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Gene analysis

Overweight prostate fat creates ideal environment for cancer

Excess fat in men can lead to conditions in the fat surrounding the prostate ideal for cancer growth. Photo: Flickr / colros
Periprostate fat affects expression of genes, potentially leading to cancer progression

Excess adiposity affects the expression of genes in the fatty tissue surrounding the prostate, creating an environment favourable to cancer progression, according to a new study.

The study, “Obesity and prostate cancer: gene expression signature of human periprostatic adipose tissue”, which claims to be the first to use microarrays to analyse cancer-related gene expression changes in human overweight and obese periprostate adipose tissue, found that the fatty tissue surrounding the prostate demonstrated altered gene expressions in overweight and obese men that could promote cancer growth, including anti-lipolytic, anti-apoptotic, proliferative, and mild local immunoinflammatory stimuli.

In overweight and obese patients with prostate cancer, wrote the authors, the altered gene expression leads to hypercellularity and reduced immunosurveillance, which would provide an environment amenable to the growth of cancer.

Overweight and obese men in the study had significantly increased levels of activity in some genes, including LEP, which encodes leptin; ANGPT1, which encodes Angiopoietin 1, a protein growth factor involved in blood vessel development; and FADS1, which helps regulates the desaturation of fatty acids (see figure 1, below).

Figure 1: changes in gene expression between lean and overweight/obese men. Taken from "Obesity and prostate cancer: gene expression signature of human periprostatic adipose tissue".

Professor Gema Frühbeck,  co-author of the study, said, “Both LEP and ANGPT1 encode proteins which are thought to have roles beyond adipose tissue itself, especially because prostate cancer cells have receptors for leptin, and angiopoietin 1. Taken together with the abnormal activity levels of other genes they will ultimately foster fat mass growth, reduce immune surveillance, and promote the formation of new blood vessels, so producing a favorable environment for prostate cancer progression.”

The study also found that the activity of other genes was altered between hyperplasia and prostate cancer, and between cancers confined to the prostate and those that spread into the surrounding fat, suggesting a gradual increase in dysregulation during cancer progression.

The study, by Dr Ricardo Ribeiro, Professor Frühbeck, et al, has been published in BioMed Central.


The investigators selected 18 patients for the study, divided into three groups based on their post-surgical diagnosis. Six patients had benign prostatic hyperplasia; the remaining 12 were divided into two groups of six, made up of those with organ-confined prostate cancer, and those with extra-prostatic prostate cancer.

Each group contained three lean patients, with a BMI under 25, and three obese or overweight patients, with a BMI exceeding 25.

The investigators extracted RNA from periprostate tissue, and analysed the difference in preponderance of a number of genes using Affymetrix GeneChip arrays.

A significant difference in expression of a gene from base levels was defined as P<0.001, and an absolute change of 1.5-fold or greater.

“In an increasingly obese population, understanding how fat, especially the fat surrounding the prostate, can influence the growth and severity of prostate cancer may provide an opportunity for implementing personalized lifestyle and therapeutic strategies,” said Ribeiro.

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