Investigational histone deacetylase inhibitors for non-Hodgkin lymphomas

Bibliography

• Marks PA, Rifkind RA, Richon VM, Histone deacetylases and cancer: causes and therapies. Nat Rev Cancer 2001;1:194-202
   PubMed Web of Science ®Google Scholar
• Redner RL, Wang J, Liu JM. Chromatin remodeling and leukemia: new therapeutic paradigms. Blood 1999;94:417-28
   PubMed Web of Science ®Google Scholar
• Marks PA, Richon VM, Rifkind RA. Histone deacetylase inhibitors: inducers of differentiation or apoptosis of transformed cells. J Natl Cancer Inst 2000;92:1210-16
   PubMed Web of Science ®Google Scholar
• Secrist JP, Zhou X, Richon VM. HDAC inhibitors for the treatment of cancer. Curr Opin Investig Drugs 2003;4:1422-7
   PubMedGoogle Scholar
• Bhalla KN. Epigenetic and chromatin modifiers as targeted therapy of hematologic malignancies. J Clin Oncol 2005;23:3971-93
   PubMed Web of Science ®Google Scholar
• Hubbert C, Guardiola A, Shao R, HDAC6 is a microtubule-associated deacetylase. Nature 2002;417:455-8
   PubMed Web of Science ®Google Scholar
• Haggarty SJ, Koeller KM, Wong JC, Domain-selective small-molecule inhibitor of histone deacetylase 6 (HDAC6)-mediated tubulin deacetylation. Proc Natl Acad Sci USA 2003;100:4389-94
   PubMed Web of Science ®Google Scholar
• Bannister AJ, Miska EA, Gorlich D, Acetylation of importin-alpha nuclear import factors by CBP/p300. Curr Biol 2000;10:467-70
   PubMed Web of Science ®Google Scholar
• Wolf D, Rodova M, Miska EA, Acetylation of beta-catenin by CREB-binding protein (CBP). J Biol Chem 2002;277:25562-7
   PubMed Web of Science ®Google Scholar
• Cohen HY, Lavu S, Bitterman KJ, Acetylation of the C terminus of Ku70 by CBP and PCAF controls Bax-mediated apoptosis. Mol Cell 2004;13:627-38
   PubMed Web of Science ®Google Scholar
• Blander G, Zalle N, Daniely Y, DNA damage-induced translocation of the Werner helicase is regulated by acetylation. J Biol Chem 2002;277:50934-40
   PubMed Web of Science ®Google Scholar
• Bali P, Pranpat M, Bradner J, Inhibition of histone deacetylase 6 acetylates and disrupts the chaperone function of heat shock protein 90: a novel basis for antileukemia activity of histone deacetylase inhibitors. J Biol Chem 2005;280:26729-34
   PubMed Web of Science ®Google Scholar
• Lindemann RK, Gabrielli B, Johnstone RW. Histone-deacetylase inhibitors for the treatment of cancer. Cell Cycle 2004;3:779-88
   PubMed Web of Science ®Google Scholar
• Taddei A, Maison C, Roche D, Reversible disruption of pericentric heterochromatin and centromere function by inhibiting deacetylases. Nat Cell Biol 2001;3:114-20
   PubMed Web of Science ®Google Scholar
• Qiu L, Burgess A, Fairlie DP, Histone deacetylase inhibitors trigger a G2 checkpoint in normal cells that is defective in tumor cells. Mol Biol Cell 2000;11:2069-83
   PubMed Web of Science ®Google Scholar
• Minucci S, Pelicci PG. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nat Rev Cancer 2006;6:38-51
   PubMed Web of Science ®Google Scholar
• Gray SG, Ekstrom TJ. The human histone deacetylase family. Exp Cell Res 2001;262:75-83
   PubMed Web of Science ®Google Scholar
• Khan N, Jeffers M, Kumar S, Determination of the class and isoform selectivity of small-molecule histone deacetylase inhibitors. Biochem J 2008;409:581-9
   PubMed Web of Science ®Google Scholar
• Mann BS, Johnson JR, He K, Vorinostat for treatment of cutaneous manifestations of advanced primary cutaneous T-cell lymphoma. Clin Cancer Res 2007;13:2318-22
   PubMed Web of Science ®Google Scholar
• Trautinger F, Knobler R, Willemze R, EORTC consensus recommendations for the treatment of mycosis fungoides/Sézary syndrome. Eur J Cancer 2006;42:1014-30
   PubMed Web of Science ®Google Scholar
• Budgin JB, Richardson SK, Newton SB, Biological effects of bexarotene in cutaneous T-cell lymphoma. Arch Dermatol 2005;141:315-21
   PubMed Web of Science ®Google Scholar
• Duvic M, Hymes K, Heald P, Bexarotene is effective and safe for treatment of refractory advanced-stage cutaneous T-cell lymphoma: multinational phase II-III trial results. J Clin Oncol 2001;19:2456-71
   PubMed Web of Science ®Google Scholar
• vanderSpek JC, Mindell JA, Finkelstein A, Murphy JR. Structure/function analysis of the transmembrane domain of DAB389-interleukin-2, an interleukin-2 receptor-targeted fusion toxin: the amphipathic helical region of the transmembrane domain is essential for the efficient delivery of the catalytic domain to the cytosol of target cells. J Biol Chem 1993;268:12077-82
   PubMed Web of Science ®Google Scholar
• Olsen E, Duvic M, Frankel A, Pivotal phase III trial of two dose levels of denileukin diftitox for the treatment of cutaneous T-cell lymphoma. J Clin Oncol 2001;19:376-88
   PubMed Web of Science ®Google Scholar
• Foss FM, Bacha P, Osann KE, Biological correlates of acute hypersensitivity events with DAB(389)IL-2 (denileukin diftitox, ONTAK) in cutaneous T-cell lymphoma: decreased frequency and severity with steroid premedication. Clin Lymphoma 2001;1:298-302
   PubMedGoogle Scholar
• Kim EJ, Hess S, Richardson SK, Immunopathogenesis and therapy of cutaneous T cell lymphoma. J Clin Invest 2005;115:798-812
   PubMed Web of Science ®Google Scholar
• Keehn CA, Belongie IP, Shistik G, The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control 2007;14:102-11
   PubMedGoogle Scholar
• O'Connor, OA, Heaney ML, Schwartz L, 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 2006;24:166-73
   PubMed Web of Science ®Google Scholar
• Watanabe T, Kato H, Kobayashi Y, Potential efficacy of the oral histone deacetylase inhibitor vorinostat in a phase I trial in follicular and mantle cell lymphoma. Cancer Sci 2010;101:196-200
   PubMed Web of Science ®Google Scholar
• Kelly WK, O'Connor OA, Krug LM, Phase I study of an oral histone deacetylase inhibitor, suberoylanilide hydroxamic acid, in patients with advanced cancer. J Clin Oncol 2005;23:3923-31
   PubMed Web of Science ®Google Scholar
• Crump M, Coiffer B, Jacobsen ED, Phase II trial of oral vorinostat (suberoylanilide hydroxamic acid) in relapsed diffuse large-B-cell lymphoma. Ann Oncol 2008;19:964-9
   PubMed Web of Science ®Google Scholar
• Duvic M, Talpur R, Ni X, Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma (CTCL). Blood 2007;109:31-9
   PubMed Web of Science ®Google Scholar
• Olsen EA, Kim YH, Kuzel TM, Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. J Clin Oncol 2007;25:3109-15
   PubMed Web of Science ®Google Scholar
• Marquard L, Poulsen CB, Gjerdrum LM, Histone deacetylase 1, 2, 6 and acetylated histone H4 in B- and T-cell lymphomas. Histopathology 2009;54:688-98
   PubMed Web of Science ®Google Scholar
• Cheson BD, Horning SJ, Coiffier B, Report of an international workshop to standardize response criteria for non-Hodgkin's lymphomas. NCI Sponsored International Working Group. J Clin Oncol 1999;17:1244-53
   PubMed Web of Science ®Google Scholar
• Friedberg JW, Taylor MD, Cerhan JR, Follicular lymphoma in the United States: first report of the national LymphoCare study. J Clin Oncol 2009;27:1202-8
   PubMed Web of Science ®Google Scholar
• Hiddemann W, Kneba M, Dreyling M, Frontline therapy with rituximab added to the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly improves the outcome for patients with advanced-stage follicular lymphoma compared with therapy with CHOP alone: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group. Blood 2005;106:3725-32
   PubMed Web of Science ®Google Scholar
• Marcus R, Imrie K, Belch A, CVP chemotherapy plus rituximab compared with CVP as first-line treatment for advanced follicular lymphoma. Blood 2005;105:1417-23
   PubMed Web of Science ®Google Scholar
• Kaminski MS, Tuck M, Estes J, 131I-tositumomab therapy as initial treatment for follicular lymphoma. N Engl J Med 2005;352:441-9
   PubMed Web of Science ®Google Scholar
• Lenz G, Dreyling M, Hoster E, Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone significantly improves response and time to treatment failure, but not long-term outcome in patients with previously untreated mantle cell lymphoma: results of a prospective randomized trial of the German Low Grade Lymphoma Study Group (GLSG). J Clin Oncol 2005;23:1984-92
   PubMed Web of Science ®Google Scholar
• Damon LE, Johnson JL, Niedzwiecki D, Immunochemotherapy and autologous stem-cell transplantation for untreated patients with mantle-cell lymphoma: CALGB 59909. J Clin Oncol 2009;27:6101-8
   PubMed Web of Science ®Google Scholar
• Husson H, Carideo EG, Neuberg D, Gene expression profiling of follicular lymphoma and normal germinal center B cells using cDNA arrays. Blood 2002;99:282-9
   PubMed Web of Science ®Google Scholar
• Salaverria I, Zettl A, Bea S, Specific secondary genetic alterations in mantle cell lymphoma provide prognostic information independent of the gene expression – based proliferation signature. J Clin Oncol 2007;25:1216-22
   PubMed Web of Science ®Google Scholar
• Kawamata N, Chen J, Koeffler PH. Suberoylanilide hydroxamic acid (SAHA; vorinostat) suppresses translation of cyclin D1 in mantle cell lymphoma cells. Blood 2007;110:2667-73
   PubMed Web of Science ®Google Scholar
• Dave SS, Wright G, Tan B, Prediction of survival in follicular lymphoma based on molecular features of tumor-infiltrating immune cells. N Engl J Med 2004;351:2159-69
   PubMed Web of Science ®Google Scholar
• Fotheringham S, Epping MT, Stimson L, Genome-wide loss-of-function screen reveals an important role for the proteasome in HDAC inhibitor-induced apoptosis. Cancer Cell 2009;15:57-66
   PubMed Web of Science ®Google Scholar
• Richon VM, Sandhoff TW, Rifkind RA, Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc Natl Acad Sci USA 2000;97:10014-19
   PubMed Web of Science ®Google Scholar
• Mitsiades CS, Mitsiades NS, McMullan CJ, Transcriptional signature of histone deacetylase inhibition in multiple myeloma: biological and clinical implications. Proc Natl Acad Sci USA 2004;101:540-5
   PubMed Web of Science ®Google Scholar
• Peart MJ, Smyth GK, van Laar RK, Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors. Proc Natl Acad Sci USA 2005;102:3697-702
   PubMed Web of Science ®Google Scholar
• Sanda T, Okamoto T, Uchida Y, Proteome analyses of the growth inhibitory effects of NCH-51, a novel histone deacetylase inhibitor, on lymphoid malignant cells. Leukemia 2007;21:2344-53
   PubMed Web of Science ®Google Scholar
• Garcia-Manero G, Yang H, Bueso-Ramos C, Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes. Blood 2008;111:1060-6
   PubMed Web of Science ®Google Scholar
• Brogdon JL, Xu Y, Szabo SJ. Histone deacetylase activities are required for innate immune cell control of Th1 but not Th2 effector cell function. Blood 2007;109:1123-30
   PubMed Web of Science ®Google Scholar
• Glas AM, Knoops L, Delahaye L, Gene-expression and immunohistochemical study of specific T-cell subsets and accessory cell types in the transformation and prognosis of follicular lymphoma. J Clin Oncol 2007;25:390-8
   PubMed Web of Science ®Google Scholar
• Farinha P, Masoudi H, Skinnider BF, Analysis of multiple biomarkers shows that lymphoma-associated macrophage (LAM) content is an independent predictor of survival in follicular lymphoma (FL). Blood 2005;106:2169-74
   PubMed Web of Science ®Google Scholar
• Nencioni A, Beck J, Werth D, Histone deacetylase inhibitors affect dendritic cell differentiation and immunogenicity. Clin Cancer Res 2007;13:3933-41
   PubMed Web of Science ®Google Scholar
• Ruefli AA, Ausserlechner MJ, Bernhard D, 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 USA 2001;98:10833-8
   PubMed Web of Science ®Google Scholar
• Inoue S, Riley J, Gant TW, Apoptosis induced by histone deacetylase inhibitors in leukemic cells is mediated by Bim and Noxa. Leukemia 2007;21:1773-82
   PubMed Web of Science ®Google Scholar
• Lindemann RK, Newbold A, Whitecross KF, Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma. Proc Natl Acad Sci USA 2007;104:8071-6
   PubMed Web of Science ®Google Scholar
• Whitecross KF, Alsop AE, Cluse LA, Defining the target specificity of ABT-737 and synergistic antitumor activities in combination with histone deacetylase inhibitors. Blood 2009;113:1982-91
   PubMed Web of Science ®Google Scholar
• Mason KD, Carpinelli MR, Fletcher JI, Programmed anuclear cell death delimits platelet life span. Cell 2007;128:1173-86
   PubMed Web of Science ®Google Scholar
• Zhang H, Nimmer PM, Tahir SK, Bcl-2 family proteins are essential for platelet survival. Cell Death Differ 2007;14:943-51
   PubMed Web of Science ®Google Scholar
• Zhang Q-L, Wang L, Zhang Y-W, The proteasome inhibitor bortezomib interacts synergistically with the histone deacetylase inhibitor suberoylanilide hydroxamic acid to induce T-leukemia/lymphoma cells apoptosis. Leukemia 2009;23:1507-14
   PubMed Web of Science ®Google Scholar
• Heider U, von Metzler I, Kaiser M, Synergistic interaction of the histone deacetylase inhibitor SAHA with the proteasome inhibitor bortezomib in mantle cell lymphoma. Eur J Haematol 2008;80:133-42
   PubMed Web of Science ®Google Scholar
• Heider U, Rademacher J, Lamottke B, Synergistic interaction of the histone deacetylase inhibitor SAHA with the proteasome inhibitor bortezomib in cutaneous T cell lymphoma. Eur J Haematol 2009;82:440-9
   PubMed Web of Science ®Google Scholar
• Bhalla S, Balasubramanian S, David K, PCI-24781 induces caspase and reactive oxygen species-dependent apoptosis through NF-kappaB mechanisms and is synergistic with bortezomib in lymphoma cells. Clin Cancer Res 2009;15:3354-65
   PubMed Web of Science ®Google Scholar
• Dasmahapatra G, Lembersky D, Kramer L, The pan-HDAC inhibitor vorinostat potentiates the activity of the proteasome inhibitor carfilzomib in human DLBCL cells in vitro and in vivo. Blood 2010;115:4478-87
   PubMed Web of Science ®Google Scholar
• Ye BH, Chaganti S, Chang CC, Chromosomal translocations cause deregulated BCL6 expression by promoter substitution in B cell lymphoma. EMBO J 1995;14:6209-17
   PubMed Web of Science ®Google Scholar
• Migliazza A, Martinotti S, Chen W, Frequent somatic hypermutation of the 5′ noncoding region of the BCL6 gene in B-cell lymphoma. Proc Natl Acad Sci USA 1995;92:12520-4
   PubMed Web of Science ®Google Scholar
• Zollman S, Godt D, Prive GG, The BTB domain, found primarily in zinc finger proteins, defines an evolutionarily conserved family that includes several developmentally regulated genes in Drosophila. Proc Natl Acad Sci USA 1994;91:10717-21
   PubMed Web of Science ®Google Scholar
• Huynh KD, Fischle W, Verdin E, Bardwell VJ. BCoR, a novel corepressor involved in BCL-6 repression. Genes Dev 2000;14:1810-23
   PubMed Web of Science ®Google Scholar
• Melnick A, Carlile G, Ahmad KF, Critical residues within the BTB domain of PLZF and Bcl-6 modulate interaction with corepressors. Mol Cell Biol 2002;22:1804-18
   PubMed Web of Science ®Google Scholar
• Ahmad KF, Melnick A, Lax S, Mechanism of SMRT corepressor recruitment by the BCL6 BTB domain. Mol Cell 2003;12:1551-64
   PubMed Web of Science ®Google Scholar
• Bereshchenko OR, Gu W, Dalla-Favera R. Acetylation inactivates the transcriptional repressor BCL6. Nat Genet 2002;32:606-13
   PubMed Web of Science ®Google Scholar
• Furumai R, Matsuyama A, Kobashi N, FK228 (depsipeptide) as a natural prodrug that inhibits class I histone deacetylases. Cancer Res 2002;62:4916-21
   PubMed Web of Science ®Google Scholar
• Byrd JC, Marcucci G, Parthun MR, A phase 1 and pharmacodynamic study of depsipeptide (FK228) in chronic lymphocytic leukemia and acute myeloid leukemia. Blood 2005;105:959-67
   PubMed Web of Science ®Google Scholar
• Piekarz RL, Robey R, Sandor V, Inhibitor of histone deacetylation, depsipeptide (FR901228), in the treatment of peripheral and cutaneous T-cell lymphoma: a case report. Blood 2001;98:2865-8
   PubMed Web of Science ®Google Scholar
• Piekarz RL, Frye R, Turner M, Phase II multi-institutional trial of the histone deacetylase inhibitor romidepsin as monotherapy for patients with cutaneous T-cell lymphoma. J Clin Oncol 2009;27:5410-7
   PubMed Web of Science ®Google Scholar
• Kim Y, Whittaker S, Demierre MF, Clinically significant responses achieved with romidepsin in treatment-refractory cutaneous T-cell lymphoma: final results from a phase 2B, international, multicenter, registration study. ASH Annual Meeting Abstracts 2008;112:263
   Google Scholar
• Piekarz R, Frye AR, Wright JJ, Update of the NCI multiinstitutional phase II trial of romidepsin, FK228, for patients with cutaneous or peripheral T-cell lymphoma. J Clin Oncol 2007;25(Suppl 18):8027
   Google Scholar
• Bates SE, Zhan Z, Steadman K, Laboratory correlates for a phase II trial of romidepsin in cutaneous and peripheral T-cell lymphoma. Br J Haematol 2010;148:256-67
   PubMed Web of Science ®Google Scholar
• Shah MH, Binkley P, Chan K, Cardiotoxicity of histone deacetylase inhibitor depsipeptide in patients with metastatic neuroendocrine tumors. Clin Cancer Res 2006;12:3997-4003
   PubMed Web of Science ®Google Scholar
• Piekarz RL, Frye AR, Wright JJ, Cardiac studies in patients treated with depsipeptide, FK228, in a phase II trial for T-cell lymphoma. Clin Cancer Res 2006;12:3762-73
   PubMed Web of Science ®Google Scholar
• Piekarz R, Wright J, Frye R, Results of a phase 2 NCI multicenter study of romidepsin in patients with relapsed peripheral T-cell lymphoma (PTCL). ASH Annual Meeting Abstracts 2008;112:1567
   Google Scholar
• Alazard N, Gruffat H, Hiriart E, Differential hyperacetylation of histones H3 and H4 upon promoter-specific recruitment of EBNA2 in Epstein-Barr virus chromatin. J Virol 2003;77:8166-72
   PubMed Web of Science ®Google Scholar
• Roychowdhury S, Baiocchi RA, Vourganti S, Selective efficacy of depsipeptide in a xenograft model of Epstein-Barr virus-positive lymphoproliferative disorder. J Natl Cancer Inst 2004;96:1447-57
   PubMed Web of Science ®Google Scholar
• He Y, Cai S, Zhang G, Interfering with cellular signaling pathways enhances sensitization to combined sodium butyrate and GCV treatment in EBV-positive tumor cells. Virus Res 2008;135:175-80
   PubMed Web of Science ®Google Scholar
• Perrine SP, Hermine O, Small T, A phase 1/2 trial of arginine butyrate and ganciclovir in patients with Epstein-Barr virus-associated lymphoid malignancies. Blood 2007;109:2571-8
   PubMed Web of Science ®Google Scholar
• Feng WH, Kenney SC. Valproic acid enhances the efficacy of chemotherapy in EBV-positive tumors by increasing lytic viral gene expression. Cancer Res 2006;66:8762-9
   PubMed Web of Science ®Google Scholar
• Fournel M, Bonfils C, Hou Y, MGCD0103, a novel isotype-selective histone deacetylase inhibitor, has broad spectrum antitumor activity in vitro and in vivo. Mol Cancer Ther 2008;7:759-68
   PubMed Web of Science ®Google Scholar
• Bonfils C, Kalita A, Dubay M, Evaluation of the pharmacodynamic effects of MGCD0103 from preclinical models to human using a novel HDAC enzyme assay. Clin Cancer Res 2008;14:3441-9
   PubMed Web of Science ®Google Scholar
• Crump M, Andreadis C, Assouline S, Treatment of relapsed or refractory non-Hodgkin lymphoma with the oral isotype-selective histone deacetylase inhibitor MGCD0103: interim results from a phase II study. J Clin Oncol (Meeting Abstracts) 2008;26(Suppl 15):8528
   Google Scholar
• Bociek RG, Kuruvilla J, Pro B, Isotype-selective histone deacetylase (HDAC) inhibitor MGCD0103 demonstrates clinical activity and safety in patients with relapsed/refractory classical Hodgkin Lymphoma (HL). J Clin Oncol (Meeting Abstracts) 2008;26:(Suppl 15);8507
   Google Scholar
• van den Berg A, Visser L, Poppema S. High expression of the CC chemokine TARC in Reed-Sternberg cells. A possible explanation for the characteristic T-cell infiltrate in Hodgkin's lymphoma. Am J Pathol 1999;154:1685-91
   PubMed Web of Science ®Google Scholar
• Buglio D, Georgakis GV, Hanabuchi S, Vorinostat inhibits STAT6-mediated TH2 cytokine and TARC production and induces cell death in Hodgkin lymphoma cell lines. Blood 2008;112:1424-33
   PubMed Web of Science ®Google Scholar
• Giles F, Fischer T, Cortes J, A phase I study of intravenous LBH589, a novel cinnamic hydroxamic acid analogue histone deacetylase inhibitor, in patients with refractory hematologic malignancies. Clin Cancer Res 2006;12:4628-35
   PubMed Web of Science ®Google Scholar
• Zhang L, Lebwohl D, Masson E, Clinically relevant QTc prolongation is not associated with current dose schedules of LBH589 (panobinostat). J Clin Oncol 2008;26:332-3
   PubMed Web of Science ®Google Scholar
• Prince HM, George D, Patnaik A, Phase I study of oral LBH589, a novel deacetylase (DAC) inhibitor in advanced solid tumors and non-Hodgkin's lymphoma. J Clin Oncol (Meeting Abstracts) 2007;25(Suppl 18):3500
   Google Scholar
• Ellis L, Pan Y, Smyth GK, Histone deacetylase inhibitor panobinostat induces clinical responses with associated alterations in gene expression profiles in cutaneous T-cell lymphoma. Clin Cancer Res 2008;14:4500-10
   PubMed Web of Science ®Google Scholar
• Duvic M, Becker JC, Dalle S, Phase II trial of oral panobinostat (LBH589) in patients with refractory cutaneous T-cell lymphoma (CTCL). ASH Annual Meeting Abstracts 2008;112:1005
   Google Scholar
• Chen J, Fiskus W, Eaton K, Cotreatment with BCL-2 antagonist sensitizes cutaneous T-cell lymphoma to lethal action of HDAC7-Nur77-based mechanism. Blood 2009;113:4038-48
   PubMed Web of Science ®Google Scholar
• Gimsing P, Hansen M, Knudsen LM, A phase I clinical trial of the histone deacetylase inhibitor belinostat in patients with advanced hematologic neoplasia. Eur J Haematol 2008;81:170-6
   PubMed Web of Science ®Google Scholar
• Gupta M, Ansell SM, Novak AJ, Inhibition of histone deacetylase overcomes rapamycin-mediated resistance in diffuse large B-cell lymphoma by inhibiting Akt signaling through mTORC2. Blood 2009;114:2926-35
   PubMed Web of Science ®Google Scholar
• cancer. gov [homepage on the Internet]. Bethesda (MD): National Cancer Institute, U.S. National Institutes of Health. Available from: http://www.cancer.gov
   Google Scholar