Moving from immune phenotyping of colorectal cancer to mechanistic insights on aspirin use

Abstract

Colorectal cancer is the third most common cancer in men and women in the US, with over 95,000 new cases expected in 2016 (1). Many preclinical, epidemiological, and clinical studies have shown that regular aspirin (acetylsalicylic acid) use, even in low-doses, prevents the development of colorectal neoplasia (2-5). In 2015, the US Preventative Services Task Force acknowledged the value of low-dose aspirin in primary prevention of colorectal cancer in adults aged 50–59 years (6). Despite this wealth of evidence, how aspirin reduces colorectal cancer risk is not fully understood. Many mechanisms have been proposed, but the most commonly cited is aspirin’s inhibition of PTGS2 (COX-2), a known mediator of inflammation and immunosuppression that is overexpressed in many colorectal neoplasms (7-12).