Researchers from the University and the Sichuan Antibiotics Industrial Institute in China have discovered a novel treatment for advanced prostate cancer.
For over forty years, ADT has been the foundation of advanced stage prostate cancer treatment. ADT is effective initially, most often measured by a drop in PSA measurement. But in almost all cases, prostate cancer returns and no longer uses androgen to fuel its growth. This is called androgen-independent cancer or castration-resistant prostate cancer (CRPC).
ADT does not have a significant effect on CRPC. So, for now, CRPC is barely treatable.
So, how are prostate cancer cells converted from androgen-dependent to androgen-independent state?
Most researchers think that the androgen receptor (AR) becomes more sensitive in CRPC cells and uses the very little amount of remaining androgen (after ADT) for the prostate cancer to revive and flourish.
Unfortunately, getting men to absolutely no addrogen production and utilization is hard to achieve and rarely is effective.
This new research has found a new target for fighting prostate cancer; a gene is called FABP5 which has acrucial role in the malignant progression of CRPC.
This study shows that FABP5-related pathway, not the androgen or AR-related pathway is the way cancer cells conduct signaling. Also, the FABP5-related pathway replaces the AR-related pathway as androgen-dependency of the CRPC cells reduces.
This highlights the fact that ADT treatment will push all cancer cells to the androgen-independent state and eventually do more harm than good.
Developing a new drug to target FABP5 to effectively treat CRPC might become a better way, and, indeed, new standard for CRPC treatment.
The full study, entitled ‘Inhibitor SBFI26 suppresses the malignant progression of castration-resistant PC3-M cells by competitively binding to oncogenic FABP5’, can be found here.
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