Experience probably tells you that cancer patients with obesity/metabolic dysfunction don’t respond as well to cancer treatment as those without obesity/metabolic dysfunction. But do you know why — and what you can do about it? Find out what our experts have to say about this challenging patient population.
Cancer patients with obesity/metabolic dysfunction have a unique tumor phenotype due to their metabolic condition as well as distinct alterations in their immune system and tumor microenvironment. Research in this nascent field is developing a clearer understanding of the pathophysiology and etiology of metabo-oncology.
Let’s say you have a patient who is over the target BMI. It would be great if you could say, “Here’s a medication you can take to address that, and here’s an exercise program that comes with it, and it has an app. We believe this will improve your response to therapy and your chance of survival, or at least your well-being.” That would be enormously appealing.
When we published recommendations on exercise oncology in 2010, we were trying to put the oncology world on notice that “rest, take it easy, don’t push yourself” is dead. Doctors need to be prescribing exercise for their patients during and after their treatment.
While the tumor-centric approach — where cancer prevention and cancer treatments are directed at the biology of the tumor itself — has been successful, we’re learning we can enhance this success by also focusing on the person as a whole and on what’s going on around the tumor. This is where metabo-oncology really becomes important, because the metabolic state of a person as a whole contributes quite a bit to how tumors develop and behave.
This is a global issue we’re dealing with. The epidemic of obesity, of excess adiposity, is here to stay. Therefore, finding strategies to alter tumor growth in those with excess adiposity is very important.
…insulin signaling can be seen as enabling tumor development by providing a mechanism for PI3K activation and enhanced glucose uptake. This idea is supported by studies showing enhanced tumor development in humans and mice with hyperinsulinemia, and reduced tumor development in states of reduced insulin levels.