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1 1 Dickinson, M., Johnstone, R.W., and Prince, H.M. (2010). Histone deacetylase inhibitors: potential targets responsible for their anti‐cancer effect. Invest New Drugs 28 (Suppl 1): S3–S20.

2 2 Choi, J., Goh, G., Walradt, T. et al. (2015). Genomic landscape of cutaneous T cell lymphoma. Nat Genet 47 (9): 1011–1019.

3 3 da Silva Almeida, A.C., Abate, F., Khiabanian, H. et al. (2015). The mutational landscape of cutaneous T cell lymphoma and Sézary syndrome. Nat Genet 47 (12): 1465–1470.

4 4 Wang, L., Ni, X., Covington, K.R. et al. (2015). Genomic profiling of Sézary syndrome identifies alterations of keyT cell signaling and differentiation genes. Nat Genet 47 (12): 1426–1434.

5 5 Whittaker, S.J., Demierre, M.F., Kim, E.J. et al. (2010). Final results from a multicenter, international, pivotal study of romidepsin in refractory cutaneous T‐cell lymphoma. J Clin Oncol 28 (29): 4485–4491.

6 6 Iqbal, J., Wright, G., Wang, C. et al. (2014). Gene expression signatures delineate biological and prognostic subgroups in peripheral T‐cell lymphoma. Blood 123 (19): 2915–2923.

7 7 Sandell, R.F., Boddicker, R.L., and Feldman, A.L. (2017). Genetic landscape and classification of peripheral T cell lymphomas. Curr Oncol Rep 19 (4): 28.

8 8 Palomero, T., Couronné, L., Khiabanian, H. et al. (2014). Recurrent mutations in epigenetic regulators, RHOA and FYN kinase in peripheral T cell lymphomas. Nat Genet 46 (2): 166–170.

9 9 Ji, M.M., Huang, Y.H., Huang, J.Y. et al. (2018). Histone modifier gene mutations in peripheral T‐cell lymphoma not otherwise specified. Haematologica 103 (4): 679–687.

10 10 Shah, U.A., Chung, E.Y., Giricz, O. et al. (2018). North American ATLL has a distinct mutational and transcriptional profile and responds to epigenetic therapies. Blood 132 (14): 1507–1518.

11 11 de Ruijter, A.J.M., van Gennip, A.H., and Caron, H.N. (2003). Histone deacetylases (HDACs): characterization of the classical HDAC family. Biochem J 370 (Pt 3): 737–749.

12 12 Bolden, J.E., Peart, M.J., and Johnstone, R.W. (2006). Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 5 (9): 769–784.

13 13 Wang, Z., Zang, C., Cui, K. et al. (2009). Genome‐wide mapping of HATs and HDACs reveals distinct functions in active and inactive genes. Cell 138 (5): 1019–1031.

14 14 Dovey, O.M., Foster, C.T., and Cowley, S.M. (2010). Emphasizing the positive: a role for histone deacetylases in transcriptional activation. Cell Cycle 9 (14): 2700–2701.

15 15 Bertrand, P. (2010). Inside HDAC with HDAC inhibitors. Eur J Med Chem 45 (6): 2095–2116.

16 16 Hubbert, C., Guardiola, A., Shao, R. et al. (2002). HDAC6 is a microtubule‐associated deacetylase. Nature 417 (6887): 455–458.

17 17 Boyault, C., Sadoul, K., Pabion, M., and Khochbin, S. (2007). HDAC6, at the crossroads between cytoskeleton and cell signaling by acetylation and ubiquitination. Oncogene 26 (37): 5468–5476.

18 18 Vernin, C., Thenoz, M., Pinatel, C. et al. (2014). HTLV‐1 bZIP factor HBZ promotes cell proliferation and genetic instability by activating oncomiRs. Cancer Res 74 (21): 6082.

19 19 Mondello, P., Tadros, S., Teater, M. et al. (2020). Selective inhibition of HDAC3 targets synthetic vulnerabilities and activates immune surveillance in lymphoma. Cancer Discov 10 (3): 440–459.

20 20 Archer, S.Y., Meng, S., Shei, A., and Hodin, R.A. (1998). p21(WAF1) is required for butyrate‐mediated growth inhibition of human colon cancer cells. Proc Natl Acad Sci U S A 95 (12): 6791–6796.

21 21 Richon, V.M., Sandhoff, T.W., Rifkind, R.A., and Marks, P.A. (2000). Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene‐associated histone acetylation. Proc Natl Acad Sci U S A 97 (18): 10014–10019.

22 22 Sasakawa, Y., Naoe, Y., Noto, T. et al. (2003). Antitumor efficacy of FK228, a novel histone deacetylase inhibitor, depends on the effect on expression of angiogenesis factors. Biochem Pharmacol 66 (6): 897–906.

23 23 Shao, Y., Gao, Z., Marks, P.A., and Jiang, X. (2004). Apoptotic and autophagic cell death induced by histone deacetylase inhibitors. Proc Natl Acad Sci U S A 101 (52): 18030–10835.

24 24 Carew, J.S., Nawrocki, S.T., Kahue, C.N. et al. (2007). Targeting autophagy augments the anticancer activity of the histone deacetylase inhibitor SAHA to overcome Bcr‐Abl‐mediated drug resistance. Blood 110 (1): 313–322.

25 25 Dunn, J., McCuaig, R., and Tu, W.J. (2015). Multi‐layered epigenetic mechanisms contribute to transcriptional memory in T lymphocytes. BMC Immunol 16: 27.

26 26 Antignano, F. and Zaph, C. (2015). Regulation of CD4 T‐cell differentiation and inflammation by repressive histone methylation. Immunol Cell Biol 93 (3): 245–252.

27 27 Toner, L.E., Vrhovac, R., Smith, E.A. et al. (2006). The schedule‐dependent effects of the novel antifolate pralatrexate and gemcitabine are superior to methotrexate and cytarabine in models of human non‐Hodgkin's lymphoma. Clin Cancer Res 12 (3): 924.

28 28 Paoluzzi, L., Scotto, L., Marchi, E. et al. (2010). Romidepsin and belinostat synergize the antineoplastic effect of bortezomib in mantle cell lymphoma. Clin Cancer Res 16 (2): 554.

29 29 Marchi, E., Paoluzzi, L., Scotto, L. et al. (2010). Pralatrexate is synergistic with the proteasome inhibitor Bortezomib in in vitro and in vivo models of T‐cell lymphoid malignancies. Clin Cancer Res 16 (14): 3648.

30 30 Kalac, M., Scotto, L., Marchi, E. et al. (2011). HDAC inhibitors and decitabine are highly synergistic and associated with unique gene‐expression and epigenetic profiles in models of DLBCL. Blood 118 (20): 5506–5516.

31 31 Jain, S., Jirau‐Serrano, X., Zullo, K.M. et al. (2015). Preclinical pharmacologic evaluation of pralatrexate and romidepsin confirms potent synergy of the combination in a murine model of human T‐cell lymphoma. Clin Cancer Res 21 (9): 2096.

32 32 Marchi, E., Zullo, K.M., Amengual, J.E. et al. (2015). The combination of hypomethylating agents and histone deacetylase inhibitors produce marked synergy in preclinical models of T‐cell lymphoma. Br J Haematol 171 (2): 215–226.

33 33 Zullo, K.M., Guo, Y., Cooke, L. et al. (2015). Aurora a kinase inhibition selectively synergizes with histone deacetylase inhibitor through cytokinesis failure in T‐cell lymphoma. Clin Cancer Res 21 (18): 4097–4109.

34 34 Odejide, O., Weigert, O., Lane, A.A. et al. (2014). A targeted mutational landscape of angioimmunoblastic T‐cell lymphoma. Blood 123 (9): 1293–1296.

35 35 Sakata‐Yanagimoto, M., Enami, T., Yoshida, K. et al. (2014). Somatic RHOA mutation in angioimmunoblastic T cell lymphoma. Nat Genet 46 (2): 171–175.

36 36 Couronné, L., Bastard, C., and Bernard, O.A. (2012). TET2 and DNMT3A mutations in human T‐cell lymphoma. N Engl J Med 366 (1): 95–96.

37 37 He, Y.F., Li, B.Z., Li, Z. et al. (2011). Tet‐mediated formation of 5‐carboxylcytosine and its excision by TDG in mammalian DNA. Science 333 (6047): 1303–1307.

38 38 Ito, S., Shen, L., Dai, Q. et al. (2011). Tet proteins can convert 5‐methylcytosine to 5‐formylcytosine and 5‐carboxylcytosine. Science 333 (6047): 1300–1303.

39 39 Tahiliani, M., Koh, K.P., Shen, Y. et al. (2009). Conversion of 5‐methylcytosine to 5‐hydroxymethylcytosine in mammalian DNA by MLL partner TET1. Science 324 (5929): 930.

40 40 Quivoron, C., Couronné, L., Della Valle, V. et al. (2011). TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis. Cancer Cell 20 (1): 25–38.

41 41 Muto, H., Sakata‐Yanagimoto, M., Nagae, G. et al. (2014). Reduced TET2 function leads to T‐cell lymphoma with follicular helper T‐cell‐like features in mice. Blood Cancer J 4 (12): e264‐e.

42 42 Lemonnier, F., Couronné, L., Parrens, M. et al. (2012). Recurrent TET2 mutations in peripheral T‐cell lymphomas correlate with TFH‐like features and adverse clinical parameters. Blood 120: 1466–1469.

43 43 Nagata, Y., Kontani, K., Enami, T. et al. (2016). Variegated RHOA mutations in adult T‐cell leukemia/lymphoma. Blood 127 (5): 596–604.

44 44 Gu, T., Lin, X., Cullen, S.M. et al. (2018). DNMT3A and TET1 cooperate to regulate promoter epigenetic landscapes in mouse embryonic stem cells. Genome Biol 19 (1): 88.

45 45 Cairns, R.A., Iqbal, J., Lemonnier, F. et al. (2012). IDH2 mutations are frequent in angioimmunoblastic T‐cell lymphoma. Blood 119 (8): 1901–1903.

46 46 Dawlaty, M.M., Breiling, A., Le, T. et al. (2014). Loss of Tet enzymes compromises proper differentiation of embryonic stem cells. Dev Cell 29 (1): 102–111.

47 47 Williams, K., Christensen, J., Pedersen, M.T. et al. (2011). TET1 and hydroxymethylcytosine in transcription and DNA methylation fidelity. Nature 473 (7347): 343–348.

48 48 Wu, H., D’Alessio, A.C., Ito, S. et al. (2011). Dual functions of Tet1 in transcriptional regulation in mouse embryonic stem cells. Nature 473 (7347): 389–393.

49 49 Lemonnier, F., Poullot, E., Dupuy, A. et al. (2018). Loss of 5‐hydroxymethylcytosine is a frequent event in peripheral T‐cell lymphomas. Haematologica 103 (3): e115.

50 50 Wang, C., McKeithan, T.W., Gong, Q. et al. (2015). IDH2R172 mutations define a unique subgroup of patients with angioimmunoblastic T‐cell lymphoma. Blood 126 (15): 1741–1752.

51 51 de Mel, S., Soon, S.G., Mok, Y. et al. (2018). The genomics and molecular biology of natural killer/T‐cell lymphoma: opportunities for translation. Int J Mol Sci 19 (7): 1931.

52 52 O’Connor, O.A., Falchi, L., Lue, J.K. et al. (2019). Oral 5‐azacytidine and romidepsin exhibit marked activity in patients with PTCL: a multicenter phase 1 study. Blood 134 (17): 1395–1405.

53 53 Yi, S., Sun, J., Qiu, L. et al. (2018). Dual role of EZH2 in cutaneous anaplastic large cell lymphoma: promoting tumor cell survival and regulating tumor microenvironment. J Invest Dermatol 138 (5): 1126–1136.

54 54 Fernandez‐Pol, S., Ma, L., Joshi, R.P., and Arber, D.A. (2019). A survey of somatic mutations in 41 genes in a cohort of T‐cell lymphomas identifies frequent mutations in genes involved in epigenetic modification. Appl Immunohistochem Mol Morphol 27 (6): 416–422.

55 55 Ng, S.Y., Brown, L., Stevenson, K. et al. (2018). RhoA G17V is sufficient to induce autoimmunity and promotes T‐cell lymphomagenesis in mice. Blood 132 (9): 935–947.

56 56 Cortes, J.R., Ambesi‐Impiombato, A., Couronné, L. et al. (2018). RHOA G17V induces T follicular helper cell specification and promotes Lymphomagenesis. Cancer Cell 33 (2): 259–273.e7.

57 57 Yoo, H.Y., Sung, M.K., Lee, S.H. et al. (2014). A recurrent inactivating mutation in RHOA GTPase in angioimmunoblastic T cell lymphoma. Nat Genet 46 (4): 371–375.

58 58 Sakata‐Yanagimoto, M., Nakamoto‐Matsubara, R., Komori, D. et al. (2017). Detection of the circulating tumor DNAs in angioimmunoblastic T‐cell lymphoma. Ann Hematol 96 (9): 1471–1475.

59 59 Pizzi, M., Margolskee, E., and Inghirami, G. (2018). Pathogenesis of peripheral T cell lymphoma. Annu Rev Pathol 13 (1): 293–320.

60 60 Iqbal, J., Amador, C., McKeithan, T.W., and Chan, W.C. (2019). Molecular and genomic landscape of peripheral T‐cell lymphoma. In: T‐Cell and NK‐Cell Lymphomas: From Biology to Novel Therapies (eds. C. Querfeld, J. Zain and S.T. Rosen), 31–68. Cham: Springer International Publishing.

61 61 Dunleavy, K., Wilson, W.H., and Jaffe, E.S. (2007). Angioimmunoblastic T cell lymphoma: pathobiological insights and clinical implications. Curr Opin Hematol 14 (4): 348–353.

62 62 Gaulard, P. and de Leval, L. (2011). Follicular helper T cells: implications in neoplastic hematopathology. Semin Diagn Pathol 28 (3): 202–213.

63 63 Zhou, Y., Attygalle, A.D., Chuang, S.S. et al. (2007). Angioimmunoblastic T‐cell lymphoma: histological progression associates with EBV and HHV6B viral load. Br J Haematol 138 (1): 44–53.

64 64 Nelson, M., Horsman, D.E., Weisenburger, D.D. et al. (2008). Cytogenetic abnormalities and clinical correlations in peripheral T‐cell lymphoma. Br J Haematol 141 (4): 461–469.

65 65 Fernández‐Piqueras, J. (2016). New mutations for nodal lymphomas of TFH origin. Blood 128 (11): 1446–1447.

66 66 Yoo, H.Y., Kim, P., Kim, W.S. et al. (2016). Frequent CTLA4‐CD28 gene fusion in diverse types of T‐cell lymphoma. Haematologica 101 (6): 757–763.

67 67 Attygalle, A., Feldman, A., and Dogan, A. (2013). ITK/SYK translocation in angioimmunoblastic T‐cell lymphoma. Am J Surg Pathol 37: 1456–1457.

68 68 Zain, J.M. (2019). Aggressive T‐cell lymphomas: 2019 updates on diagnosis, risk stratification, and management. Am J Hematol 94 (8): 929–946.

69 69 Yabe, M., Dogan, A., Horwitz, S.M., and Moskowitz, A.J. (2019). Angioimmunoblastic T‐cell lymphoma. In: T‐Cell and NK‐Cell Lymphomas: From Biology to Novel Therapies (eds. C. Querfeld, J. Zain and S.T. Rosen), 99–126. Cham: Springer International Publishing.

70 70 O’Connor, O.A., Horwitz, S., Masszi, T. et al. (2015). Belinostat in patients with relapsed or refractory peripheral T‐cell lymphoma: results of the pivotal phase II BELIEF (CLN‐19) study. J Clin Oncol 33 (23): 2492–2499.

71 71 Coiffier, B., Pro, B., Prince, H.M. et al. (2014). Romidepsin for the treatment of relapsed/refractory peripheral T‐cell lymphoma: pivotal study update demonstrates durable responses. J Hematol Oncol 7: –11.

72 72 Delarue, R., Dupuis, J., Sujobert, P. et al. (2016). Treatment with hypomethylating agent 5‐azacytidine induces sustained response in angioimmunoblastic T cell lymphomas. Blood 128 (22): 4164.

73 73 Savage, K.J., Harris, N.L., Vose, J.M. et al. (2008). ALK− anaplastic large‐cell lymphoma is clinically and immunophenotypically different from both ALK+ ALCL and peripheral T‐cell lymphoma, not otherwise specified: report from the international peripheral T‐cell lymphoma project. Blood 111 (12): 5496–5504.

74 74 Shustov, A. and Soma, L. Anaplastic large cell lymphoma: contemporary concepts and optimal management. In: T‐Cell and NK‐Cell Lymphomas: From Biology to Novel Therapies (eds. C. Querfeld, J. Zain and S.T. Rosen), 127–144. Cham: Springer International Publishing.

75 75 Fujikawa, D., Nakagawa, S., Hori, M. et al. (2016). Polycomb‐dependent epigenetic landscape in adult T‐cell leukemia. Blood 127 (14): 1790–1802.

76 76 Swerdlow, S.H., Campo, E., Pileri, S.A. et al. (2016). The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood 127 (20): 2375–2390.

77 77 Pfister, S.X., Ahrabi, S., Zalmas, L.P. et al. (2014). SETD2‐dependent histone H3K36 trimethylation is required for homologous recombination repair and genome stability. Cell Rep 7 (6): 2006–2018.

78 78 Küçük, C., Jiang, B., Hu, X. et al. (2015). Activating mutations of STAT5B and STAT3 in lymphomas derived from γδ‐T or NK cells. Nat Commun 6 (1): 6025.

79 79 Vaqué, J., Gómez‐López, G., Monsálvez, V. et al. (2014). PLCG1 mutations in cutaneous T‐cell lymphomas. Blood 123 (13): 2034–2043.

80 80 Woollard, W.J., Pullabhatla, V., Lorenc, A. et al. (2016). Candidate driver genes involved in genome maintenance and DNA repair in Sézary syndrome. Blood 127 (26): 3387–3397.

81 81 van Doorn, R., Slieker, R.C., Boonk, S.E. et al. (2016). Epigenomic analysis of Sézary syndrome defines patterns of aberrant DNA methylation and identifies diagnostic markers. J Invest Dermatol 136 (9): 1876–1884.

82 82 Cancer Genome Atlas Research Network, Weinstein, J.N., Collisson, E.A. et al. (2013). The Cancer Genome Atlas Pan‐Cancer analysis project. Nat Genet 45 (10): 1113–1120.

83 83 Chihara, D. and Oki, Y. NK‐cell lymphomas. In: T‐Cell and NK‐Cell Lymphomas: From Biology to Novel Therapies (eds. C. Querfeld, J. Zain and S.T. Rosen), 163–184. Cham: Springer International Publishing.

84 84 Kiel, M.J., Sahasrabuddhe, A.A., Rolland, D.C.M. et al. (2015). Genomic analyses reveal recurrent mutations in epigenetic modifiers and the JAK–STAT pathway in Sézary syndrome. Nat Commun 6 (1): 8470.

85 85 Ungewickell, A., Bhaduri, A., Rios, E. et al. (2015). Genomic analysis of mycosis fungoides and Sézary syndrome identifies recurrent alterations in TNFR2. Nat Genet 47 (9): 1056–1060.

86 86 Michel, L., Jean‐Louis, F., and Begue, E. (2013). Use of PLS3, Twist, CD158k/KIR3DL2, and NKp46 gene expression combination for reliable Sézary syndrome diagnosis. Blood 121 (8): 1477–1478.

87 87 Jones, C.L., Ferreira, S., McKenzie, R.C.T. et al. (2012). Regulation of T‐plastin expression by promoter hypomethylation in primary cutaneous T‐cell lymphoma. J Invest Dermatol 132 (8): 2042–2049.

88 88 Coiffier, B., Pro, B., Prince, H.M. et al. (2012). Results from a pivotal, open‐label, phase II study of romidepsin in relapsed or refractory peripheral T‐cell lymphoma after prior systemic therapy. J Clin Oncol 30 (6): 631–636.

89 89 Olsen, E.A., Kim, Y.H., Kuzel, T.M. et al. (2007). 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.

90 90 Shi, Y., Dong, M., Hong, X. et al. (2015). Results from a multicenter, open‐label, pivotal phase II study of chidamide in relapsed or refractory peripheral T‐cell lymphoma. Ann Oncol 26 (8): 1766–1771.

91 91 O’Connor, O.A., Pro, B., Pinter‐Brown, L. et al. (2011). Pralatrexate in patients with relapsed or refractory peripheral T‐cell lymphoma: results from the pivotal PROPEL study. J Clin Oncol 29 (9): 1182–1189.

92 92 Clozel, T., Yang, S., Elstrom, R.L. et al. (2013). Mechanism‐based epigenetic chemosensitization therapy of diffuse large B‐cell lymphoma. Cancer Discov 3 (9): 1002–1019.

93 93 Uenogawa, K., Hatta, Y., Arima, N. et al. (2011). Azacitidine induces demethylation of p16INK4a and inhibits growth in adult T‐cell leukemia/lymphoma. Int J Mol Med 28 (5): 835–839.

94 94 Lemonnier, F., Dupuis, J., Sujobert, P. et al. (2018). Treatment with 5‐azacytidine induces a sustained response in patients with angioimmunoblastic T‐cell lymphoma. Blood 132 (21): 2305–2309.

95 95 Gregory, G.P., Dickinson, M., Yannakou, C.K. et al. (2019). Rapid and durable complete remission of refractory AITL with azacitidine treatment in absence of TET2 mutation or concurrent MDS. Hemasphere 3 (2): e187.

96 96 Figueroa, M.E., Abdel‐Wahab, O., Lu, C. et al. (2010). Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation. Cancer Cell 18 (6): 553–567.

97 97 Lemonnier, F., Cairns, R.A., Inoue, S. et al. (2016). The IDH2 R172K mutation associated with angioimmunoblastic T‐cell lymphoma produces 2HG in T cells and impacts lymphoid development. Proc Natl Acad Sci U S A 113 (52): 15084–15089.

98 98 Nguyen, T.B., Sakata‐Yanagimoto, M., Asabe, Y. et al. (2017). Identification of cell‐type‐specific mutations in nodal T‐cell lymphomas. Blood Cancer J 7 (1): e516‐e.

99 99 Stein, E.M., DiNardo, C.D., Pollyea, D.A. et al. (2017). Enasidenib in mutant IDH2 relapsed or refractory acute myeloid leukemia. Blood 130 (6): 722–731.

100 100 DiNardo, C.D., Stein, E.M., de Botton, S. et al. (2018). Durable remissions with Ivosidenib in IDH1‐mutated relapsed or refractory AML. N Engl J Med 378 (25): 2386–2398.

101 101 Yamaguchi, H. and Hung, M.‐C. (2014). Regulation and role of EZH2 in cancer. Cancer Res. Treat. 46 (3): 209–222.

102 102 Béguelin, W., Rivas, M.A., Calvo Fernández, M.T. et al. (2017). EZH2 enables germinal Centre formation through epigenetic silencing of CDKN1A and an Rb‐E2F1 feedback loop. Nat Commun 8 (1): 877.

103 103 Béguelin, W., Popovic, R., Teater, M. et al. (2013). EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. Cancer Cell 23 (5): 677–692.

104 104 Caganova, M., Carrisi, C., Varano, G. et al. (2013). Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis. J Clin Invest 123 (12): 5009–5022.

105 105 Morin, R.D., Johnson, N.A., Severson, T.M. et al. (2010). Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B‐cell lymphomas of germinal‐center origin. Nat Genet 42 (2): 181–185.

106 106 Bödör, C., Grossmann, V., Popov, N. et al. (2013). EZH2 mutations are frequent and represent an early event in follicular lymphoma. Blood 122 (18): 3165–3168.

107 107 Sneeringer, C.J., Scott, M.P., Kuntz, K.W. et al. (2010). Coordinated activities of wild‐type plus mutant EZH2 drive tumor‐associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B‐cell lymphomas. Proc Natl Acad Sci U S A 107 (49): 20980.

108 108 Italiano, A., Soria, J.C., Toulmonde, M. et al. (2018). Tazemetostat, an EZH2 inhibitor, in relapsed or refractory B‐cell non‐Hodgkin lymphoma and advanced solid tumours: a first‐in‐human, open‐label, phase 1 study. Lancet Oncol 19 (5): 649–659.

109 109 Yap, T.A., Johnson, P.W.M., Winter, J. et al. (2016). A phase I, open‐label study of GSK2816126, an enhancer of zeste homolog 2 (EZH2) inhibitor, in patients with relapsed/refractory diffuse large B‐cell lymphoma (DLBCL), transformed follicular lymphoma (tFL), other non‐Hodgkin's lymphomas (NHL), multiple myeloma (MM) and solid tumor. J Clin Oncol 34 (15 Suppl): TPS2595.

110 110 Maruyama, D., Tobinai, K., Makita, S. et al. (2017). First‐in‐human study of the EZH1/2 dual inhibitor DS‐3201b in patients with relapsed or refractory non‐Hodgkin lymphomas: preliminary results. Blood 130 (Suppl 1): 4070.

111 111 Ntziachristos, P., Tsirigos, A., Vlierberghe, P.V. et al. (2012). Genetic inactivation of the polycomb repressive complex 2 in T cell acute lymphoblastic leukemia. Nat Med 18 (2): 298–302.

112 112 Zhang, J., Ding, L., Holmfeldt, L. et al. (2012). The genetic basis of early T‐cell precursor acute lymphoblastic leukaemia. Nature 481 (7380): 157–163.

113 113 Danis, E., Yamauchi, T., Echanique, K. et al. (2016). Ezh2 controls an early hematopoietic program and growth and survival signaling in early T cell precursor acute lymphoblastic leukemia. Cell Rep 14 (8): 1953–1965.

114 114 Shi, M., Shahsafaei, A., and Liu, C. (2015). Enhancer of zeste homolog 2 is widely expressed in T‐cell neoplasms, is associated with high proliferation rate and correlates with MYC and pSTAT3 expression in a subset of cases. Leuk Lymphoma 56 (7): 2087–2091.

115 115 Yamagishi, M., Hori, M., Fujikawa, D. et al. (2016). Development and molecular analysis of synthetic lethality by targeting EZH1 and EZH2 in non‐Hodgkin lymphomas. Blood 128 (22): 462.

116 116 Yamagishi, M., Fujikawa, D., Honma, D. et al. (2015). Polycomb‐dependent epigenetic landscape in Adult T Cell Leukemia (ATL); providing proof of concept for targeting EZH1/2 to selectively eliminate the HTLV‐1 infected population. Blood 126 (23): 572.

117 117 Honma, D., Kanno, O., Watanabe, J. et al. (2017). Novel orally bioavailable EZH1/2 dual inhibitors with greater antitumor efficacy than an EZH2 selective inhibitor. Cancer Sci 108 (10): 2069–2078.

118 118 Shortt, J., Ott, C.J., Johnstone, R.W., and Bradner, J.E. (2017). A chemical probe toolbox for dissecting the cancer epigenome. Nat Rev Cancer 17 (3): 160–183.

119 119 Doroshow, D.B., Eder, J.P., and LoRusso, P.M. (2017). BET inhibitors: a novel epigenetic approach. Ann Oncol 28 (8): 1776–1787.

120 120 Ozer, H.G., El‐Gamal, D., Powell, B. et al. (2018). BRD4 profiling identifies critical chronic lymphocytic leukemia oncogenic circuits and reveals sensitivity to PLX51107, a novel structurally distinct BET inhibitor. Cancer Discov 8 (4): 458–477.

121 121 Vázquez, R., Riveiro, M.E., Astorgues‐Xerri, L. et al. (2017). The bromodomain inhibitor OTX015 (MK‐8628) exerts anti‐tumor activity in triple‐negative breast cancer models as single agent and in combination with everolimus. Oncotarget 8 (5): 7598–7613.

122 122 Wang, L., Matkar, S., Xie, G. et al. (2017). BRD4 inhibitor IBET upregulates p27kip/cip protein stability in neuroendocrine tumor cells. Cancer Biol Ther 18 (4): 229–236.

123 123 Yokoyama, Y., Zhu, H., Lee, J.H. et al. (2016). BET inhibitors suppress ALDH activity by targeting ALDH1A1 super‐enhancer in ovarian cancer. Cancer Res 76 (21): 6320–6330.

124 124 Piunti, A., Hashizume, R., Morgan, M.A. et al. (2017). Therapeutic targeting of polycomb and BET bromodomain proteins in diffuse intrinsic pontine gliomas. Nat Med 23 (4): 493–500.

125 125 Gryder, B., Yohe, M., Chou, H.C. et al. (2017). PAX3‐FOXO1 establishes myogenic super enhancers and confers BET Bromodomain vulnerability. Cancer Discov 7 (8): 884–899.

126 126 Kohnken, R., Wen, J., Mundy‐Bosse, B. et al. (2018). Diminished microRNA‐29b level is associated with BRD4‐mediated activation of oncogenes in cutaneous T‐cell lymphoma. Blood 131 (7): 771–781.

127 127 He, A. and Miranda, J.L. (2018). JQ1 reduces Epstein–Barr virus‐associated lymphoproliferative disease in mice without sustained oncogene repression. Leuk Lymphoma 59 (5): 1248–1251.

128 128 Gopalakrishnan, R., Matta, H., Tolani, B. et al. (2016). Immunomodulatory drugs target IKZF1‐IRF4‐MYC axis in primary effusion lymphoma in a cereblon‐dependent manner and display synergistic cytotoxicity with BRD4 inhibitors. Oncogene 35 (14): 1797–1810.

129 129 Dickinson, M., Kamdar, M., Huntly, B. et al. (2018). A phase I study of molibresib (GSK525762), a selective Bromodomain (BRD) and extra terminal protein (BET) inhibitor: results from part 1 of a phase I/II open label single agent study in subjects with Non‐Hodgkin's Lymphoma (NHL). Blood 132: 1682.

130 130 Panfil, A.R., Al‐Saleem, J., Howard, C.M. et al. (2015). PRMT5 is upregulated in HTLV‐1‐mediated T‐cell transformation and selective inhibition alters viral gene expression and infected cell survival. Viruses 8 (1): 7.

131 131 Li, Y., Chitnis, N., Nakagawa, H. et al. (2015). PRMT5 is required for lymphomagenesis triggered by multiple oncogenic drivers. Cancer Discov 5 (3): 288–303.

132 132 Tan, D., Phipps, C., Hwang, W.Y.K. et al. (2015). Panobinostat in combination with bortezomib in patients with relapsed or refractory peripheral T‐cell lymphoma: an open‐label, multicentre phase 2 trial. Lancet Haematol 2 (8): e326–e333.

133 133 Amengual, J.E., Lichtenstein, R., Lue, J. et al. (2018). A phase 1 study of romidepsin and pralatrexate reveals marked activity in relapsed and refractory T‐cell lymphoma. Blood 131 (4): 397–407.

134 134 Strati, P., Nastoupil, L.J., Davis, R.E. et al. (2020). A phase 1 trial of alisertib and romidepsin for relapsed/refractory aggressive B‐cell and T‐cell lymphomas. Haematologica 105 (1): e26–e28.

135 135 Moskowitz, A.J., Koch, R., Mehta‐Shah, N. et al. (2017). In vitro, in vivo, and parallel phase I evidence support the safety and activity of duvelisib, a PI3K‐δ,γ inhibitor, in combination with romidepsin or bortezomib in relapsed/refractory T‐cell lymphoma. Blood 130 (Suppl 1): 819.

136 136 Mehta‐Shah, N., Lunning, M.A., Boruchov, A.M. et al. (2015). A phase I/II trial of the combination of romidepsin and lenalidomide in patients with relapsed/refractory lymphoma and myeloma: activity in T‐cell lymphoma. J Clin Oncol 33 (15 Suppl): 8521.

137 137 Cycon, K.A., Mulvaney, K., Rimsza, L.M. et al. (2013). Histone deacetylase inhibitors activate CIITA and MHC class II antigen expression in diffuse large B‐cell lymphoma. Immunology 140 (2): 259–272.

138 138 Tiper, I.V. and Webb, T.J. (2016). Histone deacetylase inhibitors enhance CD1d‐dependent NKT cell responses to lymphoma. Cancer Immunol Immunother 65 (11): 1411–1421.

139 139 Ghoneim, H.E., Fan, Y., Moustaki, A. et al. (2017). De novo epigenetic programs inhibit PD‐1 blockade‐mediated T cell rejuvenation. Cell 170 (1): 142–157.e19.

140 140 Lai, Q., Wang, H., Li, A. et al. (2018). Decitibine improve the efficiency of anti‐PD‐1 therapy via activating the response to IFN/PD‐L1 signal of lung cancer cells. Oncogene 37 (17): 2302–2312.

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