Interplay between inflammatory and estrogen signaling in breast cancer

Abstract Inflammation is known to have a paradoxical effect in cancers, in some cases promoting pathogenesis while in others inhibiting pathogenesis, depending on the cellular context. In an effort to answer a number of fundamental questions about two of the major signaling cascades that affect breast tumorigenesis and impact clinical outcome, we examined the genome-wide consequences of treating ERα-positive breast cancer cells with both estrogen and TNFα. Below, we highlight our observations, their biological significance, and how they provide a framework for understanding the molecular basis for integration of proinflammatory and estrogen signaling in breast cancer.