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Research Article

The p53 pathway induction is not primarily dependent on Ataxia Telangiectasia Mutated (ATM) gene activity after fludarabine treatment in chronic lymphocytic leukemia cells

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Pages 1840-1843 | Received 01 Apr 2013, Accepted 10 Apr 2013, Published online: 01 Jul 2013

References

  • Meyn MS. Ataxia-telangiectasia, cancer and the pathobiology of the ATM gene. Clin. Genet. 1999;55(5):289–304.
  • Uziel T, Lerenthal Y, Moyal L, et al. Requirement of the MRN complex for ATM activation by DNA damage. EMBO J. 2003;22(20):5612–5621.
  • Canman CE, Lim DS, Cimprich KA, et al. Activation of the ATM kinase by ionizing radiation and phosphorylation of p53. Science. 1998;281(5383):1677–1679.
  • Skowronska A, Parker A, Ahmed G, et al. Biallelic ATM inactivation significantly reduces survival in patients treated on the united kingdom leukemia research fund chronic lymphocytic leukemia 4 trial. J. Clin. Oncol. 2012;30(36):4524–4532.
  • Austen B, Skowronska A, Baker C, et al. Mutation status of the residual ATM allele is an important determinant of the cellular response to chemotherapy and survival in patients with chronic lymphocytic leukemia containing an 11q deletion. J. Clin. Oncol. 2007;25(34):5448–5457.
  • Austen B, Powell JE, Alvi A, et al. Mutations in the ATM gene lead to impaired overall and treatment-free survival that is independent of IGVH mutation status in patients with B-CLL. Blood. 2005;106(9):3175–3182.
  • Kojima K, Konopleva M, McQueen T, et al. MDM2 inhibitor nutlin-3a induces p53-mediated apoptosis by transcription-dependent and transcription-independent mechanisms and may overcome ATM-mediated resistance to fludarabine in chronic lymphocytic leukemia. Blood. 2006;108(3):993–1000.
  • Gandhi V, Plunkett W. Cellular and clinical pharmacology of fludarabine. Clin Pharmacokinet. 2002;41(2):93–103.
  • Kurz EU, Douglas P, Lees-Miller SP. Doxorubicin activates ATM-dependent phosphorylation of multiple downstream targets in part through the generation of reactive oxygen species. J. Biol. Chem. 2004;279(51):53272–53281.
  • Jones GG, Reaper PM, Pettitt AR, Sherrington PD. The ATR-p53 pathway is suppressed in noncycling normal and malignant lymphocytes. Oncogene. 2004;23(10):1911–1921.
  • De Campos-Nebel M, Larripa I, González-Cid M. Non-homologous end joining is the responsible pathway for the repair of fludarabine-induced DNA double strand breaks in mammalian cells. Mutat. Res. 2008;646(1-2):8–16.
  • Shieh SY, Ikeda M, Taya Y, Prives C. DNA damage-induced phosphorylation of p53 alleviates inhibition by MDM2. Cell. 1997;91(3): 325–334.
  • Willmore E, Elliott SL, Mainou-Fowler T, et al. DNA-dependent protein kinase is a therapeutic target and an indicator of poor prognosis in B-cell chronic lymphocytic leukemia. Clin. Cancer Res. 2008;14(12):3984–3992.
  • Chehab NH, Malikzay A, Stavridi ES, Halazonetis TD. Phosphorylation of Ser-20 mediates stabilization of human p53 in response to DNA damage. Proc. Natl. Acad. Sci. U.S.A. 1999;96(24):13777–13782.
  • Lin K, Adamson J, Johnson GG, et al. Functional analysis of the ATM-p53-p21 pathway in the LRF CLL4 trial: blockade at the level of p21 is associated with short response duration. Clin. Cancer Res. 2012;18(15):4191–4200.

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