215
Views
78
CrossRef citations to date
0
Altmetric
Review

Histone deacetylase inhibitors in lymphoma and solid malignancies

, , &
Pages 413-432 | Published online: 10 Jan 2014

References

  • Minucci S, Pelicci PG. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nat. Rev. Cancer6(1), 38–51 (2006).
  • Dokmanovic M, Clarke C, Marks PA. Histone deacetylase inhibitors: overview and perspectives. Mol. Cancer Res.5(10), 981–989 (2007).
  • Xu WS, Parmigiani RB, Marks PA. Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene26(37), 5541–5552 (2007).
  • Gregoretti IV, Lee YM, Goodson HV. Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. J. Mol. Biol.338(1), 17–31 (2004).
  • Bhalla KN. Epigenetic and chromatin modifiers as targeted therapy of hematologic malignancies. J. Clin. Oncol.23(17), 3971–3993 (2005).
  • Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors. Nat. Rev. Drug Discov.5(9), 769–784 (2006).
  • Lund AH, Van Lohuizen M. Epigenetics and cancer. Genes Dev.18(19), 2315–2335 (2004).
  • Baylin SB, Ohm JE. Epigenetic gene silencing in cancer – a mechanism for early oncogenic pathway addiction? Nat. Rev. Cancer6(2), 107–116 (2006).
  • Rice JC, Allis CD. Histone methylation versus histone acetylation: new insights into epigenetic regulation. Curr. Opin. Cell Biol.13(3), 263–273 (2001).
  • Redner RL, Wang J, Liu JM. Chromatin remodeling and leukemia: new therapeutic paradigms. Blood94(2), 417–428 (1999).
  • Jones LK, Saha V. Chromatin modification, leukaemia and implications for therapy. Br. J. Haematol.118(3), 714–727 (2002).
  • Timmermann S, Lehrmann H, Polesskaya A, Harel-Bellan A. Histone acetylation and disease. Cell. Mol. Life Sci.58(5–6), 728–736 (2001).
  • Cress WD, Seto E. Histone deacetylases, transcriptional control, and cancer. J. Cell. Physiol.184(1), 1–16 (2000).
  • Vigushin DM, Coombes RC. Histone deacetylase inhibitors in cancer treatment. Anticancer Drugs13(1), 1–13 (2002).
  • Santini V, Gozzini A, Ferrari G. Histone deacetylase inhibitors: molecular and biological activity as a premise to clinical application. Curr. Drug Metab.8(4), 383–393 (2007).
  • Fenrick R, Hiebert SW. Role of histone deacetylases in acute leukemia. J. Cell. Biochem. Suppl.30–31, 194–202 (1998).
  • Wang J, Hoshino T, Redner RL, Kajigaya S, Liu JM. Eto, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex. Proc. Natl Acad. Sci. USA95(18), 10860–10865 (1998).
  • Lin RJ, Sternsdorf T, Tini M, Evans RM. Transcriptional regulation in acute promyelocytic leukemia. Oncogene20(49), 7204–7215 (2001).
  • Pasqualucci L, Bereschenko O, Niu H et al. Molecular pathogenesis of non-Hodgkin’s lymphoma: the role of Bcl-6. Leuk. Lymphoma44(Suppl. 3), S5–S12 (2003).
  • Marchion D, Munster P. Development of histone deacetylase inhibitors for cancer treatment. Expert. Rev. Anticancer Ther.7(4), 583–598 (2007).
  • Fraga MF, Ballestar E, Villar-Garea A et al. Loss of acetylation at Lys16 and trimethylation at Lys20 of histone H4 is a common hallmark of human cancer. Nat. Genet.37(4), 391–400 (2005).
  • Guarente L. Sirtuins as potential targets for metabolic syndrome. Nature444(7121), 868–874 (2006).
  • Dokmanovic M, Marks PA. Prospects: histone deacetylase inhibitors. J. Cell. Biochem.96(2), 293–304 (2005).
  • Munster PN, Troso-Sandoval T, Rosen N et al. The histone deacetylase inhibitor suberoylanilide hydroxamic acid induces differentiation of human breast cancer cells. Cancer Res.61(23), 8492–8497 (2001).
  • Zhou Q, Melkoumian ZK, Lucktong A et al. Rapid induction of histone hyperacetylation and cellular differentiation in human breast tumor cell lines following degradation of histone deacetylase-1. J. Biol. Chem.275(45), 35256–35263 (2000).
  • Bishton M, Kenealy M, Johnstone R, Rasheed W, Prince HM. Epigenetic targets in hematological malignancies: combination therapies with HDACis and demethylating agents. Expert. Rev. Anticancer Ther.7(10), 1439–1449 (2007).
  • Vrana JA, Decker RH, Johnson CR et al. Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid (SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53. Oncogene18(50), 7016–7025 (1999).
  • Richon VM, Sandhoff TW, Rifkind RA, Marks PA. Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc. Natl Acad. Sci. USA97(18), 10014–10019 (2000).
  • Burgess AJ, Pavey S, Warrener R et al. Up-regulation of p21(WAF1/CIP1) by histone deacetylase inhibitors reduces their cytotoxicity. Mol. Pharmacol.60(4), 828–837 (2001).
  • Zhang K, Dent SY. Histone modifying enzymes and cancer: going beyond histones. J. Cell. Biochem.96(6), 1137–1148 (2005).
  • Jones PA, Baylin SB. The fundamental role of epigenetic events in cancer. Nat. Rev. Genet.3(6), 415–428 (2002).
  • Druesne N, Pagniez A, Mayeur C et al. Diallyl disulfide (DADS) increases histone acetylation and p21(waf1/cip1) expression in human colon tumor cell lines. Carcinogenesis25(7), 1227–1236 (2004).
  • Myzak MC, Karplus PA, Chung FL, Dashwood RH. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Cancer Res.64(16), 5767–5774 (2004).
  • Zhu P, Martin E, Mengwasser J et al. Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis. Cancer Cell5(5), 455–463 (2004).
  • Butler LM, Zhou X, Xu WS et al. The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin. Proc. Natl Acad. Sci. USA99(18), 11700–11705 (2002).
  • Ruefli AA, Ausserlechner MJ, Bernhard D et al. The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species. Proc. Natl Acad. Sci. USA98(19), 10833–10838 (2001).
  • Peart MJ, Tainton KM, Ruefli AA et al. Novel mechanisms of apoptosis induced by histone deacetylase inhibitors. Cancer Res.63(15), 4460–4471 (2003).
  • Lindemann RK, Newbold A, Whitecross KF et al. Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma. Proc. Natl Acad. Sci. USA104(19), 8071–8076 (2007).
  • Zhang C, Richon V, Ni X, Talpur R, Duvic M. Selective induction of apoptosis by histone deacetylase inhibitor SAHA in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. J. Invest. Dermatol.125(5), 1045–1052 (2005).
  • O’Connor OA, Heaney ML, Schwartz L et al. Clinical experience with intravenous and oral formulations of the novel histone deacetylase inhibitor suberoylanilide hydroxamic acid in patients with advanced hematologic malignancies. J. Clin. Oncol.24(1), 166–173 (2006).
  • Duvic M, Talpur R, Ni X et al. Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma (CTCL). Blood109(1), 31–39 (2007).
  • Olsen EA, Kim YH, Kuzel TM et al. Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. J. Clin. Oncol.25(21), 3109–3115 (2007).
  • Marks PA, Breslow R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nat. Biotechnol.25(1), 84–90 (2007).
  • Mann BS, Johnson JR, He K et al. Vorinostat for treatment of cutaneous manifestations of advanced primary cutaneous T-cell lymphoma. Clin. Cancer Res.13(8), 2318–2322 (2007).
  • Piekarz RL, Robey RW, Zhan Z et al. T-cell lymphoma as a model for the use of histone deacetylase inhibitors in cancer therapy: impact of depsipeptide on molecular markers, therapeutic targets, and mechanisms of resistance. Blood103(12), 4636–4643 (2004).
  • Piekarz RL, Robey R, Sandor V et al. Inhibitor of histone deacetylation, depsipeptide (FR901228), in the treatment of peripheral and cutaneous T-cell lymphoma: a case report. Blood98(9), 2865–2868 (2001).
  • Nebozhyn M, Loboda A, Kari L et al. Quantitative PCR on 5 genes reliably identifies CTCL patients with 5% to 99% circulating tumor cells with 90% accuracy. Blood107(8), 3189–3196 (2006).
  • Piekarz R, Frye R, Wright J et al. Update of the NCI multiinstitutional Phase II trial of romidepsin, FK228, for patients with cutaneous or peripheral T-cell lymphoma. J. Clin. Oncol.250(18 Suppl.), (2007) (Abstract 8027).
  • Kim YH, Reddy S, Kim EJ et al. Romidepsin (depsipeptide) induces clinically significant responses in treatment-refractory CTCL. An International, Multicenter Study. American Society of Hematology Annual Meeting Abstracts110(11), (2007) (Abstract 123).
  • Ellis L, Pan Y, Smyth G et al. The histone deacetylase inhibitor LBH589 induces responses with associated alterations in gene expression profiles in cutaneous T cell lymphoma. Clin. Cancer Res.(2008) (In press).
  • Sharma S, Vogelzang NJ, Beck J et al. Phase I pharmacokinetic (PK) and pharmacodynamic (PD) study of LBH589, a novel deacetylase (DAC) inhibitor given intravenously on a new once weekly schedule. J. Clin. Oncol.28(18 Suppl.), (2007) (Abstract 14019).
  • Ryan QC, Headlee D, Acharya M et al. Phase I and pharmacokinetic study of MS-275, a histone deacetylase inhibitor, in patients with advanced and refractory solid tumors or lymphoma. J. Clin. Oncol.23(17), 3912–3922 (2005).
  • Spencer A, Prince M, Deangelo DJ et al. Phase IA/II study of oral LBH589, a novel deacetylase inhibitor (DACi), administered on 2 schedules, in patients with advanced hematologic malignancies. ASH Annual Meeting Abstracts110(11), (2007 (Abstract 907).
  • Georgakis GV, Yazbeck VY, Li Y, Younes A. The histone deacetylase inhibitor vorinostat (SAHA) induces apoptosis and cell-cycle arrest in Hodgkin lymphoma (HL) cell lines by altering several survival signaling pathways and synergizes with doxorubicin, gemcitabine and bortezomib. American Society of Hematology Annual Meeting Abstracts108(11), (2006) (Abstract 2260).
  • Buglio D, Georgakis G, Arima K, Liu Y-J, Younes A. Vorinostat (SAHA) inhibits STAT6 phosphorylation and transcription, downregulates Bcl-xL, and induces apoptosis in Hodgkin lymphoma (HL) cell lines. American Society of Hematology Annual Meeting Abstracts110(11), (2007) (Abstract 380).
  • Younes A, Pro B, Fanale M et al. Isotype-selective HDAC inhibitor MGCD0103 decreases serum TARC concentrations and produces clinical responses in heavily pretreated patients with relapsed classical Hodgkin lymphoma (HL). American Society of Hematology Annual Meeting Abstracts110(11), (2007) (Abstract 2566).
  • Younes A, Wedgwood A, Mclaughlin P et al. Treatment of relapsed or refractory lymphoma with the oral isotype-selective histone deacetylase inhibitor MGCD0103: interim results from a Phase II study. American Society of Hematology Annual Meeting Abstracts110(11), (2007) (Abstract 2571).
  • Crump M, Coiffier B, Jacobsen ED et al. Oral vorinostat (suberoylanilide hydroxamic acid, SAHA) in relapsed diffuse large B-cell lymphoma (DLBCL): final results of a Phase II trial. J. Clin. Oncol.25(Suppl. 18), (2007) (Abstract 18511).
  • Gimsing P, Wu F, Qian X et al. Activity of the histone deacetylase (HDAC) inhibitor PXD101 in preclinical studies and in a Phase I study in patients with advanced haematological tumors. American Society of Hematology Annual Meeting Abstracts106(11), (2005) (Abstract 3337).
  • Duan H, Heckman CA, Boxer LM. Histone deacetylase inhibitors down-regulate bcl-2 expression and induce apoptosis in t(14;18) lymphomas. Mol. Cell Biol.25(5), 1608–1619 (2005).
  • Tobinai K, Watanabe T, Kobayashi Y et al. Phase I study of vorinostat (suberoylanilide hydroxamic acid, SAHA) in patients (pts) with non-Hodgkin lymphoma (NHL) in Japan. J. Clin. Oncol.25(Suppl. 18), (2007) (Abstract 18521).
  • Paner GP, Alkan S. Analysis of the effect of the novel histone deacetylase inhibitor, depsipeptide (FK228/FR901228) on mantle cell lymphoma. American Society of Hematology Annual Meeting Abstracts104(11), (2004) (Abstract 2499).
  • Kawamata N, Chen J, Koeffler HP. Suberoylanilide hydroxamic acid (SAHA; vorinostat) suppresses translation of cyclin D1 in mantle cell lymphoma cells. Blood110(7), 2667–2673 (2007).
  • Heider U, Kaiser M, Sterz J et al. Histone deacetylase inhibitors reduce VEGF production and induce growth suppression and apoptosis in human mantle cell lymphoma. Eur. J. Haematol.76(1), 42–50 (2006).
  • Yazbeck VY, Georgakis GV, Li Y et al. Molecular mechanisms of the mtor inhibitor temsirolimus (CCI-779) antiproliferative effects in mantle cell lymphoma: induction of cell-cycle arrest, autophagy, and synergy with vorinostat (SAHA). American Society of Hematology Annual Meeting Abstracts108(11), (2006) (Abstract 2493).
  • Kirschbaum MH, Zain JM, Popplewell L et al. A Phase 2 study of Vorinostat (suberoylanilide hydroxamic acid, SAHA) in relapsed or refractory indolent non Hodgkin lymphoma. A California Cancer Consortium Study. American Society of Hematology Annual Meeting Abstracts110(11), (2007) (Abstract 2568).
  • Roychowdhury S, Baiocchi RA, Vourganti S et al. Selective efficacy of depsipeptide in a xenograft model of Epstein-Barr virus-positive lymphoproliferative disorder. J. Natl Cancer Inst.96(19), 1447–1457 (2004).
  • Nishioka C, Ikezoe T, Yang J et al. Histone deacetylase inhibitors induce growth arrest and apoptosis of HTLV-1-infected T-cells via blockade of signaling by nuclear factor kB. Leuk. Res.32(2), 287–296 (2008).
  • Zhao WL, Wang L, Liu YH et al. Combined effects of histone deacetylase inhibitor and rituximab on non-Hodgkin’s B-lymphoma cells apoptosis. Exp. Hematol.35(12), 1801–1811 (2007).
  • Plumas J, Jacob MC, Chaperot L et al. Tumor B cells from non-Hodgkin’s lymphoma are resistant to CD95 (Fas/Apo-1)-mediated apoptosis. Blood91(8), 2875–2885 (1998).
  • Wajant H, Pfizenmaier K, Scheurich P. TNF-related apoptosis inducing ligand (TRAIL) and its receptors in tumor surveillance and cancer therapy. Apoptosis7(5), 449–459 (2002).
  • Inoue S, Macfarlane M, Harper N et al. Histone deacetylase inhibitors potentiate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in lymphoid malignancies. Cell Death Differ.11(Suppl. s2), S193–S206 (2004).
  • Rephaeli A, Rabizadeh E, Aviram A et al. Derivatives of butyric acid as potential anti-neoplastic agents. Int. J. Cancer49(1), 66–72 (1991).
  • Siu LL, Von Hoff DD, Rephaeli A et al. Activity of pivaloyloxymethyl butyrate, a novel anticancer agent, on primary human tumor colony-forming units. Invest. New Drugs16(2), 113–119 (1998).
  • Rephaeli A, Entin-Meer M, Angel D et al. The selectivty and anti-metastatic activity of oral bioavailable butyric acid prodrugs. Invest. New Drugs24(5), 383–392 (2006).
  • Loprevite M, Tiseo M, Grossi F et al. In vitro study of CI-994, a histone deacetylase inhibitor, in non-small cell lung cancer cell lines. Oncol. Res.15(1), 39–48 (2005).
  • Moody TW, Nakagawa T, Kang Y et al. Bombesin/gastrin-releasing peptide receptor antagonists increase the ability of histone deacetylase inhibitors to reduce lung cancer proliferation. J. Mol. Neurosci.28(3), 231–238 (2006).
  • Yu XD, Wang SY, Chen GA et al. Apoptosis induced by depsipeptide FK228 coincides with inhibition of survival signaling in lung cancer cells. Cancer J.13(2), 105–113 (2007).
  • Aviram A, Rephaeli A, Shaklai M et al. Effect of the cytostatic butyric acid pro-drug, pivaloyloxymethyl butyrate, on the tumorigenicity of cancer cells. J. Cancer Res. Clin. Oncol.123(5), 267–271 (1997).
  • Desai D, Das A, Cohen L, El-Bayoumy K, Amin S. Chemopreventive efficacy of suberoylanilide hydroxamic acid (SAHA) against 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis in female A/J mice. Anticancer Res.23(1A), 499–503 (2003).
  • Kelly WK, O’Connor OA, Krug LM et al. Phase I study of an oral histone deacetylase inhibitor, suberoylanilide hydroxamic acid, in patients with advanced cancer. J. Clin. Oncol.23(17), 3923–3931 (2005).
  • Krug LM, Curley T, Schwartz L et al. Potential role of histone deacetylase inhibitors in mesothelioma: clinical experience with suberoylanilide hydroxamic acid. Clin. Lung Cancer7(4), 257–261 (2006).
  • Wozniak A, O’Shaughnessy J, Fiorica J, Grove W. Phase II Trial of CI-994 in patients (pts) with advanced nonsmall cell lung cancer (NSCLC). J. Clin. Oncol. (1999) (Abstract 1878.)
  • Reid T, Valone F, Lipera W et al. Phase II trial of the histone deacetylase inhibitor pivaloyloxymethyl butyrate (Pivanex, AN-9) in advanced non-small cell lung cancer. Lung Cancer45(3), 381–386 (2004).
  • Traynor AM, Dubey S, Eickhoff J et al. A Phase II study of vorinostat (NSC 701852 ) in patients (pts) with relapsed non-small cell lung cancer (NSCLC). J. Clin. Oncol.25(18 Suppl.), (2007) (Abstract 18044).
  • Luong QT, O’Kelly J, Braunstein GD, Hershman JM, Koeffler HP. Antitumor activity of suberoylanilide hydroxamic acid against thyroid cancer cell lines in vitro and in vivo. Clin. Cancer Res.12(18), 5570–5577 (2006).
  • Catalano MG, Fortunati N, Pugliese M et al. Valproic acid induces apoptosis and cell-cycle arrest in poorly differentiated thyroid cancer cells. J. Clin. Endocrinol. Metab.90(3), 1383–1389 (2005).
  • Kitazono M, Robey R, Zhan Z et al. Low concentrations of the histone deacetylase inhibitor, depsipeptide (FR901228), increase expression of the Na(+)/I(-) symporter and iodine accumulation in poorly differentiated thyroid carcinoma cells. J. Clin. Endocrinol. Metab.86(7), 3430–3435 (2001).
  • Greenberg VL, Williams JM, Cogswell JP, Mendenhall M, Zimmer SG. Histone deacetylase inhibitors promote apoptosis and differential cell-cycle arrest in anaplastic thyroid cancer cells. Thyroid11(4), 315–325 (2001).
  • Su YB, Tuttle RM, Fury M et al. A Phase II study of single agent depsipeptide (DEP) in patients (pts) with radioactive iodine (RAI)-refractory, metastatic, thyroid carcinoma: preliminary toxicity and efficacy experience. J. Clin. Oncol.24(Suppl. 18), (2006) (Abstract 5554).
  • Butler LM, Agus DB, Scher HI et al. Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses the growth of prostate cancer cells in vitro and in vivo. Cancer Res.60(18), 5165–5170 (2000).
  • Shabbeer S, Kortenhorst MS, Kachhap S et al. Multiple molecular pathways explain the anti-proliferative effect of valproic acid on prostate cancer cells in vitro and in vivo. Prostate67(10), 1099–1110 (2007).
  • Park WH, Jung CW, Park JO et al. Trichostatin inhibits the growth of ACHN renal cell carcinoma cells via cell-cycle arrest in association with p27, or apoptosis. Int. J. Oncol.22(5), 1129–1134 (2003).
  • Wang X-F, Qian DZ, Ren M et al. Epigenetic modulation of retinoic acid receptor b2 by the histone deacetylase inhibitor MS-275 in human renal cell carcinoma. Clin. Cancer Res.11(9), 3535–3542 (2005).
  • Stadler WM, Margolin K, Ferber S, Mcculloch W, Thompson JA. A Phase II study of depsipeptide in refractory metastatic renal cell cancer. Clin. Genitourin. Cancer5(1), 57–60 (2006).
  • O’Shaughnessy J, Flaherty L, Fiorica J, Grove W. Phase II trial of CI-994 in patients (pts) with metastatic renal cell carcinoma (RCC). J. Clin. Oncol. (1999) (Abstract 1346).
  • Rundall BK, Denlinger CE, Jones DR. Suberoylanilide hydroxamic acid combined with gemcitabine enhances apoptosis in non-small cell lung cancer. Surgery138(2), 360–367 (2005).
  • Ramalingam SS, Parise RA, Ramananthan RK et al. Phase I and pharmacokinetic study of vorinostat, a histone deacetylase inhibitor, in combination with carboplatin and paclitaxel for advanced solid malignancies. Clin. Cancer Res.13(12), 3605–3610 (2007).
  • Richards DA, Boehm KA, Waterhouse DM et al. Gemcitabine plus CI-994 offers no advantage over gemcitabine alone in the treatment of patients with advanced pancreatic cancer: results of a Phase II randomized, double-blind, placebo-controlled, multicenter study. Ann. Oncol.17(7), 1096–1102 (2006).
  • Pili R, Kruszewski MP, Hager BW, Lantz J, Carducci MA. Combination of phenylbutyrate and 13-cis retinoic acid inhibits prostate tumor growth and angiogenesis. Cancer Res.61(4), 1477–1485 (2001).
  • Verheul HM, Qian DZ, Carducci MA, Pili R. Sequence-dependent antitumor effects of differentiation agents in combination with cell cycle-dependent cytotoxic drugs. Cancer Chemother. Pharmacol.60(3), 329–339 (2007).
  • Marrocco DL, Tilley WD, Bianco-Miotto T et al. Suberoylanilide hydroxamic acid (vorinostat) represses androgen receptor expression and acts synergistically with an androgen receptor antagonist to inhibit prostate cancer cell proliferation. Mol. Cancer Ther.6(1), 51–60 (2007).
  • Pili R, Rudek M, Altiok S et al. Phase 1 pharmacokinetic and pharmacodynamic study of the histone deacetylase inhibitor MS-275 in combination with 13-cis retinoic acid in patients with advanced solid tumors. J. Clin. Oncol.24(18 Suppl.) (2006) (Abstract 3055).
  • Munster P, Marchion D, Bicaku E et al. Phase I trial of histone deacetylase inhibition by valproic acid followed by the topoisomerase II inhibitor epirubicin in advanced solid tumors: a clinical and translational study. J. Clin. Oncol.25(15), 1979–1985 (2007).
  • Rho JH, Kang DY, Park KJ et al. Doxorubicin induces apoptosis with profile of large-scale DNA fragmentation and without DNA ladder in anaplastic thyroid carcinoma cells via histone hyperacetylation. Int. J. Oncol.27(2), 465–471 (2005).
  • Catalano MG, Fortunati N, Pugliese M et al. Valproic acid, a histone deacetylase inhibitor, enhances sensitivity to doxorubicin in anaplastic thyroid cancer cells. J. Endocrinol.191(2), 465–472 (2006).
  • Catalano MG, Poli R, Pugliese M, Fortunati N, Boccuzzi G. Valproic acid enhances tubulin acetylation and apoptotic activity of paclitaxel on anaplastic thyroid cancer cell lines. Endocr. Relat. Cancer14(3), 839–845 (2007).
  • Imanishi R, Ohtsuru A, Iwamatsu M et al. A histone deacetylase inhibitor enhances killing of undifferentiated thyroid carcinoma cells by p53 gene therapy. J. Clin. Endocrinol. Metab.87(10), 4821–4824 (2002).
  • Piekarz RL, Sackett DL, Bates SE. Histone deacetylase inhibitors and demethylating agents: clinical development of histone deacetylase inhibitors for cancer therapy. Cancer J.13(1), 30–39 (2007).
  • Rasheed WK, Johnstone RW, Prince HM. Histone deacetylase inhibitors in cancer therapy. Expert Opin. Investig. Drugs16(5), 659–678 (2007).
  • Page JG, Rodman LE, Heath JE, Tomaszewski JE, Smith AC. Effect of infusion rate on the toxicity of depsipeptide (NCS-63–176) in Beagle dogs. Proc. Am. Assoc. Cancer Res.36, 368 (1995) (Abstract 2193).
  • Page JG, Rodman LE, Heath JE, Thomaszewski JE, Smith AC. Comparison of toxicity of depsipeptide (NSC-630176) in dogs and rats. Proc. Am. Assoc. Cancer Res.37, 374 (1996) (Abstract 2549).
  • Piekarz RL, Frye AR, Wright JJ et al. Cardiac studies in patients treated with depsipeptide, FK228, in a Phase II trial for T-cell lymphoma. Clin. Cancer Res.12(12), 3762–3773 (2006).
  • Sandor V, Bakke S, Robey RW et al. Phase I trial of the histone deacetylase inhibitor, depsipeptide (FR901228, NSC 630176), in patients with refractory neoplasms. Clin. Cancer Res.8(3), 718–728 (2002).
  • Marshall JL, Rizvi N, Kauh J et al. A Phase I trial of depsipeptide (FR901228) in patients with advanced cancer. J. Exp. Ther. Oncol.2(6), 325–332 (2002).
  • Whittaker S, Mcculloch W, Robak T, Baran E, Prentice A; ALL Investigators. International multicenter Phase II study of the HDAC inhibitor (HDACi) depsipeptide (FK228) in cutaneous T-cell lymphoma (CTCL): Interim report. J. Clin. Oncol.24(Suppl. 18), (2006) (Abstract 3063).
  • Parker C, Molife R, Karavasilis V et al. Romidepsin (FK228), a histone deacetylase inhibitor: final results of a Phase II study in metastatic hormone refractory prostate cancer (HRPC). J. Clin. Oncol.25(18 Suppl.), (2007) (Abstract 15507).
  • Niesvizky R, Ely S, Diliberto M et al. Multicenter Phase II trial of the histone deacetylase inhibitor depsipeptide (FK228) for the treatment of relapsed or refractory multiple myeloma (MM). American Society of Hematology Annual Meeting Abstracts106(11), (2005) (Abstract 2574).
  • Shah MH, Binkley P, Chan K et al. Cardiotoxicity of histone deacetylase inhibitor depsipeptide in patients with metastatic neuroendocrine tumors. Clin. Cancer Res.12(13), 3997–4003 (2006).
  • Bates SE, Rosing DR, Fojo T, Piekarz RL. Challenges of evaluating the cardiac effects of anticancer agents. Clin. Cancer Res.12(13), 3871–3874 (2006).
  • Rowinsky EK, de Bono J, Deangelo DJ et al. Cardiac monitoring in Phase I trials of a novel histone deacetylase (HDAC) inhibitor LAQ824 in patients with advanced solid tumors and hematologic malignancies. J. Clin. Oncol.23(Suppl. 16), 2005) (Abstract 3131).
  • Fischer T, Patnaik A, Bhalla K et al. Results of cardiac monitoring during Phase I trials of a novel histone deacetylase (HDAC) inhibitor LBH589 in patients with advanced solid tumors and hematologic malignancies. J. Clin. Oncol.23(Suppl. 16), (2005) (Abstract 3106).
  • Prince HM, George D, Patnaik A et al. Phase I study of oral LBH589, a novel deacetylase (DAC) inhibitor in advanced solid tumors and non-hodgkin’s lymphoma. J. Clin. Oncol.25(Suppl. 18), (2007) (Abstract 3500).
  • Zhang L, Lebwohl D, Masson E et al. Clinically relevant QTc prolongation is not associated with current dose schedules of LBH589 (panobinostat). J. Clin. Oncol.26(2), 332–333 (2008).
  • Kelly WK, Richon VM, O’Connor O et al. Phase I clinical trial of histone deacetylase inhibitor: suberoylanilide hydroxamic acid administered intravenously. Clin. Cancer Res.9(10 Pt 1), 3578–3588 (2003).
  • Strevel EL, Ing DJ, Siu LL. Molecularly targeted oncology therapeutics and prolongation of the QT interval. J. Clin. Oncol.25(22), 3362–3371 (2007).
  • Prince HM, George DJ, Johnstone R et al. LBH589, a novel histone deacetylase inhibitor (HDACi), treatment of patients with cutaneous T-cell lymphoma (CTCL). Changes in skin gene expression profiles related to clinical response following therapy. J. Clin. Oncol.24(18 Suppl.), (2006) (Abstract 7501).
  • Gojo I, Gore SD, Jiemjit A et al. Phase I study of histone deacetylase inhibitor (HDI) MS-275 in adults with refractory or relapsed hematologic malignancies. Blood102(11), (2006) (Abstract 1408).
  • Gilbert J, Baker SD, Bowling MK et al. A Phase I dose escalation and bioavailability study of oral sodium phenylbutyrate in patients with refractory solid tumor malignancies. Clin. Cancer Res.7(8), 2292–2300 (2001).
  • Carducci MA, Gilbert J, Bowling MK et al. A Phase I clinical and pharmacological evaluation of sodium phenylbutyrate on an 120-h infusion schedule. Clin. Cancer Res.7(10), 3047–3055 (2001).
  • Phuphanich S, Baker SD, Grossman SA et al. Oral sodium phenylbutyrate in patients with recurrent malignant gliomas: a dose escalation and pharmacologic study. Neuro-oncol.7(2), 177–182 (2005).
  • Chang SM, Kuhn JG, Robins HI et al. Phase II study of phenylacetate in patients with recurrent malignant glioma: a North American Brain Tumor Consortium report. J. Clin. Oncol.17(3), 984–990 (1999).
  • Chang SM, Kuhn JG, Ian Robins H et al. A study of a different dose-intense infusion schedule of phenylacetate in patients with recurrent primary brain tumors consortium report. Invest. New Drugs21(4), 429–433 (2003).
  • Blumenschein G, Lu C, Kies M et al. Phase II clinical trial of suberoylanilide hydroxamic acid (SAHA) in patients (pts) with recurrent and/or metastatic head and neck cancer(SCCHN). J. Clin. Oncol.22(14 Suppl.), (2004) (Abstract 5578).
  • Galanis E, Jaeckle KA, Maurer MJ et al. N047B: NCCTG Phase II trial of vorinostat (suberoylanilide hydroxamic acid) in recurrent glioblastoma multiforme (GBM). J. Clin. Oncol.25(18 Suppl.), (2007) (Abstract 2004).
  • Whitehead RP, McCoy S, Wollner IS et al. Phase II trial of depsipeptide (NSC-630176) in colorectal cancer patients who have received either one or two prior chemotherapy regimens for metastatic or locally advanced, unresectable disease: a Southwest Oncology Group study. J. Clin. Oncol.24(18 Suppl.), (2006) (Abstract 3598).
  • Fouladi M, Furman WL, Chin T et al. Phase I Study of Depsipeptide in pediatric patients with refractory solid tumors: a Children’s Oncology Group Report. J. Clin. Oncol.24(22), 3678–3685 (2006).
  • Haigentz M Jr, Kim M, Sarta C et al. Clinical and translational studies of depsipeptide (romidepsin), a histone deacetylase (HDAC) inhibitor, in patients with squamous cell carcinoma of the head and neck (SCCHN): New York Cancer Consortium Trial P6335. J. Clin. Oncol.25(18 Suppl.), (2007) (Abstract 6065).
  • Rowinsky EK, Pacey S, Patnaik A et al. A Phase I, pharmacokinetic (PK) and pharmacodynamic (PD) study of a novel histone deacetylase inhibitor LAQ824 in patients with advanced solid tumours. J. Clin. Oncol.22(14 Suppl.), (2004) (Abstract 3022).
  • Beck J, Fischer T, Rowinsky E et al. Phase I pharmacokinetic (PK) and pharmacodynamic (PD) study of LBH589: a novel histone deacetylase inhibitor.J. Clin. Oncol.22(14 Suppl.), (2004) (Abstract 3025).
  • Gore L, Holden SN, Basche M et al. Updated results from a Phase I trial of histone deacetylase (HDAC) inhibitor MS-275 in patients with refractory solid tumours. J. Clin. Oncol.22(14 Suppl.), (2004) (Abstract 3026).
  • Hauschild A, Trefzer U, Garbe C et al. A Phase II multicenter study on the histone deacetylase (HDAC) inhibitor MS-275, comparing two dosage schedules in metastatic melanoma. J. Clin. Oncol.24(Suppl. 18), (2006) (Abstract 8044).
  • Donovan EA, Sparreboom A, Figg W et al. Phase I trial of the oral histone deacetylase inhibitor MS-275 administered with food. J. Clin. Oncol.24(18 Suppl.), (2006) (Abstract 13036).
  • Prakash S, Foster BJ, Meyer M et al. Chronic oral administration of CI-994: a Phase 1 study. Invest. New Drugs19(1), 1–11 (2001).
  • Zalupski M, O’shaughnessy J, Vukelja S et al. Phase II Trial of CI-994 in patients (PTS) with advanced pancreatic cancer (APC). Proc. Am. Soc. Clin. Oncol.19, 285a (2000) (Abstract 1115).
  • Conley BA, Egorin MJ, Tait N et al. Phase I study of the orally administered butyrate prodrug, tributyrin, in patients with solid tumors. Clin. Cancer Res.4(3), 629–634 (1998).
  • Edelman MJ, Bauer K, Khanwani S et al. Clinical and pharmacologic study of tributyrin: an oral butyrate prodrug. Cancer. Chemother. Pharmacol.51(5), 439–444 (2003).
  • Patnaik A, Rowinsky EK, Villalona MA et al. A Phase I study of pivaloyloxymethyl butyrate, a prodrug of the differentiating agent butyric acid, in patients with advanced solid malignancies. Clin. Cancer Res.8(7), 2142–2148 (2002).
  • Carducci M, Siu LL, Sullivan R et al. Phase I study of isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 given as three-times weekly oral dose in patients (pts) with advanced solid tumors. J. Clin. Oncol.24(18 Suppl.), (2006) (Abstract 3007).
  • Gelmon K, Tolcher A, Carducci M et al. Phase I trials of the oral histone deacetylase (HDAC) inhibitor MGCD0103 given either daily or 3x weekly for 14 days every 3 weeks in patients (pts) with advanced solid tumors. J. Clin. Oncol.23(16 Suppl.), (2005) (Abstract 3147).
  • Steele N, Vidal L, Plumb J et al. A Phase 1 pharmacokinetic (PK) and pharmacodynamic (PD) study of the histone deacetylase (HDAC) inhibitor PXD101 in patients (pts) with advanced solid tumours. J. Clin. Oncol.23(16 Suppl.), (2005) (Abstract 3035).
  • Fakih MG, Pendyala L, Smith P et al. A Phase I study of vorinostat (suberoylanilide hydroxamic acid) in combination with 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) in patients with advanced colorectal cancer (CRC). J. Clin. Oncol.25(18 Suppl.), (2007) (Abstract 4088).
  • Schelman WR, Kolesar J, Schell K et al. A Phase I study of vorinostat in combination with bortezomib in refractory solid tumors. J. Clin. Oncol.25(Suppl. 18), (2007) (Abstract 3573).
  • Nemunaitis JJ, Orr D, Eager R et al. Phase I study of oral CI-994 in combination with gemcitabine in treatment of patients with advanced cancer. Cancer J.9(1), 58–66 (2003).
  • Undevia SD, Kindler HL, Janisch L et al. A Phase I study of the oral combination of CI-994, a putative histone deacetylase inhibitor, and capecitabine. Ann. Oncol.15(11), 1705–1711 (2004).
  • Pauer LR, Olivares J, Cunningham C et al. Phase I study of oral CI-994 in combination with carboplatin and paclitaxel in the treatment of patients with advanced solid tumors. Cancer Invest.22(6), 886–896 (2004).
  • Reid T, Weeks A, Vakil M et al. Dose escalation study of pivanex (a histone deacetylase inhibitor) in combination with docetaxel for advanced non-small cell lung cancer. J. Clin. Oncol.22(14 Suppl.), (2004) (Abstract 7279).
  • Sung MW, Waxman S. Combination of cytotoxic-differentiation therapy with 5-fluorouracil and phenylbutyrate in patients with advanced colorectal cancer. Anticancer Res.27(2), 995–1001 (2007).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.