TGF-β’s role in Immune Evasion of Colorectal Cancer and Anti-TGF-β Therapies

Abstract

Colon cancer is a cancer that begins in the large intestine, or colon. When detected early, colon cancer will often begin as benign polyps in the color that over time, turn malignant. These tumors begin in the mucosa of the color and work out to the outermost layer of sub serosa and serosa. As of recent research, no mutations have been correlated with aggressive, metastatic cancer. However, the tumor microenvironment of aggressive subtypes of Colon cancer have been discovered to have elevated TGFβ levels. Due to TGF-B’s role in promotin immunosuppression, angiogenesis, metastasis, and tumor cell epithelial-to mesenchymal transitions (EMT)², TGF-B serves as a theoretically good target for anti-cancer pharmaceuticals. However, preclinical studies in-vitro and in-vivo employing animal models are exhibiting drastically different results when compared to the current clinical study. This begs the question, are we overlooking key features of TGF-B in human models that lead to poor results in clinical trials? This question will be examined in this microreview.