Low-dose aspirin confers no survival benefit in oesophageal or gastric cancer
Use of low-dose aspirin does not appear to positively influence survival of patients with oesophageal or gastric cancer, a study from UK has found.
The study analysed two large independent cohorts of oesophageal or gastric cancer patients identified from the English and Scottish cancer registries. Low-dose aspirin prescription data were obtained from linkages to the United Kingdom Clinical Research Practice Datalink in England and the Prescribing Information System in Scotland. On the other hand, data on deaths were acquired from linkage to national mortality records.
Pooled data comprised 4,654 oesophageal cancer patients and 3,833 gastric cancer patients, with 3,240 and 2,392 cancer-specific deaths, respectively. The proportions of patients surviving 1 year, based upon cancer-specific mortality, did not significantly differ between aspirin users and nonusers following diagnosis of oesophageal cancer (48 vs 50 percent in England and 49 vs 46 percent in Scotland, respectively) or gastric cancer (58 vs 57 percent in England and 59 vs 55 percent in Scotland, respectively).
Time-dependent Cox regression models showed no association between postdiagnosis exposure to low-dose aspirin and cancer-specific mortality among patients with oesophageal cancer (pooled adjusted hazard ratio [aHR], 0.98; 95 percent CI, 0.89 to 1.09) or gastric cancer (pooled aHR, 0.96; 0.85 to 1.08).
Furthermore, long-term aspirin use was not related to cancer-specific mortality after diagnosis of oesophageal cancer (pooled aHR, 1.03; 0.85 to 1.25) or gastric cancer (pooled aHR, 1.06; 0.85 to 1.32).
While unknown, the mechanism responsible for the effect of aspirin on cancer may involve the reduction in prostanoid generation by irreversible inhibition of platelet COX-1 (cyclooxygenase-1) and COX-2 isozymes. This is in light of evidence suggesting that activated platelets release several growth factors that impact on tumour progression and metastasis. Low-dose aspirin (75 to 100 mg/day) is believed to induce maximum platelet inactivation by COX-1, with over 95 percent of platelet activity being inhibited for up to 24 hours. [Br J Cancer 2017;116:405–413]