Metabolites from a fatty diet join forces with the cancer-driving gene MYC to reprogram prostate cancer cells to grow faster, finds new study. This discovery solidifies a direct link between obesity and lethal prostate cancer.

your-questions-answeredAt the 2016 Annual American Association for Cancer Research (AACR) Conference, Giorgia Zadra, PhD, of the Harvard: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, presented results from a study that helped to clarify the relationship between obesity and prostate cancer.

The skinny? Fat increases the activity of a critical cancer-driving gene called MYC.

Cancer is a greedy disease. Tumors plunder the body’s resources – vitamins and nutrients, energy and oxygen, and vital space as tumors grow to ultimately cause lethal damage. Worst of all, cancer steals precious time away from patients and their loved ones.

It follows then, that having a high-fat diet may be like pouring fuel on the fire, by providing cancer cells with even more of the resources they need. In fact, a number of recent population studies have linked obesity and a high-fat diet with an increased risk for advanced, lethal prostate cancer, especially among African-American men. Unfortunately, the exact biological reasons behind this phenomenon have remained elusive.

Investigating this important question required the intersection of four distinct fields of study: dietary metabolism, “epigenetics” (a mechanism of gene regulation), the biology of cancer-causing genes, and public health sciences.

To develop a comprehensive understanding of how obesity and a high-fat diet promote prostate cancer progression, Zadra, who studies cancer cell metabolism, teamed up with Prostate Cancer Foundation (PCF) Young Investigator David P. Labbé, PhD, of the Harvard: Dana-Farber Cancer Institute, who studies the regulation of gene expression in healthy and malignant cells by epigenetics.  Read the full story …

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