No abstract

Oesophageal and gastric adenocarcinoma share an unexplained male predominance, which would be explained by the hypothesis that oestrogens are protective in this respect. We carried out a nested case -control study of hormone replacement therapy (HRT) among 299 women with oesophageal cancer, 313 with gastric cancer, and 3191 randomly selected control women, frequency matched by age and calendar year in the General Practitioners Research Database in the United Kingdom. Data were adjusted for age, calendar year, tobacco smoking, alcohol consumption, body mass index, hysterectomy, and upper gastrointestinal disorders. Among 1 619 563 person-years of follow-up, more than 50% reduced risk of gastric adenocarcinoma was found among users of HRT compared to nonusers (odds ratio (OR), 0.48, 95% confidence interval (CI) 0.29 -0.79). This inverse association appeared to be stronger for gastric noncardia (OR 0.34, 95% CI 0.14 -0.78) and weaker for gastric cardia tumours (OR 0.68, 95% CI 0.23 -2.01). There was no association between HRT and oesophageal adenocarcinoma (OR 1.17, 95% CI 0.41 -3.32).

No abstract

In a population-based cohort study of all women aged over 50 years with breast cancer in the Swedish Cancer Register in 1961 -2003, those diagnosed before 31 December 1987 were regarded as unexposed to tamoxifen, whereas those diagnosed after that date were considered potentially exposed. Crosslinkages within the Cancer Register and the Registers of Death and Emigration enabled follow-up. Standardised incidence ratios (SIRs) of oesophageal and gastric cancer represented relative risks. Among 138 885 cohort members contributing with 1 075 724 person-years of follow-up, we found a nonsignificantly increased risk of oesophageal adenocarcinoma during the potential tamoxifen exposure period (SIR 1.60, 95% confidence interval (CI) 0.83 -3.08), but the risk estimates decreased with increasing latency interval. No association was observed during the unexposed period. No increased risk of cardia adenocarcinoma was identified in either period. The risk of non-cardia gastric adenocarcinoma was increased in the potential tamoxifen period (SIR 1.27, 1.03 -1.57), and almost doubled (SIR 1.86, 95% CI 1.10 -3.14) in the period of longest latency (10 -14 years). The corresponding overall SIR was increased in the unexposed group also, but here SIR did not increase with longer latency intervals. An increased risk of tobacco-related tumours, that is, oesophageal squamous-cell carcinoma and lung cancer, was limited to the unexposed cohort, indicating that confounding by smoking might explain the increased SIR during the unexposed period. We concluded that there might be a link between tamoxifen and risk of non-cardia gastric adenocarcinoma.

Gastric adenocarcinoma of the intestinal type is less common in women with high endogenous estrogen exposure, indicating a preventive effect of estrogen. No differences in the distribution of ERs was found between the three estrogen exposure groups. The presence of ERbeta cx in gastric cancer warrants further investigation.