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Ras oncogene-induced sensitization to 1-beta-D-arabinofuranosylcytosine

  1. Author:
    Koo, H. M.
    McWilliams, M. J.
    Alvord, W. G.
    Woude, G. F. V.

  2. Author Address

    Woude GFV Van Andel Res Inst 201 Monroe Ave NW,Suite 400 Grand Rapids, MI 49503 USA NCI, Frederick Canc Res & Dev Ctr, Adv Biosci Labs, Basic Res Program Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Data Management Serv Frederick, MD 21702 USA NCI, Div Basic Sci, NIH Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Cancer Research
    1. 59
    2. 24
    3. Pages: 6057-6062
  4. Type of Article: Article
  1. Abstract:

    Human tumor cells containing ras oncogenes display enhanced sensitivity to 1-beta-D-arabinofuranosylcytosine (Ara-C) and other deoxycytidine analogues (H-M. Koo, et al., Cancer Res., 56: 5211-5216, 1996). Human tumor cell lines with or without a ras oncogene as well as a pair of isogenic cell lines with one containing an activated ras oncogene were used to study the basis for differential sensitivity. We found that human tumor cells containing ras oncogenes upon entry into the S phase of the cell cycle underwent apoptosis in response to Ara-C treatment. By contrast, human tumor cells harboring wild-type ras alleles were only delayed in the S phase when exposed to Ara-C. Thus, the ras oncogene specifically renders human cells more sensitive to Ara-C by preventing S-phase arrest. This may occur by the ras oncogene compromising an S-phase checkpoint. [References: 23]

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