Sensitivity of p53-deficient cells to oxaliplatin and thio-tepa (n, n′, n′ triethylenethiophosphoramide)

Young R. Seo, Edmund I.T. Chen, Martin L. Smith

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

P53 is known as a determinant of cellular responses to DNA damage, including apoptosis, cell cycle arrest, and DNA repair. Its role is most easily understood in the context of Burkitt lymphoma and other apoptosis-prone cell types. A number of epithelial cancer cell types, by contrast, exhibit a higher threshold for apoptosis induction in response to DNA damage. In fact, p53 mediates DNA repair and protective responses in the latter cell types, in some cases p53-deficient cells being more sensitive to DNA damage, antithetical to the situation in Burkitt lymphoma and other apoptosis-prone cell types. Ultraviolet light, cisplatin, and nitrogen mustards produce damage that is repaired by a p53-regulated pathway. Here, we explore the sensitivity of the platinum compound oxaliplatin and thio-TEPA (N, N′, N″, triethylenethiophosphoramide), a cancer chemotherapeutic agent that produces largely base damage, in p53-defective cells. This work demonstrates that the contribution of p53 temporally correlates with DNA repair pathways to produce a resistant phenotype, while the p53-defective cells are more sensitive to certain DNA-damaging chemotherapeutic agents.

Original languageEnglish
Pages (from-to)255-263
Number of pages9
JournalBreast Cancer Research and Treatment
Volume72
Issue number3
DOIs
StatePublished - 2002

Keywords

  • Chemosensitivity
  • p53

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