Outsmarting prostate cancer

FFCMH Researchers Professor Wayne Tilley and Dr Luke Selth from the Dame Roma Mitchell Cancer Research Laboratories, Uni of Adelaide, are senior co-authors on a paper published recently in Nucleic Acids Research which has been classified as a  ‘Breakthrough Article’ and may lead to better patient management and new drugs for men with advanced prostate cancer. Such papers present high-impact studies answering long-standing questions in the field of nucleic acids research and/or opening up new areas and mechanistic hypotheses for investigation. These articles are chosen by the Editors on the recommendation of Editorial Board Members and Referees. They represent the very best papers published in this high profile journal.

Until now, it has been unclear how prostate cancer cells evade common hormone therapy treatments. In this study with the Masonic Cancer Centre at the University of Minnesota, the Researchers have shown that a variant of a protein present in most tumours is an important driver of resistance to hormone therapy in advanced prostate cancer.  This research provides important insight into how prostate cancers advance to a lethal phase. They have shown that a drug  not previously used in prostate cancer could effectively inhibit the variant protein that drives drug resistance and lethal disease.  The cancer cells are resilient and highly adaptive, and this research is aimed at addressing how to outsmart them. “Many men can be cured of their prostate cancer if it is diagnosed early, through surgery and radiation therapy. However, for some men, their cancer will progress to a stage that is invariably lethal. This research is especially targeted at this group of men. The next stage will see us further testing and developing newer generation drugs.

This is the Nuclei Acids Research Journal Editors summary:

“Understanding and overcoming mechanisms of resistance to second-generation endocrine-targeted androgen receptor (AR) inhibitors are arguably the most urgent priorities in the field of prostate cancer research. This article demonstrates that AR variants (AR-Vs) arising from alterations in AR mRNA splicing broadly recapitulate chromatin binding events that are otherwise suppressed during endocrine-targeted therapy. Additionally, this work reveals that the bromodomain inhibitor JQ1 down-regulates AR-V expression, which leads to impaired AR-V chromatin binding, impaired transcriptional activation of target genes, and impaired growth of AR-V-driven prostate cancer cells in vitro and in vivo. “

This research was supported by National Institutes of Health, the American Cancer Society, US Department of Defense Prostate Cancer Research Program, Prostate Cancer Foundation of Australia, Masonic Cancer Center, Ray and Shirl Norman Cancer Research Trust and Prostate Cancer Foundation Australia.


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