We recently reported that frequent low-dose intake of aspirin reduces the risk of developing colorectal and bile duct cancers (read it here). Now a new study from Norway shows that taking aspirin after cancer diagnosis improves survival of people diagnosed with colorectal cancer. In a collaboration between the Cancer Registry of Norway, the Norwegian Institute of Public Health, Oslo University Hospital, and University of Oslo, researchers analyzed nearly the entire population of Norway between 2004 and 2011 with a focus on colorectal cancer patients. Through the Cancer Registry of Norway, researchers had access to the complete medical history of colorectal cancer patients in the 5 million population, and could track which patients took aspirin and at what dose.
They found that patients who, in addition to the prescribed colorectal cancer treatment, took enteric-coated (to protect the stomach) aspirin at a daily dose of as little as 75 mg within a month of diagnosis, had better survival at 1, 2, and 3 years post-diagnosis. The survival advantage conferred by aspirin was less evident past the 3-year period. However, the group of patients who took aspirin were on average 74 year-old at diagnosis and suffered of several other advanced age-related diseases. It would therefore be interesting to conduct a similar study on younger patients to fully assess the long-term effectiveness of aspirin supplementation on colorectal cancer survival.
The best results were obtained in patients whose tumor was confined to the rectum, and in those whose tumor presented with a stage II, or was either moderately or poorly differentiated. Some advantage to aspirin intake was also seen in patients with a tumor localized to the right colon.
While how aspirin improves colorectal cancer patient’s survival is still unknown, one likely scenario may be through the inhibition of metastasis (cancer spreading) through an anti-platelet effect. As an anti-inflammatory drug, it is also likely that aspirin reverses an epigenetic program known to be induced by inflammation in experimental colorectal cancer mouse models and in patients. This epigenetic program affects DNA methylation and leads to the silencing of a large number of genes important for intestinal cellular differentiation (identity), thus leading to poorly differentiated cells, a hallmark of poor-prognosis cancer. By reducing inflammation, aspirin may restore the epigenetic program and intestinal cellular differentiation to their original states, ipso facto reverting colorectal cancer cells to a state approaching normalcy. This would explain why aspirin improved survival most in patients with poorly differentiated colorectal tumors. Future studies will hopefully put this speculation and its implications in cancer patient’s care to the test (Cancer Epigenetics Society news; Ref: J. Clin. Oncol. 34(21):2501. doi: 10.1200/JCO.2015.65.3519).