There is a lot of medical evidence that obesity is linked to the growth of cancer cells. But what doctors have also noticed is that obese patients tend to respond better to anticancer drugs than other patients.
So, what could be the reason for such paradox?
A protein called PD-1 is naturally produced by our immune system to protect our cells. Tumor cells also trigger the production of this protein to protect themselves. Anticancer drugs block the activation of PD-1 so they can target and kill tumor cells.
However, very few patients seem to respond to this treatment, and another study published earlier this year showed that overweight patients had a far better response to the drugs than other patients.
William Murphy of the University of California (UC), Davis, and UC Davis oncologist Arta Monjazeb have started carrying out clinical observations on overweight mice, monkeys and humans. They noticed that, although their T-cells (our immune sentinels) are too “exhausted” to trigger immune system helpers, their bodies also produce an excess of leptin, a hormone made by fat cells that signals our brains that we have already had enough to eat. Leptin also affects the immune system and may trigger the production of PD-1 on T-cells.
Dr. Murphy’s team suspect that, while obesity is linked to the formation of cancer cells, it may surprisingly be a “benefit” to cancer treatment. Leptin makes T-cells “unusually responsive” to anticancer drugs, says Harvard University immunologist Lydia Lynch.
However, this study does not support the fact that obesity can prevent or fight cancer cells. The researchers warn that it is too early to predict that treatments that use a high-fat diet could mimic some effects of obesity to boost a response to PD-1 inhibitors in cancer patients.
MD Anderson melanoma researcher Jennifer McQuade, lead author on The Lancet Oncology study, says “Ultimately, we need an integrative analysis to understand the contributions of body mass index (BMI), sex, age, and how these interact with each other.”
This post is an excerpt of the original article published in Science by Jocelyn Kaiser on