We are analyzing https://link.springer.com/article/10.1007/s10552-012-9950-9.

Title:
Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database | Cancer Causes & Control
Description:
Esophageal adenocarcinoma (EAC) is five times more common among men. EAC tissue exhibits an increased concentration of androgen receptors. We previously reported lower EAC incidence following prostate cancer (PC), suggesting androgen deprivation therapy may reduce EAC incidence, but were unable to demonstrate reducing incidence of EAC with time (latency effect) that would support a cumulative effect of anti-androgen treatment. The Survival Epidemiology and End Results (SEER9) dataset from 1977–2004 was therefore examined to identify subjects with a first malignant primary of PC. Subjects were followed until second primary cancer diagnosis, death, or time period end. Age- and period-adjusted standardized incidence ratios (SIR) were calculated as an estimate of relative risk of an esophageal second malignant primary. Between 1977 and 2004, 343,538 subjects (following exclusion criteria) developed PC as a first primary malignant tumor, providing 2,014,337 years of follow-up. Subsequently 604 esophageal cancers developed, with 763 expected. The incidence of EAC fell following PC [SIR 0.83 (95 % CI 0.74–0.93)] with a latency effect identified with SIR 1.1 3 months to 1 year post-PC, SIR 0.85 1–5 years post-PC, and SIR 0.75 greater than five years post-PC. The incidence of esophageal squamous cell carcinoma (ESCC) after PC was also reduced [SIR, 0.79 (0.69−0.89)], with evidence of a latency effect also seen. There is a reduced risk of developing esophageal cancer, both EAC and ESCC, following PC. Androgen deprivation therapy may contribute, but changes in lifestyle following PC diagnosis and decrease in ESCC incidence are also plausible explanations.
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Keywords {🔍}

cancer, google, scholar, article, pubmed, esophageal, adenocarcinoma, cas, prostate, incidence, risk, androgen, gastric, research, control, subjects, cooper, eac, squamous, cell, seer, primary, sir, cancers, carcinoma, oesophageal, cardia, privacy, cookies, content, trudgill, deprivation, diagnosis, access, trends, esophagus, prev, natl, inst, west, analysis, data, publish, search, men, therapy, effect, epidemiology, end, thomson,

Topics {✒️}

month download article/chapter prostate-specific antigen screening squamous cell carcinoma cancer research uk full article pdf develop esophageal cancer developing esophageal cancer esophageal cancer trends privacy choices/manage cookies prostate cancer detection short-term hormones develop oesophageal adenocarcinoma anti-androgen therapy prostate cancer diagnosis androgen deprivation therapy sex hormones play prostate cancer patients oesophageal carcinoma primary cancer diagnosis european economic area scope submit manuscript check access fraumeni jf jr population attributable risks androgen receptor expression bianco fj jr african-american race pre-biopsy nomogram sandwell general hospital instant access article cancer conditions privacy policy demonstrate reducing incidence dataset time period end primary malignant tumor symptomatic gastroesophageal reflux population based cohort comparative epidemiological characteristics national practice patterns statistical methodology programming cancer research esophageal cancer eac tissue exhibits accepting optional cookies esophageal adenocarcinoma anti-androgen treatment vaughan tl iarc scientific publication 1 year post-pc

Questions {❓}

Brower V (2009) Long- or short-term hormones for locally advanced prostate cancer?
Lagergren J, Nyren O (1998) Do sex hormones play a role in the etiology of esophageal adenocarcinoma?

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         headline:Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database
         description:Esophageal adenocarcinoma (EAC) is five times more common among men. EAC tissue exhibits an increased concentration of androgen receptors. We previously reported lower EAC incidence following prostate cancer (PC), suggesting androgen deprivation therapy may reduce EAC incidence, but were unable to demonstrate reducing incidence of EAC with time (latency effect) that would support a cumulative effect of anti-androgen treatment. The Survival Epidemiology and End Results (SEER9) dataset from 1977–2004 was therefore examined to identify subjects with a first malignant primary of PC. Subjects were followed until second primary cancer diagnosis, death, or time period end. Age- and period-adjusted standardized incidence ratios (SIR) were calculated as an estimate of relative risk of an esophageal second malignant primary. Between 1977 and 2004, 343,538 subjects (following exclusion criteria) developed PC as a first primary malignant tumor, providing 2,014,337 years of follow-up. Subsequently 604 esophageal cancers developed, with 763 expected. The incidence of EAC fell following PC [SIR 0.83 (95 % CI 0.74–0.93)] with a latency effect identified with SIR 1.1 3 months to 1 year post-PC, SIR 0.85 1–5 years post-PC, and SIR 0.75 greater than five years post-PC. The incidence of esophageal squamous cell carcinoma (ESCC) after PC was also reduced [SIR, 0.79 (0.69−0.89)], with evidence of a latency effect also seen. There is a reduced risk of developing esophageal cancer, both EAC and ESCC, following PC. Androgen deprivation therapy may contribute, but changes in lifestyle following PC diagnosis and decrease in ESCC incidence are also plausible explanations.
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      description:Esophageal adenocarcinoma (EAC) is five times more common among men. EAC tissue exhibits an increased concentration of androgen receptors. We previously reported lower EAC incidence following prostate cancer (PC), suggesting androgen deprivation therapy may reduce EAC incidence, but were unable to demonstrate reducing incidence of EAC with time (latency effect) that would support a cumulative effect of anti-androgen treatment. The Survival Epidemiology and End Results (SEER9) dataset from 1977–2004 was therefore examined to identify subjects with a first malignant primary of PC. Subjects were followed until second primary cancer diagnosis, death, or time period end. Age- and period-adjusted standardized incidence ratios (SIR) were calculated as an estimate of relative risk of an esophageal second malignant primary. Between 1977 and 2004, 343,538 subjects (following exclusion criteria) developed PC as a first primary malignant tumor, providing 2,014,337 years of follow-up. Subsequently 604 esophageal cancers developed, with 763 expected. The incidence of EAC fell following PC [SIR 0.83 (95 % CI 0.74–0.93)] with a latency effect identified with SIR 1.1 3 months to 1 year post-PC, SIR 0.85 1–5 years post-PC, and SIR 0.75 greater than five years post-PC. The incidence of esophageal squamous cell carcinoma (ESCC) after PC was also reduced [SIR, 0.79 (0.69−0.89)], with evidence of a latency effect also seen. There is a reduced risk of developing esophageal cancer, both EAC and ESCC, following PC. Androgen deprivation therapy may contribute, but changes in lifestyle following PC diagnosis and decrease in ESCC incidence are also plausible explanations.
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