Defective DNA repair systems and the development of breast and prostate cancer (Review)

  • Authors:
    • Yasuko Kitagishi
    • Mayumi Kobayashi
    • Satoru Matsuda
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  • Published online on: November 14, 2012     https://doi.org/10.3892/ijo.2012.1696
  • Pages: 29-34
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Abstract

Genetic defects in DNA repair and DNA damage response genes often lead to an increase in cancer incidence. The role of defects is also associated with the modulation of hormone signaling pathways. A number of studies have suggested a role for estrogen in the regulation of DNA repair activity. Furthermore, mutations or epigenetic silencing in DNA repair genes have been associated with the sensitivity of cancers to hormonal therapy. The molecular basis for the progression of cancers from hormone-dependent to hormone-independent remains a critical issue in the management of these types of cancer. In the present review, we aimed to summarize the function of DNA repair molecules from the viewpoint of carcinogenesis and hormone-related cell modulation, providing a comprehensive view of the molecular mechanisms by which hormones may exert their effects on the regulation of tumor progression.
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January 2013
Volume 42 Issue 1

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Copy and paste a formatted citation
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Spandidos Publications style
Kitagishi Y, Kobayashi M and Matsuda S: Defective DNA repair systems and the development of breast and prostate cancer (Review). Int J Oncol 42: 29-34, 2013
APA
Kitagishi, Y., Kobayashi, M., & Matsuda, S. (2013). Defective DNA repair systems and the development of breast and prostate cancer (Review). International Journal of Oncology, 42, 29-34. https://doi.org/10.3892/ijo.2012.1696
MLA
Kitagishi, Y., Kobayashi, M., Matsuda, S."Defective DNA repair systems and the development of breast and prostate cancer (Review)". International Journal of Oncology 42.1 (2013): 29-34.
Chicago
Kitagishi, Y., Kobayashi, M., Matsuda, S."Defective DNA repair systems and the development of breast and prostate cancer (Review)". International Journal of Oncology 42, no. 1 (2013): 29-34. https://doi.org/10.3892/ijo.2012.1696