New research suggests that aggressive prostate cancer blocker can be the key to better treatment options, saving millions. Insights from the study show that cancer evolution might help prevent treatment resistance in prostate cancer patients.

What is Prostate Cancer?

Cancer begins when cells begin to grow substantially. Cells from any part of the body can become cancer cells and spread to different areas in the body.

According to UCLA Health, prostate cancer manifests an uncontrolled growth of cells in the prostate gland.  The prostate is a walnut-sized gland located below the bladder. It cab only found in males, it in part, is responsible for the fluid that can be found with semen. 

Prostate cancer is one of the most common forms of cancer in men in the United States, second only to skin cancer. It often begins without any physical symptoms. 

There are many forms of prostate cancer, such as small cell carcinomas, transitional cell carcinomas, neuroendocrine tumors, and sarcomas. But the most common form of prostate cancer is adenocarcinomas, according to the American Cancer Society.

Despite prostate cancer, most often not developing symptoms, the causes of the cancer are still unknown. Many types of research and studies are on their way with hopes of establishing concrete evidence in the near future.

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A Breakthrough in Prostate Cancer

In a study published in the Cell Reports, cancer cells' evolution holds the key to preventing patients' treatment resistance. 

Common hormone treatment involves decreasing androgen receptor activity--responsible for binding hormones such as testosterone and transportation deep within the cell. 

Prostate cancer cells depend on such hormones, and blocking the receptors would, in turn, starve the cancer cells.

However, cancer cells can quickly adapt to the treatment and promptly change to resists hormone therapy and evolve to a more aggressive neuroendocrine subtype of prostate cancer.

The resistance occurs in up to 15% of patients. Currently, there are no established effective treatments for these potentially lethal forms of prostate cancer.

Researchers have evidence that tumor adaptation is enhanced by microRNA called miR-194. This leads to the development of neuroendocrine prostate in patients post-therapy. Successful inhibition of miR-194 may slow down and even prevent the growth of cancer cells.

The team found out that miR-194 significantly increased when androgen receptors were turned off. Evidence also suggests that miR-194 regulates genes' process, creating proteins, which allowed the cancer cells to show features of neuroendocrine cancers that resist conventional hormone therapy.

To test their hypothesis, the research team used cancer cells from a deceased patient. The findings are far from clinical trials; however, it is a significant stepping stone in overcoming prostate cancer treatment roadblocks. 


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