PMID: 25773832Mar 17, 2015Paper

Conditional PTEN-deficient mice as a prostate cancer chemoprevention model

Asian Pacific Journal of Cancer Prevention : APJCP
Hiroyuki KoikeHirotsugu Uemura

Abstract

We generated a mouse model of prostate cancer based on the adult-prostate-specific inactivation of phosphatase and tensin homolog (PTEN) using the Cre-loxP system. The potential of our mice as a useful animal model was examined by evaluating the chemopreventive efficacy of the anti-androgen, chlormadinone acetate (CMA). Six-week-old mice were treated subcutaneously with 50 μg/g of CMA three times a week for 9 or 14 weeks and sacrificed at weeks 15 and 20. Macroscopic change of the entire genitourinary tract (GUT) and histologically evident prostate gland tumor development were evaluated. Proliferation and apoptosis status in the prostate were examined by immunohistochemistry. CMA triggered significant shrinkage of not only the GUT but also prostate glands at 15 weeks compared to the control (p=0.017 and p=0.010, respectively), and the trend became more marked after a further five-weeks of treatment. The onset of prostate adenocarcinoma was not prevented but the proliferation of cancer cells was inhibited by CMA, which suggested the androgen axis is critical for cancer growth in these mice. Conditional PTEN-deficient mice are useful as a preclinical model for chemoprevention studies and serve as a valuable tool for the future sc...Continue Reading

References

Feb 1, 1980·Endocrinologia Japonica·T KodamaJ Shimazaki
Mar 23, 2006·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Kenneth J Pienta, Deborah Bradley
Oct 16, 2008·British Journal of Cancer·P McCallJ Edwards
Oct 26, 2011·Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology·Michael A Davies
Apr 17, 2012·Asian Pacific Journal of Cancer Prevention : APJCP·Donovan A McGrowderTazhmoye V Crawford
Aug 17, 2012·The New England Journal of Medicine·Howard I ScherUNKNOWN AFFIRM Investigators
Mar 14, 2013·Molecular Oncology·Maxime Parisotto, Daniel Metzger
Mar 29, 2013·Asian Pacific Journal of Cancer Prevention : APJCP·Yukiko SugiyamaTaiji Tsukamoto
Jun 4, 2013·Asian Pacific Journal of Cancer Prevention : APJCP·Lei YangXiao-Hou Wu
Sep 3, 2013·Asian Pacific Journal of Cancer Prevention : APJCP·Xiao-Feng ZhouNai-Bo Liu
Jan 9, 2014·CA: a Cancer Journal for Clinicians·Rebecca SiegelAhmedin Jemal
Apr 11, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Manish GargSatya Narayan Sankhwar
Apr 11, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Faezeh AskariBahram Rashidkhani
Dec 19, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Muhammad DaniyalAsmatullah Khan
Dec 19, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Hoang Van DongColin W Binns
Dec 19, 2014·Asian Pacific Journal of Cancer Prevention : APJCP·Reshu TewariSingh Rajender

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Citations

Feb 14, 2018·International Journal of Molecular Medicine·Chun-Lin ZhaoJia-Xiang Wang

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