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Original Articles

MDMX/MDM4 is highly expressed and contributes to cell growth and survival in anaplastic large cell lymphoma

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Pages 1563-1573 | Received 27 Jul 2020, Accepted 07 Jan 2021, Published online: 11 Feb 2021

References

  • Leventaki V, Bhattacharyya S, Lim MS. Pathology and genetics of anaplastic large cell lymphoma. Semin Diagn Pathol. 2020;37(1):57–71.
  • Montes-Mojarro I, Steinhilber J, Bonzheim I, et al. The pathological spectrum of systemic anaplastic large cell lymphoma (ALCL). Cancers. 2018;10(4):107.
  • Mereu E, Pellegrino E, Scarfò I, et al. The heterogeneous landscape of ALK negative ALCL. Oncotarget. 2017;8(11):18525–18536.
  • Hallberg B, Palmer RH. Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology. Nat Rev Cancer. 2013;13(10):685–700.
  • Crescenzo R, Abate F, Lasorsa E, European T-Cell Lymphoma Study Group, T-Cell Project: Prospective Collection of Data in Patients with Peripheral T-Cell Lymphoma and the AIRC 5xMille Consortium “Genetics-Driven Targeted Management of Lymphoid Malignancies”, et al. Convergent mutations and kinase fusions lead to oncogenic STAT3 activation in anaplastic large cell lymphoma. Cancer Cell. 2015;27(4):516–532.
  • Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature. 2000;408(6810):307–310.
  • Hollstein M, Sidransky D, Vogelstein B, et al. p53 mutations in human cancers. Science. 1991;253(5015):49–53.
  • Rassidakis GZ, Thomaides A, Wang S, et al. p53 gene mutations are uncommon but p53 is commonly expressed in anaplastic large-cell lymphoma. Leukemia. 2005;19(9):1663–1669.
  • Drakos E, Atsaves V, Schlette E, et al. The therapeutic potential of p53 reactivation by nutlin-3a in ALK + anaplastic large cell lymphoma with wild-type or mutated p53. Leukemia. 2009;23(12):2290–2299.
  • Shvarts A, Bazuine M, Dekker P, et al. Isolation and Identification of the Human Homolog of a New p53-Binding Protein, Mdmx. Genomics. 1997;43(1):34–42.
  • Parant J, Chavez-Reyes A, Little NA, et al. Rescue of embryonic lethality in Mdm4-null mice by loss of Trp53 suggests a nonoverlapping pathway with MDM2 to regulate p53. Nat Genet. 2001;29(1):92–95.
  • Wade M, Li Y-C, Wahl GM. MDM2, MDMX and p53 in oncogenesis and cancer therapy. Nat Rev Cancer. 2013;13(2):83–96.
  • Karni-Schmidt O, Lokshin M, Prives C. The roles of MDM2 and MDMX in cancer. Annu Rev Pathol. 2016;11(1):617–644.
  • Liang M, Han X, Vadhan-Raj S, et al. HDM4 is overexpressed in mantle cell lymphoma and its inhibition induces p21 expression and apoptosis. Mod Pathol. 2010;23(3):381–391.
  • Leventaki V, Rodic V, Tripp SR, et al. TP53 pathway analysis in paediatric Burkitt lymphoma reveals increased MDM4 expression as the only TP53 pathway abnormality detected in a subset of cases. Br J Haematol. 2012;158(6):763–771.
  • Hüllein J, Słabicki M, Rosolowski M, et al. MDM4 is targeted by 1q gain and drives disease in Burkitt lymphoma. Cancer Res. 2019;79(12):3125–3138.
  • Han X, Medeiros LJ, Zhang YH, et al. High expression of human homologue of murine double minute 4 and the short splicing variant, HDM4-S, in bone marrow in patients with acute myeloid leukemia or myelodysplastic syndrome. Clin Lymphoma Myeloma Leuk. 2016;16:S30–S38.
  • Drakos E, Leventaki V, Schlette EJ, et al. c-Jun expression and activation are restricted to CD30+ lymphoproliferative disorders. Am J Surg Pathol. 2007;31(1):447–453.
  • Kwiecinska A, Tsesmetzis N, Ghaderi M, et al. CD274 (PD-L1)/PDCD1 (PD-1) expression in de novo and transformed diffuse large B-cell lymphoma. Br J Haematol. 2018;180(5):744–748.
  • Drakos E, Rassidakis GZ, Lai R, et al. Caspase-3 activation in systemic anaplastic large-cell lymphoma. Mod Pathol. 2004;17(1):109–116.
  • Ventura A, Kirsch DG, McLaughlin ME, et al. Restoration of p53 function leads to tumour regression in vivo. Nature. 2007;445(7128):661–665.
  • Xue W, Zender L, Miething C, et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature. 2007;445(7128):656–660.
  • Martins CP, Brown-Swigart L, Evan GI. Modeling the therapeutic efficacy of p53 restoration in tumors. Cell. 2006;127(7):1323–1334.
  • Toufektchan E, Toledo F. The guardian of the genome revisited: p53 downregulates genes required for telomere maintenance, DNA repair, and centromere structure. Cancers. 2018;10(5):135.
  • 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.
  • Gilkes DM, Pan Y, Coppola D, et al. Regulation of MDMX expression by mitogenic signaling. Mol Cell Biol. 2008;28(6):1999–2010.
  • Markey MP. Regulation of MDM4. Front Biosci (Landmark Ed)). 2011;16(1):1144–1156.
  • Xiong S, Pant V, Zhang Y, et al. The p53 inhibitor Mdm4 cooperates with multiple genetic lesions in tumourigenesis: increased Mdm4 cooperates in tumourigenesis. J Pathol. 2017;241(4):501–510.
  • Ng SY, Yoshida N, Christie AL, et al. Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models. Nat Commun. 2018;9(1):2024.
  • Tisato V, Voltan R, Gonelli A, et al. MDM2/X inhibitors under clinical evaluation: perspectives for the management of hematological malignancies and pediatric cancer. J Hematol Oncol. 2017;10(1):133.
  • Bo MD, Secchiero P, Degan M, et al. MDM4 (MDMX) is overexpressed in chronic lymphocytic leukaemia (CLL) and marks a subset of p53wild-type CLL with a poor cytotoxic response to Nutlin-3: correspondence. Br J Haematol. 2010;150(2):237–239.
  • Patton JT, Mayo LD, Singhi AD, et al. Levels of HdmX expression dictate the sensitivity of normal and transformed cells to Nutlin-3. Cancer Res. 2006;66(6):3169–3176.
  • Hu B, Gilkes DM, Farooqi B, et al. MDMX overexpression prevents p53 activation by the MDM2 inhibitor nutlin. J Biol Chem. 2006;281(44):33030–33035.

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