musculus 139-144 31346162-6 2019 Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Panobinostat 102-114 E2F transcription factor 2 Mus musculus 146-150 31346162-6 2019 Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Panobinostat 102-114 v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived Mus musculus 152-157 31346162-6 2019 Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Panobinostat 102-114 MYC proto-oncogene, bHLH transcription factor Homo sapiens 159-164 31346162-6 2019 Combination therapy with the CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistically reduces JMJD6, E2F2, N-Myc, c-Myc expression, induces apoptosis in vitro and leads to neuroblastoma tumor regression in mice, which are significantly reversed by forced JMJD6 over-expression. Panobinostat 102-114 jumonji domain containing 6 Mus musculus 300-305 31136571-7 2019 We functionally validate one such novel association: that increased expression of the cell-cycle regulator C/EBPdelta decreases sensitivity to the histone deacetylase (HDAC) inhibitor panobinostat. Panobinostat 184-196 CCAAT enhancer binding protein delta Homo sapiens 107-117 30753450-6 2019 Our data reveal that panobinostat (LBH-589) and romidepsin (FK-228) provide functional correction of Class II and III CFTR variants, restoring cell surface chloride channel activity in primary human bronchial epithelial cells. Panobinostat 21-33 CF transmembrane conductance regulator Homo sapiens 118-122 30815722-4 2019 In this study, we evaluated the feasibility of using a histone deacetylase (HDAC) inhibitor, panobinostat, to upregulate RALDH2 expression and restore the angiogenic potential of MMD ECFCs. Panobinostat 93-105 aldehyde dehydrogenase 1 family member A2 Homo sapiens 121-127 30849634-1 2019 Panobinostat, a histone deacetylase inhibitor, induces histone acetylation and acts against cancer but attenuates its anticancer activity by activating the mammalian target of rapamycin (mTOR) pathway. Panobinostat 0-12 mechanistic target of rapamycin kinase Homo sapiens 156-185 30987296-5 2019 We revealed that panobinostat inhibits MM cell growth by degrading the protein PPP3CA, a catalytic subunit of calcineurin. Panobinostat 17-29 protein phosphatase 3 catalytic subunit alpha Homo sapiens 79-85 30849634-1 2019 Panobinostat, a histone deacetylase inhibitor, induces histone acetylation and acts against cancer but attenuates its anticancer activity by activating the mammalian target of rapamycin (mTOR) pathway. Panobinostat 0-12 mechanistic target of rapamycin kinase Homo sapiens 187-191 30849634-7 2019 Furthermore, the AMPK activation by metformin enhanced panobinostat-induced histone and non-histone acetylation. Panobinostat 55-67 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 17-21 30956773-3 2019 As HDAC inhibitors alter the immunogenicity and anti-tumor immune responses, we here explored the regulation of PD-L1 expression in MM cells by the clinically available HDAC inhibitor panobinostat in the presence of IFN-gamma. Panobinostat 184-196 CD274 molecule Homo sapiens 112-117 30956773-7 2019 These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-gamma-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-gamma. Panobinostat 27-39 CD274 molecule Homo sapiens 49-54 30956773-7 2019 These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-gamma-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-gamma. Panobinostat 27-39 interferon gamma Homo sapiens 86-95 30956773-7 2019 These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-gamma-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-gamma. Panobinostat 27-39 signal transducer and activator of transcription 1 Homo sapiens 96-101 30956773-7 2019 These results suggest that panobinostat enhances PD-L1 expression by facilitating the IFN-gamma-STAT1 pathway in a ligand-dependent manner in MM cells with ambient IFN-gamma. Panobinostat 27-39 interferon gamma Homo sapiens 164-173 30303565-0 2019 The histone deacetylase inhibitor LBH589 inhibits undifferentiated pleomorphic sarcoma growth via downregulation of FOS-like antigen 1. Panobinostat 34-40 FOS like 1, AP-1 transcription factor subunit Homo sapiens 116-134 30301863-7 2019 Corroborating the basis of sensitivity, transcriptional profiling of platinum-resistant ARID1A-mutated HT1197 cells treated with panobinostat reveals negative enrichment for both cyto-proliferative (MYC and E2F targets) and DNA repair gene sets, and positive enrichment for TP53 and inflammatory gene sets. Panobinostat 129-141 AT-rich interaction domain 1A Homo sapiens 88-94 30301863-7 2019 Corroborating the basis of sensitivity, transcriptional profiling of platinum-resistant ARID1A-mutated HT1197 cells treated with panobinostat reveals negative enrichment for both cyto-proliferative (MYC and E2F targets) and DNA repair gene sets, and positive enrichment for TP53 and inflammatory gene sets. Panobinostat 129-141 MYC proto-oncogene, bHLH transcription factor Homo sapiens 199-202 30301863-7 2019 Corroborating the basis of sensitivity, transcriptional profiling of platinum-resistant ARID1A-mutated HT1197 cells treated with panobinostat reveals negative enrichment for both cyto-proliferative (MYC and E2F targets) and DNA repair gene sets, and positive enrichment for TP53 and inflammatory gene sets. Panobinostat 129-141 tumor protein p53 Homo sapiens 274-278 30369061-5 2019 A docking study was performed comparing panobinostat derivatives in both HDAC2 and HDAC8. Panobinostat 40-52 histone deacetylase 2 Homo sapiens 73-78 30369061-5 2019 A docking study was performed comparing panobinostat derivatives in both HDAC2 and HDAC8. Panobinostat 40-52 histone deacetylase 8 Homo sapiens 83-88 30847387-4 2019 We found that panobinostat alone increased iodine-metabolizing gene expression, promoted radioiodine uptake and toxicity, and suppressed GLUT1 expression in all the cells. Panobinostat 14-26 solute carrier family 2 member 1 Homo sapiens 137-142 30847387-6 2019 Combined treatment with panobinostat and MAPKi (dabrafenib or selumetinib) displayed a more robust BRAF V600E-dependent redifferentiation effect than panobinostat alone via further improving the acetylation level of histone at the sodium-iodide symporter (NIS) promoter. Panobinostat 24-36 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 99-103 30847387-6 2019 Combined treatment with panobinostat and MAPKi (dabrafenib or selumetinib) displayed a more robust BRAF V600E-dependent redifferentiation effect than panobinostat alone via further improving the acetylation level of histone at the sodium-iodide symporter (NIS) promoter. Panobinostat 150-162 B-Raf proto-oncogene, serine/threonine kinase Homo sapiens 99-103 30962658-0 2019 Enhanced efficacy of histone deacetylase inhibitor panobinostat combined with dual PI3K/mTOR inhibitor BEZ235 against glioblastoma. Panobinostat 51-63 histone deacetylase 9 Homo sapiens 21-40 30962658-3 2019 This study aimed to evaluate the efficacy of combination treatment of GBM with the histone deacetylase (HDAC) inhibitor panobinostat and dual phosphoinositide 3-kinase (PI3K) and mammalian target of rapamycin (mTOR) inhibitor BEZ235. Panobinostat 120-132 histone deacetylase 9 Homo sapiens 83-102 30962658-3 2019 This study aimed to evaluate the efficacy of combination treatment of GBM with the histone deacetylase (HDAC) inhibitor panobinostat and dual phosphoinositide 3-kinase (PI3K) and mammalian target of rapamycin (mTOR) inhibitor BEZ235. Panobinostat 120-132 histone deacetylase 9 Homo sapiens 104-108 30224345-6 2019 RESULTS: In the model, panobinostat/bicalutamide demonstrated synergistic antitumor effect while reducing AR activity. Panobinostat 23-35 androgen receptor Homo sapiens 106-108 30481203-0 2018 Comparison of the antifibrotic effects of the pan-histone deacetylase-inhibitor panobinostat versus the IPF-drug pirfenidone in fibroblasts from patients with idiopathic pulmonary fibrosis. Panobinostat 80-92 histone deacetylase 9 Homo sapiens 50-69 30481203-12 2018 Furthermore, panobinostat-treatment enhanced alpha-tubulin-acetylation, decreased the expression of survival-related genes Bcl-XL and BIRC5/survivin, and was associated with induction of ER stress and apoptosis in IPF-fibroblasts. Panobinostat 13-25 BCL2 like 1 Homo sapiens 123-129 30481203-12 2018 Furthermore, panobinostat-treatment enhanced alpha-tubulin-acetylation, decreased the expression of survival-related genes Bcl-XL and BIRC5/survivin, and was associated with induction of ER stress and apoptosis in IPF-fibroblasts. Panobinostat 13-25 baculoviral IAP repeat containing 5 Homo sapiens 134-139 30481203-17 2018 The pan-HDAC-inhibitor panobinostat reduces profibrotic phenotypes while inducing cell cycle arrest and apoptosis in IPF-fibroblasts, thus indicating more efficiency than pirfenidone in inactivating IPF-fibroblasts. Panobinostat 23-35 histone deacetylase 9 Homo sapiens 8-12 30481203-18 2018 We therefore believe that HDAC-inhibitors such as panobinostat can present a novel therapeutic strategy for IPF. Panobinostat 50-62 histone deacetylase 9 Homo sapiens 26-30 30404918-6 2018 Pharmacologic induction of NOXA, using the histone deacetylase inhibitor panobinostat, decreased MCL1 protein abundance and increased lymphoma cell vulnerability to BCL2 inhibitors in vitro and in vivo. Panobinostat 73-85 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 27-31 30404918-6 2018 Pharmacologic induction of NOXA, using the histone deacetylase inhibitor panobinostat, decreased MCL1 protein abundance and increased lymphoma cell vulnerability to BCL2 inhibitors in vitro and in vivo. Panobinostat 73-85 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 97-101 30039622-6 2018 Furthermore, we showed that simvastatin prevented, whereas LBH589 promoted, the progression of Hsp90 chaperone cycling and client maturation, resulting in an increment of cell apoptosis by the combination of simvastatin and LBH589 in a mouse xenograft model. Panobinostat 59-65 heat shock protein, 3 Mus musculus 95-100 30484863-8 2018 Taken together, we propose that LBH589 inhibits ESCC cell proliferation mainly through inducing cell cycle arrest by increasing p21 and decreasing cyclin D1 in a p53-independent manner. Panobinostat 32-38 cyclin dependent kinase inhibitor 1A Homo sapiens 128-131 30484863-8 2018 Taken together, we propose that LBH589 inhibits ESCC cell proliferation mainly through inducing cell cycle arrest by increasing p21 and decreasing cyclin D1 in a p53-independent manner. Panobinostat 32-38 cyclin D1 Homo sapiens 147-156 30484863-8 2018 Taken together, we propose that LBH589 inhibits ESCC cell proliferation mainly through inducing cell cycle arrest by increasing p21 and decreasing cyclin D1 in a p53-independent manner. Panobinostat 32-38 tumor protein p53 Homo sapiens 162-165 30014555-2 2018 Here, we report effects of panobinostat and 5-azacytidine on the proliferation of juvenile myelomonocytic leukemia (JMML) CD34+ cells. Panobinostat 27-39 CD34 antigen Mus musculus 122-126 30014555-4 2018 Using this culture system, we evaluated effects of panobinostat and 5-azacytidine on the proliferation of JMML CD34+ cells. Panobinostat 51-63 CD34 antigen Mus musculus 111-115 30014555-5 2018 RESULTS: Panobinostat dose dependently reduced the numbers of day 7 CD34+ cells generated under stimulation of hematopoietic growth factors on AGM-S3 cells in all eight patients with JMML. Panobinostat 9-21 CD34 antigen Mus musculus 68-72 30014555-7 2018 CD34+ CD38- cells were substantially more sensitive to panobinostat at 10 and 20 nM than CD34+ CD38+ cells. Panobinostat 55-67 CD34 antigen Mus musculus 0-4 30014555-7 2018 CD34+ CD38- cells were substantially more sensitive to panobinostat at 10 and 20 nM than CD34+ CD38+ cells. Panobinostat 55-67 CD38 antigen Mus musculus 6-10 30348136-5 2018 RESULTS: We demonstrated that KLF9 expression combined with HDAC inhibitor panobinostat (LBH589) dramatically induced glioma stem cell death via both apoptosis and necroptosis in a synergistic manner. Panobinostat 75-87 histone deacetylase 9 Homo sapiens 60-64 30348136-5 2018 RESULTS: We demonstrated that KLF9 expression combined with HDAC inhibitor panobinostat (LBH589) dramatically induced glioma stem cell death via both apoptosis and necroptosis in a synergistic manner. Panobinostat 89-95 Kruppel like factor 9 Homo sapiens 30-34 30348136-5 2018 RESULTS: We demonstrated that KLF9 expression combined with HDAC inhibitor panobinostat (LBH589) dramatically induced glioma stem cell death via both apoptosis and necroptosis in a synergistic manner. Panobinostat 89-95 histone deacetylase 9 Homo sapiens 60-64 30039622-6 2018 Furthermore, we showed that simvastatin prevented, whereas LBH589 promoted, the progression of Hsp90 chaperone cycling and client maturation, resulting in an increment of cell apoptosis by the combination of simvastatin and LBH589 in a mouse xenograft model. Panobinostat 224-230 heat shock protein, 3 Mus musculus 95-100 29956350-1 2018 This is a phase II study of panobinostat, an oral pan-HDAC inhibitor, combined with rituximab in patients with relapsed diffuse large B cell lymphoma. Panobinostat 28-40 histone deacetylase 9 Homo sapiens 54-58 30285808-4 2018 METHODS: The synergistic effects of cotreatment with the histone deacetylase (HDAC) inhibitor panobinostat and bromodomain inhibitor JQ1 or OTX015 were validated using cell viability assays in GBM cell lines. Panobinostat 94-106 histone deacetylase 9 Homo sapiens 57-76 30285808-4 2018 METHODS: The synergistic effects of cotreatment with the histone deacetylase (HDAC) inhibitor panobinostat and bromodomain inhibitor JQ1 or OTX015 were validated using cell viability assays in GBM cell lines. Panobinostat 94-106 histone deacetylase 9 Homo sapiens 78-82 29482060-0 2018 Inhibition of class IIa histone deacetylase activity by gallic acid, sulforaphane, TMP269, and panobinostat. Panobinostat 95-107 ATPase, class II, type 9A Mus musculus 20-23 30081552-5 2018 Panobinostat produced concentration-dependent reductions in ventricular gj, peak INa density, and NaV1.5 protein expression levels. Panobinostat 0-12 internexin neuronal intermediate filament protein alpha Homo sapiens 81-84 30081552-5 2018 Panobinostat produced concentration-dependent reductions in ventricular gj, peak INa density, and NaV1.5 protein expression levels. Panobinostat 0-12 sodium voltage-gated channel alpha subunit 5 Homo sapiens 98-104 29669761-6 2018 Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor-suppressor miRNAs such as miR-449, another member of the miR-34 family, and synergistically induced antiproliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Panobinostat 0-12 microRNA 449a Mus musculus 125-132 29669761-6 2018 Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor-suppressor miRNAs such as miR-449, another member of the miR-34 family, and synergistically induced antiproliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Panobinostat 0-12 anaplastic lymphoma kinase Mus musculus 230-233 29669761-6 2018 Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor-suppressor miRNAs such as miR-449, another member of the miR-34 family, and synergistically induced antiproliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Panobinostat 0-12 echinoderm microtubule associated protein like 4 Mus musculus 281-285 29669761-6 2018 Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor-suppressor miRNAs such as miR-449, another member of the miR-34 family, and synergistically induced antiproliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Panobinostat 0-12 anaplastic lymphoma kinase Mus musculus 286-289 29482060-5 2018 The selective class IIa HDAC inhibitor, TMP269, and the pan-HDAC inhibitor, panobinostat, but not MC1568, clearly inhibited class IIa HDAC activities. Panobinostat 76-88 histone deacetylase 6 Mus musculus 60-64 29482060-5 2018 The selective class IIa HDAC inhibitor, TMP269, and the pan-HDAC inhibitor, panobinostat, but not MC1568, clearly inhibited class IIa HDAC activities. Panobinostat 76-88 ATPase, class II, type 9A Mus musculus 130-133 29482060-5 2018 The selective class IIa HDAC inhibitor, TMP269, and the pan-HDAC inhibitor, panobinostat, but not MC1568, clearly inhibited class IIa HDAC activities. Panobinostat 76-88 histone deacetylase 6 Mus musculus 60-64 29774113-5 2018 Pre-treatment with EZH2 inhibitors greatly enhanced the sensitivity of HMCLs to the pan-HDAC inhibitor panobinostat in nearly all cases regardless of single agent EZH2 inhibitor sensitivity. Panobinostat 103-115 enhancer of zeste 2 polycomb repressive complex 2 subunit Homo sapiens 19-23 29306016-0 2018 Pan-HDAC inhibition by panobinostat mediates chemosensitization to carboplatin in non-small cell lung cancer via attenuation of EGFR signaling. Panobinostat 23-35 epidermal growth factor receptor Homo sapiens 128-132 29306016-2 2018 Here we report that panobinostat (LBH589), a potent pan-HDAC inhibitor, effectively curbed the proliferation of non-small cell lung cancer (NSCLC) cell lines A549, Calu-1, H226, H460, H838 and SKMES-1 at IC50 concentrations between 4 and 31 nmol/L via pleiotropic mechanisms, including crosstalk with EGFR signal transduction cascades. Panobinostat 20-32 epidermal growth factor receptor Homo sapiens 301-305 29306016-2 2018 Here we report that panobinostat (LBH589), a potent pan-HDAC inhibitor, effectively curbed the proliferation of non-small cell lung cancer (NSCLC) cell lines A549, Calu-1, H226, H460, H838 and SKMES-1 at IC50 concentrations between 4 and 31 nmol/L via pleiotropic mechanisms, including crosstalk with EGFR signal transduction cascades. Panobinostat 34-40 epidermal growth factor receptor Homo sapiens 301-305 29317217-0 2018 Crucial role of HO-1/IRF4-dependent apoptosis induced by panobinostat and lenalidomide in multiple myeloma. Panobinostat 57-69 heme oxygenase 1 Homo sapiens 16-20 28792260-1 2018 This phase-I/phase-II study evaluated panobinostat in combination with ifosfamide, carboplatin, etoposide (P-ICE) in relapsed/refractory classical Hodgkin lymphoma. Panobinostat 38-50 carboxylesterase 2 Homo sapiens 109-112 28792260-2 2018 During phase I, panobinostat was given daily on Monday/Wednesday/Friday starting one week prior to Cycle 1 (C1) of ICE and during two weeks of C1-2 of ICE (Schedule A). Panobinostat 16-28 carboxylesterase 2 Homo sapiens 115-118 29317217-0 2018 Crucial role of HO-1/IRF4-dependent apoptosis induced by panobinostat and lenalidomide in multiple myeloma. Panobinostat 57-69 interferon regulatory factor 4 Homo sapiens 21-25 29317217-7 2018 Herein, panobinostat induced acetylation of histone H3K9 and activation of caspase-3 in MM cells, being inversely correlated with the reduction of HO-1/IRF4/MYC protein levels. Panobinostat 8-20 caspase 3 Homo sapiens 75-84 29317217-7 2018 Herein, panobinostat induced acetylation of histone H3K9 and activation of caspase-3 in MM cells, being inversely correlated with the reduction of HO-1/IRF4/MYC protein levels. Panobinostat 8-20 heme oxygenase 1 Homo sapiens 147-151 29317217-7 2018 Herein, panobinostat induced acetylation of histone H3K9 and activation of caspase-3 in MM cells, being inversely correlated with the reduction of HO-1/IRF4/MYC protein levels. Panobinostat 8-20 interferon regulatory factor 4 Homo sapiens 152-156 29317217-7 2018 Herein, panobinostat induced acetylation of histone H3K9 and activation of caspase-3 in MM cells, being inversely correlated with the reduction of HO-1/IRF4/MYC protein levels. Panobinostat 8-20 MYC proto-oncogene, bHLH transcription factor Homo sapiens 157-160 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. Panobinostat 79-91 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. Panobinostat 79-91 heme oxygenase 1 Homo sapiens 56-60 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. Panobinostat 79-91 interferon regulatory factor 4 Homo sapiens 61-65 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. Panobinostat 79-91 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. Panobinostat 79-91 heme oxygenase 1 Homo sapiens 170-174 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. Panobinostat 79-91 interferon regulatory factor 4 Homo sapiens 175-179 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. Panobinostat 79-91 MYC proto-oncogene, bHLH transcription factor Homo sapiens 180-183 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. Panobinostat 0-6 interferon regulatory factor 4 Homo sapiens 197-201 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. Panobinostat 0-6 MYC proto-oncogene, bHLH transcription factor Homo sapiens 206-209 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. Panobinostat 57-63 heme oxygenase 1 Homo sapiens 191-195 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. Panobinostat 57-63 interferon regulatory factor 4 Homo sapiens 197-201 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. Panobinostat 57-63 MYC proto-oncogene, bHLH transcription factor Homo sapiens 206-209 29468194-6 2018 We found that proportions of CD4+ and CD8+ T cells expressing CD69 increased 24 h after initial panobinostat administration (P < 0.01), followed by an increase in the proportions of CD38+ HLA-DR+-coexpressing CD4+ T cells on day 4 (P = 0.02). Panobinostat 96-108 CD69 molecule Homo sapiens 62-66 28839000-9 2018 Radiosensitization by panobinostat was effective in hypoxic bladder cancer cells and associated with class I HDAC inhibition, and protein downregulation of HDAC2 and MRE11. Panobinostat 22-34 histone deacetylase 2 Mus musculus 156-161 28839000-9 2018 Radiosensitization by panobinostat was effective in hypoxic bladder cancer cells and associated with class I HDAC inhibition, and protein downregulation of HDAC2 and MRE11. Panobinostat 22-34 MRE11A homolog A, double strand break repair nuclease Mus musculus 166-171 28667459-2 2018 Panobinostat is a first-in-line HDAC inhibitor approved for treating multiple myeloma in combination with bortezomib and dexamethasone. Panobinostat 0-12 histone deacetylase 9 Homo sapiens 32-36 28667459-11 2018 Panobinostat itself is a CYP2D6 inhibitor, which influences the plasma levels of the CYP2D6 substrate dexamethasone. Panobinostat 0-12 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 25-31 28667459-11 2018 Panobinostat itself is a CYP2D6 inhibitor, which influences the plasma levels of the CYP2D6 substrate dexamethasone. Panobinostat 0-12 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 85-91 29080797-8 2017 Adding DNMT1 inhibitor (5-Aza-2dc) or HDAC1 inhibitor (LBH589) depressed the up-regulation of DNMT1 or HDAC1 expression, the decreases of GSH levels and increases of ROS production induced by OTA, respectively. Panobinostat 55-61 DNA methyltransferase 1 Sus scrofa 7-12 29136455-0 2017 LBH589 Inhibits Glioblastoma Growth and Angiogenesis Through Suppression of HIF-1alpha Expression. Panobinostat 0-6 hypoxia inducible factor 1 subunit alpha Homo sapiens 76-86 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 19-31 lysine methyltransferase 2A Homo sapiens 88-91 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 19-31 ring finger protein 20 Homo sapiens 150-155 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 19-31 ring finger protein 40 Homo sapiens 156-161 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 33-39 lysine methyltransferase 2A Homo sapiens 88-91 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 33-39 ring finger protein 20 Homo sapiens 150-155 28690313-0 2018 The HDAC inhibitor panobinostat (LBH589) exerts in vivo anti-leukaemic activity against MLL-rearranged acute lymphoblastic leukaemia and involves the RNF20/RNF40/WAC-H2B ubiquitination axis. Panobinostat 33-39 ring finger protein 40 Homo sapiens 156-161 28690313-4 2018 Here we demonstrate the in vivo efficacy of the histone deacetylase inhibitor panobinostat (LBH589) using xenograft mouse models of MLL-rearranged ALL. Panobinostat 78-90 lysine (K)-specific methyltransferase 2A Mus musculus 132-135 28690313-4 2018 Here we demonstrate the in vivo efficacy of the histone deacetylase inhibitor panobinostat (LBH589) using xenograft mouse models of MLL-rearranged ALL. Panobinostat 92-98 lysine (K)-specific methyltransferase 2A Mus musculus 132-135 29080797-8 2017 Adding DNMT1 inhibitor (5-Aza-2dc) or HDAC1 inhibitor (LBH589) depressed the up-regulation of DNMT1 or HDAC1 expression, the decreases of GSH levels and increases of ROS production induced by OTA, respectively. Panobinostat 55-61 histone deacetylase 1 Sus scrofa 38-43 29080797-8 2017 Adding DNMT1 inhibitor (5-Aza-2dc) or HDAC1 inhibitor (LBH589) depressed the up-regulation of DNMT1 or HDAC1 expression, the decreases of GSH levels and increases of ROS production induced by OTA, respectively. Panobinostat 55-61 DNA methyltransferase 1 Sus scrofa 94-99 29080797-8 2017 Adding DNMT1 inhibitor (5-Aza-2dc) or HDAC1 inhibitor (LBH589) depressed the up-regulation of DNMT1 or HDAC1 expression, the decreases of GSH levels and increases of ROS production induced by OTA, respectively. Panobinostat 55-61 histone deacetylase 1 Sus scrofa 103-108 28814661-4 2017 Importantly, we demonstrate that clinical administration of histone deacetylase inhibitors (HDACis; vorinostat and panobinostat) induced HIV gag p24, and ex vivo stimulation produced sufficient viral antigen to elicit immune-mediated cell killing using anti-gp120/CD3 bispecific antibody. Panobinostat 115-127 transmembrane p24 trafficking protein 2 Homo sapiens 145-148 28912253-3 2017 Panobinostat was also an in vitro reversible and time-dependent inhibitor of CYP3A4/5 and a reversible inhibitor of CYP2D6 and CYP2C19. Panobinostat 0-12 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 77-83 28912253-3 2017 Panobinostat was also an in vitro reversible and time-dependent inhibitor of CYP3A4/5 and a reversible inhibitor of CYP2D6 and CYP2C19. Panobinostat 0-12 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 116-122 28912253-3 2017 Panobinostat was also an in vitro reversible and time-dependent inhibitor of CYP3A4/5 and a reversible inhibitor of CYP2D6 and CYP2C19. Panobinostat 0-12 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 127-134 28860561-5 2017 Like butyrate and propionate, the prototypical hydroxyamic acid-derived histone deacetylase (HDAC) inhibitors Panobinostat and Vorinostat also enhanced AhR ligand-mediated induction and this was accompanied by enhanced histone acetylation. Panobinostat 110-122 aryl hydrocarbon receptor Homo sapiens 152-155 28710768-6 2017 In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild-type NSCLC. Panobinostat 36-48 KRAS proto-oncogene, GTPase Homo sapiens 85-89 28710768-6 2017 In this study, we demonstrated that panobinostat overcame resistance to gefitinib in KRAS-mutant/EGFR-wild-type NSCLC. Panobinostat 36-48 epidermal growth factor receptor Homo sapiens 97-101 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 36-48 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 77-80 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 36-48 epidermal growth factor receptor Homo sapiens 218-222 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 36-48 epidermal growth factor receptor Homo sapiens 227-231 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 119-131 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 176-179 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 119-131 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 176-179 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 119-131 epidermal growth factor receptor Homo sapiens 218-222 28710768-8 2017 Mechanistically, we identified that panobinostat-but not gefitinib-inhibited TAZ transcription, and the combination of panobinostat and gefitinib synergistically downregulated TAZ and TAZ downstream targets, including EGFR and EGFR ligand. Panobinostat 119-131 epidermal growth factor receptor Homo sapiens 227-231 28710768-9 2017 Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Panobinostat 21-33 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 14-17 28710768-9 2017 Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Panobinostat 21-33 KRAS proto-oncogene, GTPase Homo sapiens 66-70 28710768-9 2017 Inhibition of TAZ by panobinostat or short hairpin RNA sensitized KRAS-mutant/EGFR-wild-type NSCLC to gefitinib through abrogating AKT/mammalian target of rapamycin (mTOR) signaling. Panobinostat 21-33 epidermal growth factor receptor Homo sapiens 78-82 29080899-10 2017 Moreover, LBH589 significantly induced hyperacetylation of histone H4, the protein level of PARP notably increased, and the level of Bcl-X decreased. Panobinostat 10-16 poly(ADP-ribose) polymerase 1 Homo sapiens 92-96 29080899-10 2017 Moreover, LBH589 significantly induced hyperacetylation of histone H4, the protein level of PARP notably increased, and the level of Bcl-X decreased. Panobinostat 10-16 BCL2 like 1 Homo sapiens 133-138 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 protein tyrosine phosphatase non-receptor type 6 Homo sapiens 80-85 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 DNA methyltransferase 1 Homo sapiens 120-125 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 DNA methyltransferase 3 alpha Homo sapiens 127-133 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 methyl-CpG binding protein 2 Homo sapiens 135-140 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 methyl-CpG binding domain protein 2 Homo sapiens 142-146 28480959-7 2017 Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Panobinostat 63-69 histone deacetylase 1 Homo sapiens 151-156 28814661-4 2017 Importantly, we demonstrate that clinical administration of histone deacetylase inhibitors (HDACis; vorinostat and panobinostat) induced HIV gag p24, and ex vivo stimulation produced sufficient viral antigen to elicit immune-mediated cell killing using anti-gp120/CD3 bispecific antibody. Panobinostat 115-127 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 258-263 28516379-8 2017 The addition of three HDAC inhibitors (panobinostat, LBH589; trichostatin A, TSA; suberoylanilide hydroxamic acid, SAHA) decreased the viability of EC cells and up-regulated the expression of PR and MIG6, and these effects were the strongest with LBH589. Panobinostat 39-51 progesterone receptor Homo sapiens 192-194 28516379-8 2017 The addition of three HDAC inhibitors (panobinostat, LBH589; trichostatin A, TSA; suberoylanilide hydroxamic acid, SAHA) decreased the viability of EC cells and up-regulated the expression of PR and MIG6, and these effects were the strongest with LBH589. Panobinostat 39-51 ERBB receptor feedback inhibitor 1 Homo sapiens 199-203 28516379-8 2017 The addition of three HDAC inhibitors (panobinostat, LBH589; trichostatin A, TSA; suberoylanilide hydroxamic acid, SAHA) decreased the viability of EC cells and up-regulated the expression of PR and MIG6, and these effects were the strongest with LBH589. Panobinostat 53-59 progesterone receptor Homo sapiens 192-194 28516379-8 2017 The addition of three HDAC inhibitors (panobinostat, LBH589; trichostatin A, TSA; suberoylanilide hydroxamic acid, SAHA) decreased the viability of EC cells and up-regulated the expression of PR and MIG6, and these effects were the strongest with LBH589. Panobinostat 247-253 progesterone receptor Homo sapiens 192-194 28476749-0 2017 Panobinostat induces CD38 upregulation and augments the antimyeloma efficacy of daratumumab. Panobinostat 0-12 CD38 molecule Homo sapiens 21-25 28363998-4 2017 Truncated MRE11 was stabilized by proteasome inhibition, exhibited a decreased half-life after treatment with panobinostat, and therefore represents a newly identified intermediate induced and degraded in response to HDAC inhibition. Panobinostat 110-122 MRE11 homolog, double strand break repair nuclease Homo sapiens 10-15 28915627-9 2017 The findings demonstrate that panobinostat suppresses MB leptomeningeal seeding through the down-regulation of ID3 and the induction of neuronal differentiation. Panobinostat 30-42 inhibitor of DNA binding 3, HLH protein Homo sapiens 111-114 28415789-6 2017 Panobinostat, an HDAC inhibitor, downregulated Hmga2 expression by preventing Hmga2 to bind its own promoter, and thus inhibiting Hmga2 promoter activity. Panobinostat 0-12 high mobility group AT-hook 2 Mus musculus 47-52 28415789-6 2017 Panobinostat, an HDAC inhibitor, downregulated Hmga2 expression by preventing Hmga2 to bind its own promoter, and thus inhibiting Hmga2 promoter activity. Panobinostat 0-12 high mobility group AT-hook 2 Mus musculus 78-83 28415789-6 2017 Panobinostat, an HDAC inhibitor, downregulated Hmga2 expression by preventing Hmga2 to bind its own promoter, and thus inhibiting Hmga2 promoter activity. Panobinostat 0-12 high mobility group AT-hook 2 Mus musculus 78-83 28505595-8 2017 Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator. Panobinostat 72-84 tumor protein p53 Homo sapiens 124-127 28505595-9 2017 A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator. Panobinostat 66-78 tumor protein p53 Homo sapiens 174-177 28505595-10 2017 Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. Panobinostat 85-97 tumor protein p53 Homo sapiens 30-33 28505595-10 2017 Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML. Panobinostat 85-97 tumor protein p53 Homo sapiens 127-130