2ⁿᵈ Edition of the Cancer R&D World Conference 2026

Abstract

Breast cancer, the second most common cancer among U.S. women, primarily arises in breast epithelial cells. Genetic and epigenetic factors contribute to the development of cancer, with BRCA mutations significantly increasing risk. DNA methylation, an epigenetic mechanism, regulates breast cancer associated genes expression, and aberrant methylation is linked to aging, chronic inflammation, and mutations. Chronic inflammation plays a crucial role in cancer development and is possibly present, often unnoticed, in up to 15% of lactating women. Chronic inflammation can alter DNA methylation patterns and can affect tumor suppressor/promoter gene expression. Investigating factors that trigger early aberrant DNA methylation, specifically chronic inflammation (that is usually associated with increased levels of cytokines), could lead to prevention of these aberrant patterns. My research examines the extent that chronic inflammation alters DNA methylation in breast cells. Specifically, I assess if prolonged exposure to physiologically relevant cytokine levels, mimicking chronic inflammation, alters DNA methylation in human breast epithelial cells in a pattern associated with increased risk of breast cancer. To test this, I exposed two immortalized human mammary epithelial cell lines, MCF-10A and BRCA1-mutated MCF-10A, to a cytokine cocktail for 30-weeks. Significant alterations in DNA methylation associated with increased risk were observed after treatment.