Mechanism Identified in Cellular Change Driving Castration-Resistant Prostate Cancer

Mechanism Identified in Cellular Change Driving Castration-Resistant Prostate Cancer
Researchers at Moffitt Cancer Center have revealed the mechanism that explains the transformation process of prostate cells into castration-resistant cancer cells. They've also identified a new drug candidate that targets this specific mechanism, preventing the growth and proliferation of these aggressive and deadly cancer cells. The findings were featured in an article titled “ACK1/TNK2 Regulates Histone H4 Tyr88-phosphorylation and AR Gene Expression in Castration-Resistant Prostate Cancer,” published in the journal Cancer Cell. Researchers have known for years that male hormones, called androgens, and their receptor-driven signals are essential for the development of prostate cancer. Therefore, the first line of treatment in most advanced prostate cancer cases are drugs that reduce the activity of androgens, such as Astellas Pharma’s Xtandi (enzalutamide), or surgical removal of the testicles – where these hormones are produced. Despite the benefits provided by these therapeutic strategies, many patients develop a more aggressive type of cancer within two or three years, called metastatic castration-resistant prostate cancer (mCRPC). It is not yet clear how cancer cells acquire this treatment resistance or how the transformation develops, making it harder to tackle. "Undoubtedly, the foremost reason for transient effectiveness of the androgen deprivation therapy is a poor understanding of th
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