This diet may drive prostate cancer development

A recent study from McGill University found that saturated fat intake induces a cellular reprogramming that is linked to prostate cancer progression.

When patients eat a high-fat diet, prostate cancer can progress faster and be deadlier.

The findings could have a clinical utility in identifying patients at higher risk of a more aggressive, lethal disease.

In addition, the study suggests that the reduction of animal fat, and specifically saturated fat intake in men with early-stage prostate cancer, could possibly diminish or delay the risk of disease progression.

The study is published in Nature Communications. One author is Dr. David P. Labbé, a scientist at the Research Institute of the McGill University Health Centre.

Some genes—called oncogenes—play a role in cancer initiation and progression. MYC is one of those.

In the study, the team showed that by mimicking an MYC overexpression, saturated fat intake makes prostate cancer worse.

MYC overexpression profoundly rewires cellular programs. It induces malignant properties in normal cells and fuels the growth of cancer cells.

The researchers stratified prostate cancer patients based on their fat intake—high-fat diet vs. low-fat diet—and the type of fat they were eating—either saturated, monounsaturated or polyunsaturated fat.

By integrating dietary and gene expression data from 319 patients, the team discovered that animal fat and specifically saturated fat consumption mimicked an MYC overexpression.

They confirmed the findings in experiments using a murine prostate cancer model.

Strikingly, patients who had the highest level of the saturated fat intake MYC signature were four times more likely to die from prostate cancer, compared to patients with the lowest level.

Since fat consumption could be linked to an increase in body fat and obesity, and since obesity is also a risk factor linked to prostate cancer, the team used the Body Mass Index (BMI) to make sure that it was only saturated fat intake—and not obesity—that promoted the progression to a metastatic and lethal disease.

The study may develop clinical tools aimed at reducing the consumption of saturated fat and increasing the odds of surviving.

The team suggests that many prostate cancer patients may benefit from therapies targeting MYC transcriptional activity or from dietary interventions targeting metabolic addictions regulated by MYC.

Knowing the dietary pattern of a patient or his level of physical activity, clinicians could eventually suggest some intervention to decrease the progression to a lethal disease.

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