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Review

Development of molecular intervention strategies for B-cell lymphoma

& ORCID Icon
Pages 241-252 | Received 02 Jul 2020, Accepted 24 Nov 2020, Published online: 12 Jan 2021

References

  • Rosenberg SA, Restifo NP.Adoptive cell transfer as personalized immunotherapy for human cancer.Science. 2015;348(6230):62–68.
  • Raut LS, Chakrabarti PP. Management of relapsed-refractory diffuse large B cell lymphoma. South Asian J Cancer. 2014;3(1):66–70.
  • Voropaeva EN, Pospelova TI,Voevoda MI, et al.Frequency, spectrum, and functional significance of TP53 mutations in patients with diffuse large B-cell lymphoma. Mol Biol (Mosk).2017;51(1):64–72.
  • Xu-Monette ZY,Medeiros LJ, Li Y,et al.Dysfunction of the TP53 tumor suppressor gene in lymphoid malignancies.Blood.2012;119(16):3668–3683.
  • Belyi VA, Ak P, Markert E, et al. The origins and evolution of the p53 family of genes. Cold Spring Harb Perspect Biol.2010;2(6):a1198.
  • Brieghel C,Kinalis S, Yde CW,et al.Deep targeted sequencing of TP53 in chronic lymphocytic leukemia: clinical impact at diagnosis and at time of treatment.Haematologica. 2019;104(4): 789–796.
  • Chipuk JE, Kuwana T, Bouchier-Hayes L, et al. Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis. Science. 2004;303(5660):1010–1014.
  • Byrd JC, Hillmen P, O’Brien S, et al. Long-term follow-up of the RESONATE phase 3 trial of ibrutinib vs ofatumumab. Blood. 2019;133(19):2031–2042.
  • Hallek M. Chronic lymphocytic leukemia: 2020 update on diagnosis, risk stratification and treatment. Am J Hematol. 2019;94(11):1266–1287.
  • Sharif-Askari B, Doyon D, Paliouras M, et al. Bruton’s tyrosine kinase is at the crossroads of metabolic adaptation in primary malignant human lymphocytes. Sci Rep. 2019;9(1):11069.
  • Gango A, Alpar D, Galik B, et al., Dissection of suBCLonal evolution by temporal mutation profiling in chronic lymphocytic leukemia patients treated with ibrutinib. Int J Cancer. 2020;146(1): 85–93.
  • Hershkovitz-Rokah O, Pulver D, Lenz G, et al., Ibrutinib resistance in mantle cell lymphoma: clinical, molecular and treatment aspects. Br J Haematol. 2018;181(3): 306–319.
  • Miao Y, Medeiros LJ, Xu-Monette ZY, et al. Dysregulation of cell survival in diffuse large b cell lymphoma: mechanisms and therapeutic targets. Front Oncol. 2019;9:107.
  • Hullein J, Slabicki M, Rosolowski M, et al., MDM4 is targeted by 1q gain and drives disease in burkitt lymphoma. Cancer Res. 2019;79(12): 3125–3138.
  • Kuruvilla J, Savona M, Baz R,et al. Selective inhibition of nuclear export with selinexor in patients with non-Hodgkin lymphoma. Blood. 2017;129(24):3175–3183.
  • Lue JK, Amengual JE. Emerging EZH2 inhibitors and their application in lymphoma.Curr Hematol Malig Rep. 2018;13(5):369–382.
  • Li B, Chng WJ. EZH2 abnormalities in lymphoid malignancies: underlying mechanisms and therapeutic implications. J Hematol Oncol. 2019;12(1):118.
  • Nielsen JS, Chang AR, Wick DA, et al. Mapping the human T cell repertoire to recurrent driver mutations in MYD88 and EZH2 in lymphoma. Oncoimmunology. 2017;6(7):e1321184.
  • Fioravanti R, Stazi G, Zwergel C, et al. Six Years (2012-2018) of researches on catalytic EZH2 inhibitors: the boom of the 2-pyridone compounds. Chem Rec. 2018;18(12):1818–1832.
  • Italiano A, Soria JC, Toulmonde M, et al. 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. 2018;19(5):649–659.
  • Gulati N, Beguelin W, Giulino-Roth L. Enhancer of zeste homolog 2 (EZH2) inhibitors. Leuk Lymphoma. 2018;59(7):1574–1585.
  • Huang S, Wang Z, Zhou J, et al., EZH2 inhibitor GSK126 suppresses antitumor immunity by driving production of Myeloid-Derived suppressor cells. Cancer Res. 2019;79(8): 2009–2020.
  • Daisuke HPENM. DS-3201, a potent EZH1/2 dual inhibitor, demonstrates antitumor activity against Non-Hodgkin lymphoma (NHL) regardless of EZH2 mutation. Blood. 2018;132(Supplement 1):2217.
  • Yap TA, Winter JN, Giulino-Roth L, et al. Phase i study of the novel enhancer of zeste homolog 2 (EZH2) inhibitor GSK2816126 in patients with advanced hematologic and solid tumors. Clin Cancer Res. 2019;25(24):7331–7339.
  • McDonnell TJ, Deane N, Platt FM, et al. BCL-2-immunoglobulin transgenic mice demonstrate extended B cell survival and follicular lymphoproliferation. Cell. 1989;57(1):79–88.
  • MS D. Targeting BCL-2 in B-cell lymphomas. Blood. 2017;130(9):1081–1088.
  • Arif A, Jamal S, Mushtaq S, et al. Frequency of BCL-2 gene rearrangement in B-cell Non-Hodgkin’s lymphoma. Asian Pac J Cancer Prev. 2009;10(2):237–240.
  • Souers AJ, Leverson JD, Boghaert ER, et al. ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets. Nat Med. 2013;19(2):202–208.
  • Tse C, Shoemaker AR, Adickes J, et al. ABT-263: A potent and orally bioavailable BCL-2 family inhibitor. Cancer Res. 2008;68(9):3421–3428. .
  • Oltersdorf T, Elmore SW, Shoemaker AR, et al. An inhibitor of BCL-2 family proteins induces regression of solid tumours. Nature. 2005;435(7042):677–681.
  • Kitada S, Leone M, Sareth S, et al. Discovery, characterization, and structure-activity relationships studies of proapoptotic polyphenols targeting B-cell lymphocyte/leukemia-2 proteins. J Med Chem. 2003;46(20):4259–4264.
  • Lessene G, Czabotar PE, Sleebs BE, et al. Structure-guided design of a selective BCL-X(L) inhibitor. Nat Chem Biol. 2013;9(6):390–397.
  • Leverson JD, Phillips DC, Mitten MJ, et al. Exploiting selective BCL-2 family inhibitors to dissect cell survival dependencies and define improved strategies for cancer therapy. Sci Transl Med. 2015;7(279):240r–279r.
  • Tao ZF, Hasvold L, Wang L, et al. Discovery of a potent and selective BCL-XL inhibitor with in vivo activity. Acs Med Chem Lett. 2014;5(10):1088–1093.
  • Abulwerdi F, Liao C, Liu M, et al. A novel small-molecule inhibitor of mcl-1 blocks pancreatic cancer growth in vitro and in vivo. Mol Cancer Ther. 2014;13(3):565–575.
  • Kotschy A, Szlavik Z, Murray J, et al. The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models. Nature. 2016;538(7626):477–482.
  • Zhu Y, Tchkonia T, Fuhrmann-Stroigg H, et al. Identification of a novel senolytic agent, navitoclax, targeting the BCL-2 family of anti-apoptotic factors. Aging Cell. 2016;15(3):428–435.
  • Kale J, Osterlund EJ, Andrews DW. BCL-2 family proteins: changing partners in the dance towards death. Cell Death Differ. 2018;25(1):65–80.
  • Roberts AW, Davids MS, Pagel JM, et al. Targeting BCL2 with venetoclax in relapsed chronic lymphocytic leukemia. N Engl J Med. 2016;374(4):311–322.
  • Stilgenbauer S, Eichhorst B, Schetelig J, et al. Venetoclax in relapsed or refractory chronic lymphocytic leukaemia with 17p deletion: A multicentre, open-label, phase 2 study. Lancet Oncol. 2016;17(6):768–778.
  • Davids MS, Roberts AW, Seymour JF, et al. Phase i First-in-Human study of venetoclax in patients with relapsed or refractory Non-Hodgkin lymphoma. J Clin Oncol. 2017;35(8):826–833.
  • Radha G, Raghavan SC. BCL2: A promising cancer therapeutic target. Biochim Biophys Acta Rev Cancer. 2017;1868(1):309–314.
  • Cheson BD. Oblimersen for the treatment of patients with chronic lymphocytic leukemia. Ther Clin Risk Manag. 2007;3(5):855–870.
  • Weber A, Cardona GY, Cinar O, et al., Oncogenic MYD88 mutations in lymphoma: novel insights and therapeutic possibilities. Cancer Immunol Immunother. 2018;67(11): 1797–1807.
  • de Groen R, Schrader A, Kersten MJ, et al. MYD88 in the driver’s seat of B-cell lymphomagenesis: from molecular mechanisms to clinical implications. Haematologica. 2019;104(12):2337–2348.
  • Treon SP, Tripsas CK, Meid K, et al. Ibrutinib in previously treated Waldenstrom’s macroglobulinemia. N Engl J Med. 2015;372(15):1430–1440.
  • Chen JG, Liu X, Munshi M, et al. BTK(Cys481Ser) drives ibrutinib resistance via ERK1/2 and protects BTK(wild-type) MYD88-mutated cells by a paracrine mechanism. Blood. 2018;131(18):2047–2059.
  • Kelly PN, Romero DL, Yang Y, et al. Selective interleukin-1 receptor-associated kinase 4 inhibitors for the treatment of autoimmune disorders and lymphoid malignancy. J Exp Med. 2015;212(13):2189–2201.
  • Scott JS, Degorce SL, Anjum R, et al., Discovery and optimization of pyrrolopyrimidine inhibitors of interleukin-1 receptor associated kinase 4 (IRAK4) for the treatment of mutant MYD88(L265P) diffuse large B-Cell lymphoma. J Med Chem. 2017;60(24): 10071–10091.
  • Improgo MR, Tesar B, Klitgaard JL, et al. MYD88 L265P mutations identify a prognostic gene expression signature and a pathway for targeted inhibition in CLL. Br J Haematol. 2019;184(6):925–936.
  • Wang X, Tan Y, Huang Z, et al. Disrupting myddosome assembly in diffuse large Bcell lymphoma cells using the MYD88 dimerization inhibitor ST2825. Oncol Rep. 2019;42(5):1755–1766.
  • Yang G, Zhou Y, Liu X, et al. A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenstrom macroglobulinemia. Blood. 2013;122(7):1222–1232.
  • Guang Yang PJWP. A novel HCK inhibitor kin-8193 blocks BTK activity in BTKCys481 mutated ibrutinib resistant B-Cell lymphomas driven by mutated MYD88. Blood. 2018;132(Supplement 1):40.
  • Pasqualucci L, Dominguez-Sola D, Chiarenza A, et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature. 2011;471(7337):189–195.
  • Pastore A, Jurinovic V, Kridel R, et al. Integration of gene mutations in risk prognostication for patients receiving first-line immunochemotherapy for follicular lymphoma: A retrospective analysis of a prospective clinical trial and validation in a population-based registry. Lancet Oncol. 2015;16(9):1111–1122.
  • Bereshchenko OR, Gu W, Dalla-Favera R. Acetylation inactivates the transcriptional repressor BCL6. Nat Genet. 2002;32(4):606–613.
  • Jiang Y, Ortega-Molina A, Geng H, et al. CREBBP inactivation promotes the development of HDAC3-Dependent lymphomas. Cancer Discov. 2017;7(1):38–53.
  • Zhang J, Vlasevska S, Wells VA, et al. The CREBBP acetyltransferase is a haploinsufficient tumor suppressor in b-cell lymphoma. Cancer Discov. 2017;7(3):322–337.
  • Ogura M, Ando K, Suzuki T, et al. A multicentre phase II study of vorinostat in patients with relapsed or refractory indolent B-cell non-Hodgkin lymphoma and mantle cell lymphoma. Br J Haematol. 2014;165(6):768–776.
  • Kirschbaum M, Frankel P, Popplewell L, et al. Phase II study of vorinostat for treatment of relapsed or refractory indolent non-Hodgkin’s lymphoma and mantle cell lymphoma. J Clin Oncol. 2011;29(9):1198–1203.
  • Liu Y, Gonzalez Y, Amengual JE. Chromatin-Remodeled state in lymphoma. Curr Hematol Malig Rep. 2019;14(5):439–450.
  • Fagan RJ, Dingwall AK. COMPASS Ascending: emerging clues regarding the roles of MLL3/KMT2C and MLL2/KMT2D proteins in cancer. Cancer Lett. 2019;458:56–65.
  • Ji MM, Huang YH, Huang JY, et al. Histone modifier gene mutations in peripheral T-cell lymphoma not otherwise specified. Haematologica. 2018;103(4):679–687.
  • Harris WJ, Huang X, Lynch JT, et al. The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells. Cancer Cell. 2012;21(4):473–487.
  • Maes TTIMC. Preclinical characterization of a potent and selective inhibitor of the histone demethylase KDM1A for MLL leukemia. J Clin Oncol. 2013;31:1.
  • van Aller M, Cusan S, Kamat Y, et al. Novel anti-tumor activity of targeted LSD1 inhibition by GSK2879552. EJC. 2014;50(Supplement 6):72.
  • Hancock RL, Dunne K, Walport LJ, et al. Epigenetic regulation by histone demethylases in hypoxia. Epigenomics-Uk. 2015;7(5):791–811.
  • Maes T, Carceller E, Salas J, et al. Advances in the development of histone lysine demethylase inhibitors. Curr Opin Pharmacol. 2015;23:52–60.
  • Vinogradova M, Gehling VS, Gustafson A, et al. An inhibitor of KDM5 demethylases reduces survival of drug-tolerant cancer cells. Nat Chem Biol. 2016;12(7):531–538.
  • Horton JR, Liu X, Gale M, et al. Structural basis for KDM5A histone lysine demethylase inhibition by diverse compounds. Cell Chem Biol. 2016;23(7):769–781.
  • Mellert K, Martin M, Lennerz JK, et al. The impact of SOCS1 mutations in diffuse large B-cell lymphoma. Br J Haematol. 2019;187(5):627–637.
  • Ying J, Qiu X, Lu Y, et al. SOCS1 and its potential clinical role in tumor. Pathol Oncol Res. 2019;25(4):1295–1301.
  • Saint-Germain E, Mignacca L, Huot G, et al. Phosphorylation of SOCS1 inhibits the SOCS1-p53 tumor suppressor axis. Cancer Res. 2019;79(13):3306–3319.
  • Lessard F, Saint-Germain E, Mignacca L, et al. SOCS1: phosphorylation, dimerization and tumor suppression. Oncoscience. 2019;6(11-12:386–389.
  • Boone DL, Turer EE, Lee EG, et al. The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses. Nat Immunol. 2004;5(10):1052–1060.
  • Compagno M, Lim WK, Grunn A, et al. Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma. Nature. 2009;459(7247):717–721.
  • Kato M, Sanada M, Kato I, et al. Frequent inactivation of A20 through gene mutation in B-cell lymphomas. Rinsho Ketsueki. 2011;52(6):313–319.
  • Vela V, Juskevicius D, Gerlach MM, et al. High throughput sequencing reveals high specificity of TNFAIP3 mutations in ocular adnexal marginal zone B-cell lymphomas. Hematol Oncol. 2020 Aug; 38(3):284-292.
  • Pasqualucci L, Dalla-Favera R. Genetics of diffuse large B-cell lymphoma. Blood. 2018;131(21):2307–2319.
  • Dong G, Chanudet E, Zeng N, et al. A20, ABIN-1/2, and CARD11 mutations and their prognostic value in gastrointestinal diffuse large B-cell lymphoma. Clin Cancer Res. 2011;17(6):1440–1451.
  • Wenzl K, Manske MK, Sarangi V, et al. Loss of TNFAIP3 enhances MYD88L265P-driven signaling in non-Hodgkin lymphoma. Blood Cancer J. 2018;8(10):97.
  • Boice M, Salloum D, Mourcin F, et al. Loss of the HVEM tumor suppressor in lymphoma and restoration by modified CAR-T cells. Cell. 2016;167(2):405–418.
  • Carreras JLAKY. High TNFRSF14 and low BTLA are associated with poor prognosis in Follicular Lymphoma and in Diffuse Large B-cell Lymphoma transformation. J Clin Exp Hematop. 2019;59(1):1–16.
  • M’Hidi H, Thibult ML, Chetaille B, et al. High expression of the inhibitory receptor BTLA in T-follicular helper cells and in B-cell small lymphocytic lymphoma/chronic lymphocytic leukemia. Am J Clin Pathol. 2009;132(4):589–596.
  • Di Pilato M, Kim EY, Cadilha BL, et al. Targeting the CBM complex causes Treg cells to prime tumours for immune checkpoint therapy. Nature. 2019;570(7759):112–116.
  • Holliday MJ, Witt A, Rodriguez GA, et al. Structures of autoinhibited and polymerized forms of CARD9 reveal mechanisms of CARD9 and CARD11 activation. Nat Commun. 2019;10(1):3070.
  • Knies N, Alankus B, Weilemann A, et al. Lymphomagenic CARD11/BCL10/MALT1 signaling drives malignant B-cell proliferation via cooperative NF-kappaB and JNK activation. Proc Natl Acad Sci U S A. 2015;112(52):E7230–E7238.
  • Chen CZ, Li L, Lodish HF, et al. MicroRNAs modulate hematopoietic lineage differentiation. Science. 2004;303(5654):83–86.
  • Alencar AJ, Malumbres R, Kozloski GA, et al. MicroRNAs are independent predictors of outcome in diffuse large B-cell lymphoma patients treated with R-CHOP. Clin Cancer Res. 2011;17(12):4125–4135.
  • Zhu D, Fang C, He W, et al. MicroRNA-181a inhibits activated B-Cell-Like diffuse large B-Cell lymphoma progression by repressing CARD11. J Oncol. 2019;2019:9832956.
  • Dominguez-Sola D, Kung J, Holmes AB, et al. The FOXO1 transcription factor instructs the germinal center dark zone program. Immunity. 2015;43(6):1064–1074.
  • Kabrani E, Chu VT, Tasouri E, et al. Nuclear FOXO1 promotes lymphomagenesis in germinal center B cells. Blood. 2018;132(25):2670–2683.
  • Silhan J, Vacha P, Strnadova P, et al. 14-3-3 protein masks the DNA binding interface of forkhead transcription factor FOXO4. J Biol Chem. 2009;284(29):19349–19360.
  • Tzivion G, Dobson M, Ramakrishnan G. FoxO transcription factors; Regulation by AKT and 14-3-3 proteins. Biochim Biophys Acta. 2011;1813(11):1938–1945.
  • Gehringer F, Weissinger SE, Swier LJ, et al. FOXO1 confers maintenance of the dark zone proliferation and survival program and can be pharmacologically targeted in burkitt lymphoma. Cancers (Basel). 2019;11:10.