All activated signaling pathways lead to anaplastic large cell lymphoma (ALCL)

References

• Stein H, Mason DY, Gerdes J, et al. The expression of the Hodgkin’s disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells. Blood. 1985;66(4):848–858.
   PubMed Web of Science ®Google Scholar
• Swerdlow S, Campo E, Harris N, et al. WHO classification of tumours of haematopoietic and lymphoid tissues. Rev. 4th ed. Vol. 2. Lyon: International Agency for Research on Cancer; 2017.
   Google Scholar
• Montes-Mojarro IA, Steinhilber J, Bonzheim I, et al. The pathological spectrum of systemic Anaplastic Large Cell Lymphoma (ALCL). Cancers. 2018;10(4):107.
   Web of Science ®Google Scholar
• Bonzheim I, Geissinger E, Roth S, et al. Anaplastic large cell lymphomas lack the expression of T-cell receptor molecules or molecules of proximal T-cell receptor signaling. Blood. 2004;104(10):3358–3360.
   PubMed Web of Science ®Google Scholar
• Ambrogio C, Martinengo C, Voena C, et al. NPM-ALK oncogenic tyrosine kinase controls T-cell identity by transcriptional regulation and epigenetic silencing in lymphoma cells [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't]. Cancer Res. 2009;69(22):8611–8619.
   PubMed Web of Science ®Google Scholar
• Turner SD, Inghirami G, Miranda RN, et al. Cell of origin and immunologic events in the pathogenesis of breast implant-associated anaplastic large-cell lymphoma. Am J Pathol. 2020;190(1):2–10.
   PubMed Web of Science ®Google Scholar
• Geissinger E, Sadler P, Roth S, et al. Disturbed expression of the T-cell receptor/CD3 complex and associated signaling molecules in CD30+ T-cell lymphoproliferations. Haematologica. 2010;t95(10):1697–1704.
   PubMed Web of Science ®Google Scholar
• Morris SW, Kirstein MN, Valentine MB, et al. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin’s lymphoma [Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.]. Science. 1994;263(5151):1281–1284.
   PubMed Web of Science ®Google Scholar
• Duyster J, Bai RY, Morris SW. Translocations involving anaplastic lymphoma kinase (ALK) [Research Support, Non-U.S. Gov’t Research Support, U.S. Gov’t, P.H.S. Review]. Oncogene. 2001;20(40):5623–5637.
   PubMed Web of Science ®Google Scholar
• Miething C, Peschel C, Duyster J. Targeting the oncogenic tyrosine kinase NPM-ALK in lymphoma: the role of murine models in defining pathogenesis and treatment options. Curr Drug Targets. 2006;7(10):1329–1334.
   PubMed Web of Science ®Google Scholar
• Ritter U, Damm-Welk C, Fuchs U, et al. Design and evaluation of chemically synthesized siRNA targeting the NPM-ALK fusion site in anaplastic large cell lymphoma (ALCL). Oligonucleotides. 2003;13(5):365–373.
   PubMed Web of Science ®Google Scholar
• Bai RY, Dieter P, Peschel C, et al. Nucleophosmin-anaplastic lymphoma kinase of large-cell anaplastic lymphoma is a constitutively active tyrosine kinase that utilizes phospholipase C-gamma to mediate its mitogenicity. Mol Cell Biol. 1998;18(12):6951–6961.
   PubMed Web of Science ®Google Scholar
• Bai RY, Ouyang T, Miething C, et al. Nucleophosmin-anaplastic lymphoma kinase associated with anaplastic large-cell lymphoma activates the phosphatidylinositol 3-kinase/Akt antiapoptotic signaling pathway. Blood. 2000;96(13):4319–4327.
   PubMed Web of Science ®Google Scholar
• Chiarle R, Voena C, Ambrogio C, et al. The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer. 2008;8(1):11–23.
   PubMed Web of Science ®Google Scholar
• Cesarman E, Inghirami G, Chadburn A, et al. High levels of p53 protein expression do not correlate with p53 gene mutations in anaplastic large cell lymphoma. Am J Pathol. 1993;143(3):845–856.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Vogelstein B, Lane D, Levine AJ. Surfing the p53 network. Nature. 2000;408(6810):307–310.
   PubMed Web of Science ®Google Scholar
• Inoue K, Kurabayashi A, Shuin T, et al. Overexpression of p53 protein in human tumors. Med Mol Morphol. 2012;45(3):115–123.
   PubMed Web of Science ®Google Scholar
• Vousden KH, Lu X. Live or let die: the cell’s response to p53. Nat Rev Cancer. 2002;2(8):594–604.
   PubMed Web of Science ®Google Scholar
• Boi M, Rinaldi A, Kwee I, et al. PRDM1/BLIMP1 is commonly inactivated in anaplastic large T-cell lymphoma. Blood. 2013;122(15):2683–2693.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Rassidakis GZ, Drakos E. The emerging role of CD30 and p53 as novel targets for therapy in anaplastic large cell lymphoma. Front Biosci (Elite Ed). 2016;8:61–71.
   PubMedGoogle Scholar
• Kruse JP, Gu W. Modes of p53 regulation. Cell. 2009;137(4):609–622.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMed Web of Science ®Google Scholar
• Karni-Schmidt O, Lokshin M, Prives C. The roles of MDM2 and MDMX in cancer. Annu Rev Pathol. 2016;11:617–644.
   PubMed Web of Science ®Google Scholar
• Sinatkas V, Stathopoulou K, Xagoraris I, et al. MDMX/MDM4 is highly expressed and contributes to cell growth and survival in anaplastic large cell lymphoma. Leuk Lymphoma. 2021;11:1.
   Google Scholar
• Stetkova M, Growkova K, Fojtik P, et al. CDK9 activity is critical for maintaining MDM4 overexpression in tumor cells. Cell Death Dis. 2020;11(9):754.
   PubMed Web of Science ®Google Scholar
• Gilkes DM, Pan Y, Coppola D, et al. Regulation of MDMX expression by mitogenic signaling. Mol Cell Biol. 2008;28(6):1999–2010.
   PubMed Web of Science ®Google Scholar
• 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.
   PubMedGoogle Scholar
• Konopleva M, Martinelli G, Daver N, et al. MDM2 inhibition: an important step forward in cancer therapy. Leukemia. 2020;34(11):2858–2874.
   PubMed Web of Science ®Google Scholar
• Yu DH, Xu ZY, Mo S, et al. Targeting MDMX for cancer therapy: rationale, strategies, and challenges. Front Oncol. 2020;10:1389.
   PubMed Web of Science ®Google Scholar