Abstract B68: Contributions of STAT3 to pro-tumorigenic alterations within the microenvironment during mammary tumorigenesis

Inflammation has long been recognized as a possible trigger that contributes to tumor initiation. Numerous studies have shown that cells of both the innate and adaptive immune systems are able to support tumor formation and growth through secretion of growth factors and cytokines and by actively shielding the tumor from wider immune surveillance. As a result, inflammation is generally linked to worse patient outcome. However, depending on factors such as tumor size, extracellular matrix, and the complex composition of immune cell infiltrates, inflammation can promote both pro- and anti-tumor properties. Our studies focus on identifying novel mechanisms through which tumor-derived cytokines act in a paracrine manner to regulate the functions of infiltrating inflammatory cells in the tumor microenvironment. We have previously shown that activation of the fibroblast growth factor receptor-1 (FGFR1) oncogene results in the production of high levels of interleukin 6 (IL-6) family members by mammary epithelial cells. Histological examination of FGFR1-driven tumors revealed high levels of STAT3 activation in both tumor cells and macrophages. Thus, further studies focused on identifying mechanisms through which STAT3 activation in different cellular compartments contributes to mammary tumor growth. Initial studies focused on the consequences of STAT3 activation in epithelial/tumor cells. We found that epithelial cell STAT3 activation resulted in accumulation of the extracellular matr...
Source: Molecular Cancer Research - Category: Cancer & Oncology Authors: Tags: Tumor Microenvironment and Immunotherapy: Poster Presentations - Proffered Abstracts Source Type: research