Obesity is a known risk factor for breast and other cancers, but knowledge about the underlying biology of how, when and by what mechanism obesity influences cancer risk is limited.

New research from The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) offers some of the first evidence that obesity alters in genes involved in inflammatory response (32 genes), hereditary disorders (48 genes) and other immunological diseases (42 genes).

Researchers presented their findings at the American Association for Cancer Research (AACR) 2017 Annual Meeting.

A multidisciplinary team made of geneticists, cell biologists, medical oncologists and epidemiologists conducted a broad spectrum gene expression analysis of tissue samples from 121 healthy women with no history of breast cancer. All women were undergoing breast reduction surgery and 51 patients were clinically obese.

The team integrated DNA methylation and mRNA expression into the analysis to identify 308 genes important in the obesity/inflammation relationship. Of these, 240 were shown to have high DNA methylation (more likely to have sporadic mutations), low gene expression in obese women and 68 gene has low DNA methylation, high gene expression status. All of the affected genes were involved in diseases and disorders for inflammatory response, hereditary disorder and immunological disease.

“Different types of breast cancer could be affected differently by obesity, A more robust understanding of how obesity triggers inflammatory cancer pathways and increases breast cancer risk could help us develop better chemoprevention strategies or early prevention strategies in women at increased risk based on their weight,” says Peter Shields, MD, senior author of the AACR abstract and deputy director of the OSUCCC – James.

Future studies would be designed to understand the specific genes identified in this study among women who ultimately develop breast cancer later.