Dr. Brenner on the Link Between Breast Cancer and Obesity

Andrew J. Brenner, MD, PhD
Published: Friday, Dec 13, 2013



Andrew J. Brenner, MD, PhD, assistant professor of medicine, clinical investigator, Cancer Therapy Research Center, The University of Texas Health Science Center, discusses the link between obesity and breast cancer.

For the investigation, serum was collected from a group of patients who had survived breast cancer, Brenner says. Once collected, the serum was developed into an assay that would assess breast cancer growth.

The serum was conditioned on adipose stromal cells before looking at the impact on breast cancer cells that were ER-positive. Brenner says the findings showed that the serum collected from obese patients indicated a stimulation in proliferation within the breast cancer cells. This added proliferation was not seen in the serum of the healthy-weight patients.

It was discovered that the mechanism of this action was dependent on conversion of a testosterone to estradiol by aromatase. The aromatase activity was increased in the adipose stromal cells by the serum, Brenner says, and this was directly caused by the increases in prostaglandin E2, which was driven by the obese serum.

As a result, it was concluded that inflammation, which is a known systemic problem in obesity, was turning on aromatase activity in obese patients with breast cancer.

<<< View more from the 2013 SABCS Meeting



Andrew J. Brenner, MD, PhD, assistant professor of medicine, clinical investigator, Cancer Therapy Research Center, The University of Texas Health Science Center, discusses the link between obesity and breast cancer.

For the investigation, serum was collected from a group of patients who had survived breast cancer, Brenner says. Once collected, the serum was developed into an assay that would assess breast cancer growth.

The serum was conditioned on adipose stromal cells before looking at the impact on breast cancer cells that were ER-positive. Brenner says the findings showed that the serum collected from obese patients indicated a stimulation in proliferation within the breast cancer cells. This added proliferation was not seen in the serum of the healthy-weight patients.

It was discovered that the mechanism of this action was dependent on conversion of a testosterone to estradiol by aromatase. The aromatase activity was increased in the adipose stromal cells by the serum, Brenner says, and this was directly caused by the increases in prostaglandin E2, which was driven by the obese serum.

As a result, it was concluded that inflammation, which is a known systemic problem in obesity, was turning on aromatase activity in obese patients with breast cancer.

<<< View more from the 2013 SABCS Meeting




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