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Potential Mechanism of Chemo-Resistance to Gemcitabine

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Listed:
  • Daekyu Sun
  • John Michael White

    (Department of Pharmacology & Toxicology, University of Arizona, Tucson, USA)

Abstract

Gemcitabine (2′,2′-difluorodeoxycytidine, Gemzar®) is a deoxycytidine analog with pronounced antitumor activity against a variety of solid tumors. As gemcitabine is widely used for the treatment of human cancer, the appearance of resistance is a major obstacle to its clinical efficacy. Therefore, it is very important to understand the mechanisms by which cancer cells evolve chemo-resistance to this drug. Through comprehensive analysis of gene -expression profiles by oligonucleotide microarray analysis and follow -up studies, we have identified a cluster of DNA repair genes whose expression is induced in MDA- MB231 cells in the presence of gemcitabine. Based upon information obtained from this analysis, a testable hypothesis was generated regarding the potential roles of identified DNA repair gene products in mediating chemo resistance to gemcitabine in human cancer. Furthermore, new insights can be gained into the potential signaling pathways that interface the DNA damage checkpoint pathways with the activation of DNA repair processes by up regulating a selected group of DNA repair genes in cancer cells treated with gemcitabine.

Suggested Citation

  • Daekyu Sun & John Michael White, 2017. "Potential Mechanism of Chemo-Resistance to Gemcitabine," Novel Approaches in Drug Designing & Development, Juniper Publishers Inc., vol. 2(3), pages 50-53, August.
    • Handle: RePEc:adp:jnapdd:v:2:y:2017:i:3:p:50-53
    DOI: 10.19080/NAPDD.2017.02.555588
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    References listed on IDEAS

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    1. Bin-Bing S. Zhou & Stephen J. Elledge, 2000. "The DNA damage response: putting checkpoints in perspective," Nature, Nature, vol. 408(6811), pages 433-439, November.
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