Abstract
In human populations, aspirin has emerged as the agent with the most consistently observed chemopreventive effect on cancer, particularly of the colorectum. Remarkably consistent data demonstrating aspirin's efficacy have accumulated from prospective studies and randomized controlled trials conducted for the prevention of polyp recurrence, hereditary colorectal cancer, cardiovascular disease, and overall cancer. In addition, there are now convincing data supporting an association between aspirin use and lower risk of metastases and improved survival among colorectal cancer patients. This substantial evidence base has stimulated interest in the molecular underpinnings of aspirin's mode of action. Although a complete understanding of aspirin's anti-cancer mechanism remains elusive, several interrelated biological pathways have been uncovered which appear to, at least in part, mediate aspirin's effect on both tumor initiation and progression. These include fundamental pathways of prostaglandin synthesis and Wnt signaling, offering additional molecular targets for chemopreventive intervention that may enhance aspirin's effectiveness and/or reduce its associated toxicities. In this presentation, we will provide an update on investigation into the mechanistic basis of the effect of aspirin on cancer with a focus on potential molecularly-targeted strategies for combinatorial chemoprevention.
Citation Format: Andrew T. Chan. Exploiting aspirin's mechanism of action for combination chemoprevention. [abstract]. In: Proceedings of the Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2014 Sep 27-Oct 1; New Orleans, LA. Philadelphia (PA): AACR; Can Prev Res 2015;8(10 Suppl): Abstract nr CN05-02.
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