Gene Defects & Prostate Cancer

As you know by now, there is no shortage of methods to treat prostate cancer.  The trick is figuring out which treatment will be best suited to each individual case, as one size doesn't fit all. A molecular biology professor at the University of Tampere in Finland is driving deep into the weeds to obtain a “holistic picture” of the cancer’s mechanisms and use those mechanisms as a basis for developing new treatments.

Professor Tapio Visakorpi notes that the disease’s underlying mechanisms vary significantly from one individual to the next. In his opinion, prostate cancer treatments should be designed individually for each patient according to their personal clinical picture.

“Recent genome studies have shown that even though prostate cancer initiates in a single cell of origin, several cancer cell subpopulations with different genome types emerge as the disease progresses. This is not a single disease; several mechanisms lead to the emergence of the disease. Therefore, it’s important to identify those genome defects in each patient that occur in all cancer cells, that is, the so-called truncal mutations, and target the treatment to them,” says Visakorpi. “This requires taking multiple samples from the patient. The processing of samples also needs to be improved to make them more suitable for molecular analysis than the current methods. We’ve developed a new processing method for cancerous tissue.”

Prostate cancer growth is stimulated by androgens, or male hormones. Hormone therapy has been a popular weapon against the advanced form of the disease, but prostate cancer has been known to reactivate the androgen receptor signaling pathway during treatment.

“It was already proven back in the 1990s that one mechanism stimulating this reactivation is the amplification of the androgen receptor (AR) gene. New research has shown that glucocorticoid medication, which is often used to treat end-stage prostate cancer, can turn against the patient. This causes a mutation in the AR gene, which leads to the activation of the signaling pathway by glucocorticoids,” Visakorpi explains.

“All this indicates that we should be able to monitor the genome changes in each patient’s cancer cells, not just at the time of diagnosis but also during treatment as the disease progresses. This would allow for the tailoring of the cancer therapy at any given time throughout the progression of the disease.”