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Results: 1 to 20 of 184

Similar articles for PubMed (Select 24023871)

1.

The HDAC inhibitor LBH589 induces ERK-dependent prometaphase arrest in prostate cancer via HDAC6 inactivation and down-regulation.

Chuang MJ, Wu ST, Tang SH, Lai XM, Lai HC, Hsu KH, Sun KH, Sun GH, Chang SY, Yu DS, Hsiao PW, Huang SM, Cha TL.

PLoS One. 2013 Sep 4;8(9):e73401. doi: 10.1371/journal.pone.0073401. eCollection 2013.

2.

The prostate cancer blocking potential of the histone deacetylase inhibitor LBH589 is not enhanced by the multi receptor tyrosine kinase inhibitor TKI258.

Vallo S, Mani J, Stastny M, Makarević J, Juengel E, Tsaur I, Bartsch G, Haferkamp A, Blaheta RA.

Invest New Drugs. 2013 Apr;31(2):265-72. doi: 10.1007/s10637-012-9851-5. Epub 2012 Jul 17.

PMID:
22801803
3.

Targeting tumor angiogenesis with histone deacetylase inhibitors: the hydroxamic acid derivative LBH589.

Qian DZ, Kato Y, Shabbeer S, Wei Y, Verheul HM, Salumbides B, Sanni T, Atadja P, Pili R.

Clin Cancer Res. 2006 Jan 15;12(2):634-42.

4.

DNA microarray profiling of genes differentially regulated by the histone deacetylase inhibitors vorinostat and LBH589 in colon cancer cell lines.

LaBonte MJ, Wilson PM, Fazzone W, Groshen S, Lenz HJ, Ladner RD.

BMC Med Genomics. 2009 Nov 30;2:67. doi: 10.1186/1755-8794-2-67.

5.

LBH589 Inhibits proliferation and metastasis of hepatocellular carcinoma via inhibition of gankyrin/STAT3/Akt pathway.

Song X, Wang J, Zheng T, Song R, Liang Y, Bhatta N, Yin D, Pan S, Liu J, Jiang H, Liu L.

Mol Cancer. 2013 Oct 5;12(1):114. doi: 10.1186/1476-4598-12-114.

6.

Panobinostat synergistically enhances the cytotoxic effects of cisplatin, doxorubicin or etoposide on high-risk neuroblastoma cells.

Wang G, Edwards H, Caldwell JT, Buck SA, Qing WY, Taub JW, Ge Y, Wang Z.

PLoS One. 2013 Sep 30;8(9):e76662. doi: 10.1371/journal.pone.0076662. eCollection 2013.

7.

Epigenetic modulation of radiation response in human cancer cells with activated EGFR or HER-2 signaling: potential role of histone deacetylase 6.

Kim IA, No M, Lee JM, Shin JH, Oh JS, Choi EJ, Kim IH, Atadja P, Bernhard EJ.

Radiother Oncol. 2009 Jul;92(1):125-32. doi: 10.1016/j.radonc.2009.03.008. Epub 2009 Mar 28.

PMID:
19329208
8.
9.

Histone acetylation-independent effect of histone deacetylase inhibitors on Akt through the reshuffling of protein phosphatase 1 complexes.

Chen CS, Weng SC, Tseng PH, Lin HP, Chen CS.

J Biol Chem. 2005 Nov 18;280(46):38879-87. Epub 2005 Sep 26.

10.

Green tea polyphenols causes cell cycle arrest and apoptosis in prostate cancer cells by suppressing class I histone deacetylases.

Thakur VS, Gupta K, Gupta S.

Carcinogenesis. 2012 Feb;33(2):377-84. doi: 10.1093/carcin/bgr277. Epub 2011 Nov 23.

11.

HDAC gene expression in pancreatic tumor cell lines following treatment with the HDAC inhibitors panobinostat (LBH589) and trichostatine (TSA).

Mehdi O, Françoise S, Sofia CL, Urs G, Kevin Z, Bernard S, Igor S, Anabela CD, Dominique L, Eric M, Ali O.

Pancreatology. 2012 Mar-Apr;12(2):146-55. doi: 10.1016/j.pan.2012.02.013. Epub 2012 Feb 25.

PMID:
22487525
12.

CG0006, a novel histone deacetylase inhibitor, induces breast cancer cell death via histone-acetylation and chaperone-disrupting pathways independent of ER status.

Kim HM, Kim CS, Lee JH, Jang SJ, Hwang JJ, Ro S, Hyun YL, Choi J.

Breast Cancer Res Treat. 2011 Nov;130(2):365-75. doi: 10.1007/s10549-010-1310-4. Epub 2010 Dec 24.

PMID:
21184271
13.

HDAC-inhibitor (S)-8 disrupts HDAC6-PP1 complex prompting A375 melanoma cell growth arrest and apoptosis.

Balliu M, Guandalini L, Romanelli MN, D'Amico M, Paoletti F.

J Cell Mol Med. 2015 Jan;19(1):143-54. doi: 10.1111/jcmm.12345. Epub 2014 Nov 6.

14.

The HDAC inhibitor, panobinostat, induces apoptosis by suppressing the expresssion of specificity protein 1 in oral squamous cell carcinoma.

Jeon YJ, Ko SM, Cho JH, Chae JI, Shim JH.

Int J Mol Med. 2013 Oct;32(4):860-6. doi: 10.3892/ijmm.2013.1451. Epub 2013 Jul 18.

PMID:
23877235
15.

DAPK plays an important role in panobinostat-induced autophagy and commits cells to apoptosis under autophagy deficient conditions.

Gandesiri M, Chakilam S, Ivanovska J, Benderska N, Ocker M, Di Fazio P, Feoktistova M, Gali-Muhtasib H, Rave-Fränk M, Prante O, Christiansen H, Leverkus M, Hartmann A, Schneider-Stock R.

Apoptosis. 2012 Dec;17(12):1300-15. doi: 10.1007/s10495-012-0757-7.

PMID:
23011180
16.

Selective inhibition of histone deacetylase 6 (HDAC6) induces DNA damage and sensitizes transformed cells to anticancer agents.

Namdar M, Perez G, Ngo L, Marks PA.

Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):20003-8. doi: 10.1073/pnas.1013754107. Epub 2010 Oct 29.

17.

Induction of cell cycle arrest and DNA damage by the HDAC inhibitor panobinostat (LBH589) and the lipid peroxidation end product 4-hydroxynonenal in prostate cancer cells.

Pettazzoni P, Pizzimenti S, Toaldo C, Sotomayor P, Tagliavacca L, Liu S, Wang D, Minelli R, Ellis L, Atadja P, Ciamporcero E, Dianzani MU, Barrera G, Pili R.

Free Radic Biol Med. 2011 Jan 15;50(2):313-22. doi: 10.1016/j.freeradbiomed.2010.11.011. Epub 2010 Nov 13.

PMID:
21078383
18.

A novel small molecule hybrid of vorinostat and DACA displays anticancer activity against human hormone-refractory metastatic prostate cancer through dual inhibition of histone deacetylase and topoisomerase I.

Yu CC, Pan SL, Chao SW, Liu SP, Hsu JL, Yang YC, Li TK, Huang WJ, Guh JH.

Biochem Pharmacol. 2014 Aug 1;90(3):320-30. doi: 10.1016/j.bcp.2014.06.001. Epub 2014 Jun 7.

PMID:
24915421
19.

Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).

Kubo M, Kanaya N, Petrossian K, Ye J, Warden C, Liu Z, Nishimura R, Osako T, Okido M, Shimada K, Takahashi M, Chu P, Yuan YC, Chen S.

Breast Cancer Res Treat. 2013 Jan;137(1):93-107. doi: 10.1007/s10549-012-2332-x. Epub 2012 Nov 18.

20.

Targeting triple-negative breast cancer cells with the histone deacetylase inhibitor panobinostat.

Tate CR, Rhodes LV, Segar HC, Driver JL, Pounder FN, Burow ME, Collins-Burow BM.

Breast Cancer Res. 2012 May 21;14(3):R79.

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