The Peripheral T-Cell Lymphomas. Группа авторов

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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.

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      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.

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