Patients with prostate cancer are less likely to develop oesophageal adenocarcinoma: could androgens have a role in the aetiology of oesophageal adenocarcinoma?

Cooper, Sheldon C.; Croft, Stacey; Day, Rosie; Thomson, Catherine S.; Trudgill, Nigel

doi:10.1007/s10552-009-9359-2

Cited by 26 publications

(27 citation statements)

References 23 publications

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“…However, a putative molecular basis for androgens contributing to the oncogenesis of EAC has been reported [9][10][11], and more recently, we reported epidemiological evidence of a reduced incidence of EAC following PC [14], a condition frequently treated with anti-androgen therapy [15]. In our previous study, we could not identify a latency effect that would support the hypothesis that androgens play a role in the etiology of EAC, but postulated that the lack of an effect was likely to be due to a relative lack of power to demonstrate it [14].…”

Section: Black Malesmentioning

confidence: 94%

“…We have previously investigated the hypothesis that androgens may contribute to the etiology of EAC by identifying subjects with a first primary of prostate cancer, an androgen-sensitive tumor [12] with a long natural history (5 year survival of over 70 % for those presenting without metastases [13]), in the West Midlands Cancer Intelligence Unit registry (UK) and examining the risk of developing a second cancer of the esophagus, compared with the general population [14]. The study identified a reduced risk of developing EAC following prostate cancer (PC), but not esophageal squamous cell carcinoma (ESCC).…”

Section: Introductionmentioning

confidence: 99%

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Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database

Cooper

Trudgill

2012

Cancer Causes Control

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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 [SIR0.83 (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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Section: Black Malesmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database

Cooper

Trudgill

2012

Cancer Causes Control

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“…The rapid rise in the incidence of oesophageal adenocarcinoma in Western societies during recent decades (Brown et al , 2008) has been especially pronounced in men (Vizcaino et al , 2002). Epidemiological studies evaluating the hypothesis that sex hormones have a role, including hormonal replacement therapy (Lindblad et al , 2006) and reproductive factors (Lagergren and Jansson, 2005), have not provided support for oestrogen as an aetiological factor, whereas reports on anti-androgen therapy have shown mixed results (Lagergren and Nyren, 1998; Cooper et al , 2009). Furthermore, there seem to be no clear sex differences in the strength of the associations between known risk factors and risk of oesophageal adenocarcinoma (Hampel et al , 2005; Lindblad et al , 2005; Kubo and Corley, 2006).…”

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confidence: 99%

Sex-specific exposure prevalence of established risk factors for oesophageal adenocarcinoma

Rutegård

Nordenstedt

et al. 2010

Br J Cancer

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Background:There is an unexplained male predominance in the incidence of oesophageal adenocarcinoma, and the sex-specific distribution of its risk factors in the general population is not known.Methods:A random sample of Swedish citizens aged 40–79 years completed a questionnaire for assessment of the prevalence of five risk factors for oesophageal adenocarcinoma: reflux symptoms, body mass index, tobacco smoking habits, socioeconomic status, and use of non-steroidal anti-inflammatory drugs (NSAIDs). Logistic regression was used to calculate odds ratios (ORs) with 95% confidence intervals (CIs) to evaluate the association of these risk factors, separately and combined, with male sex, with women as reference.Results:Among 6969 invited people, 4906 (70.4%) completed the questionnaire. Adjusted prevalence estimates showed a negative association with male sex with regard to reflux disease (OR=0.70, 95% CI=0.58–0.84), whereas overweight (OR=1.98, 95% CI=1.72–2.27) and obesity (OR=1.22, 95% CI=1.01–1.47), previous smoking (OR=1.50, 95% CI=1.30–1.72), and no NSAID use (OR=1.35, 95% CI=1.15–1.49) were positively associated.Conclusions:Exposure to some but not all established risk factors for oesophageal adenocarcinoma seems to be more common in men than in women, but the differences are small and unlikely to explain the male predominance of this tumour.

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“…Individuals diagnosed with prostate cancer, who often receive some form of androgen deprivation therapy which severely reduces testosterone and DHT levels, have shown reduced risks of esophageal adenocarcinoma with standardized incidence ratios (SIR) of 0.83 (p<0.05) in a US population 29 and 0.70 (p<0.05) in a UK population 30 .…”

Section: Discussionmentioning

confidence: 99%

Association Between Circulating Levels of Sex Steroid Hormones and Barrett’s Esophagus in Men: A Case–Control Analysis

Cook

Wood

Cash

et al. 2015

Clinical Gastroenterology and Hepatology

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Background & Aims Esophageal adenocarcinoma is believed to result from the progression of gastroesophageal reflux disease to erosive esophagitis and re-epithelialization of the esophagus with a columnar cell population termed Barrett's esophagus (BE). Men develop BE and esophageal adenocarcinoma more frequently than women, and the ratio is increasing; approximately 7 men are diagnosed with malignancy for every woman, yet little is known about the mechanisms of this difference. We assessed whether sex steroid hormones were associated with BE in a male population. Methods We analyzed data from the Barrett's Esophagus Early Detection Case Control Study, based at the Walter Reed National Military Medical Center. Blood samples were collected from 173 men with BE and 213 men without BE (controls, based on endoscopic analysis); 13 sex steroid hormones were measured by mass spectrometry and sex hormone binding globulin was measured by ELISA. We also calculated free estradiol, free testosterone and free dihydrotestosterone (DHT). We used multivariable logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for age, race, smoking status, alcohol consumption, body mass index (BMI; kg/m2), heartburn, regurgitation, and gastroesophageal symptom score (excluding heartburn and regurgitation). Results Levels of free testosterone and free DHT were positively associated with BE risk; patients in the highest quartile for these hormones were most likely to have BE (for free testosterone, OR=5.36; 95% CI, 2.21–13.03; P=0.0002 and for free DHT, OR=4.25, 95% CI, 1.87–9.66; P=.001). Level of estrone sulfate was inversely associated with BE risk (P for trend=.02). No other hormone was associated with BE risk. Relationships were not modified by age or BMI. Conclusions In an analysis of men, levels of free testosterone and free DHT were significantly associated with risk of BE.

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Patients with prostate cancer are less likely to develop oesophageal adenocarcinoma: could androgens have a role in the aetiology of oesophageal adenocarcinoma?

Cited by 26 publications

References 23 publications

Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database

Subjects with prostate cancer are less likely to develop esophageal cancer: analysis of SEER 9 registries database

Sex-specific exposure prevalence of established risk factors for oesophageal adenocarcinoma

Association Between Circulating Levels of Sex Steroid Hormones and Barrett’s Esophagus in Men: A Case–Control Analysis

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