If you lack this gene, you’re more prone to deadly prostate cancer

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Prostate Cancer If you lack this gene you're at higher risk of the cancer
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A recent study conducted by the Cleveland Clinic has revealed that men who lack the gene HSD17B4 are more likely to develop fatal and treatment-resistant prostate cancer. This is the first time a physically provable link has been established between the gene subtype and this particular cancer. The HSD17B4 gene encrypts enzymes that activate male hormones called androgens. These hormones are vital to the growth of the prostate cancer and so, inactivating them should prevent the growth of the cancer. However, these enzymes are present in large quantities in advanced prostate cancer. The therapy for this type of cancer is called the Androgen Deprivation Therapy (ADT) or chemical castration, which blocks the cell's supply of androgens. The ADT treatment may be successful early on, but it could eventually fail and allow the cancer to transition into the fatal phase called Castration-Resistant Prostate Cancer (CRPC).

These findings come after prior work on the subject showed that when a gene called HSD3B1 is altered, it enables prostate cancer to dodge treatment and spread further. Dr. Nima Sharifi, the lead researcher of the project, was quoted by Economic Times as saying, "We are hopeful that these findings will lead to more precise and effective treatments for prostate cancer. If men lack a specific isoform of this gene, we may be able to personalize their therapy."

For this study, the researchers analysed the expression of HSD17B4 in the tissue of patients having healthy prostates, along with those with localized prostate cancer and those with CRPC. They found that the expression levels of the gene were almost the same in the benign and local prostate cancer tissue. But they were a lot less in the CRPC tissue.

These findings suggest that not only does HSD17B4 have a role in preventing CRPC but that only one specific isoform - isoform 2 - was capable of inactivating androgens, and thus prevent tumor growth.


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