Cancer risk factors, such as obesity, inflammation, and diabetes, have been associated with carcinogenesis by a wide variety of molecular mechanisms; however, ecological, evolutionary and microenvironment-centered mechanisms are under- explored. A common theme underlying these risk factors is the creation of resource oversupply. We propose normal physiology restricts resource availability to a bare maintenance level, limiting proliferation. Furthermore, we conjecture that lifting this restriction allows for abnormal proliferation and creates a selective pressure for cancer-associated phenotypes, accelerating carcinogenesis. This evolutionary mechanism suggests generalizable treatment and prevention strategies.
We built an agent-based model of tissue, and simulated the development of cancer under various resource access conditions. We found that resource oversupply significantly expedites clonal expansion and metastasis.
This research was published in 2019 in Evolutionary Medicine and Public Health, and can be found here.
Here's a poster we presented on the work.
