BACKGROUND: The incidence of esophageal and gastric cardia adenocarcinoma is, for unknown reasons, increasing dramatically. A weak and inconsistent association between body mass index (BMI) and adenocarcinoma of the esophagus and gastric cardia has been reported. OBJECTIVE: To reexamine the association between BMI and development of adenocarcinoma of the esophagus and gastric cardia. DESIGN: Nationwide, population-based case-control study. SETTING: Sweden, 1995 through 1997. PATIENTS: Patients younger than 80 years of age who had recently received a diagnosis were eligible. Comprehensive organization ensured rapid case ascertainment. Controls were randomly selected from the continuously updated population register. Interviews were conducted with 189 patients with adenocarcinoma of the esophagus and 262 patients with adenocarcinoma of the gastric cardia; for comparison, 167 patients with incident esophageal squamous-cell carcinoma and 820 controls were also interviewed. MEASUREMENTS: Odds ratios were determined from BMI and cancer case-control status. Odds ratios estimated the relative risk for the two adenocarcinomas studied and were calculated by multivariate logistic regression with adjustment for potential confounding factors. RESULTS: A strong dose-dependent relation existed between BMI and esophageal adenocarcinoma. The adjusted odds ratio was 7.6 (95% CI, 3.8 to 15.2) among persons in the highest BMI quartile compared with persons in the lowest. Obese persons (persons with a BMI > 30 kg/m2) had an odds ratio of 16.2 (CI, 6.3 to 41.4) compared with the leanest persons (persons with a BMI
BACKGROUND: The incidence of esophageal adenocarcinoma is increasing rapidly. Gastroesophageal reflux is a strong risk factor for this disease. The increase in incidence of esophageal adenocarcinoma coincided with the introduction of medications that promote reflux by relaxing the lower esophageal sphincter (LES), such as nitroglycerin, anticholinergics, beta-adrenergic agonists, aminophyllines, and benzodiazepines. OBJECTIVE: To test the possible association between use of LES-relaxing medications and risk for adenocarcinoma of the esophagus and gastric cardia. DESIGN: A nationwide population-based case-control study with in-person interviews. SETTING: Sweden, 1995 through 1997. PATIENTS: 189 patients with newly diagnosed esophageal adenocarcinoma, 262 with adenocarcinoma of the gastric cardia, and 167 with esophageal squamous-cell carcinoma were compared with 820 population-based controls. MEASUREMENTS: Estimated incidence rate ratios, calculated by using multivariate logistic regression from case-control data with adjustment for potential confounding. RESULTS: Past use of LES-relaxing drugs was positively associated with risk for esophageal adenocarcinoma. Among daily, long-term users (>5 years) of LES-relaxing drugs, the estimated incidence rate ratio was 3.8 (95% CI, 2.2 to 6.4) compared with persons who had never used these drugs. Drugs of all classes contributed to the increased risk, but the association was particularly strong for anticholinergics. Short-term use of other types of LES-relaxing drugs did not seem to be strongly associated with risk. The association almost disappeared after adjustment for reflux symptoms, indicating that promotion of reflux is the link between use of LES-relaxing drugs and esophageal adenocarcinoma. If 15,490 men in any age group take LES-relaxing drugs daily for 5 years, 1 additional case of adenocarcinoma would be expected (number needed to treat for harm); in men older than 60 years of age, the number needed to treat for harm is 5,570. Assuming a causal relation, about 10% of the esophageal adenocarcinomas occurring in the population may be attributable to intake of LES-relaxing drugs. Cardia adenocarcinoma and esophageal squamous-cell carcinoma were not associated with use of LES-relaxing drugs. CONCLUSIONS: The widespread use of LES-relaxing drugs may have contributed to the increasing incidence of esophageal adenocarcinoma.
Notes
Comment In: Ann Intern Med. 2000 Aug 1;133(3):227-910906839
A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
Notes
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Unit of Esophageal and Gastric Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, P9:03, 17176 Stockholm, Sweden. jesper.lagergren@ki.se
The aim of this study was to test the hypothesis that chewing gum is associated with risk of oesophageal and cardia adenocarcinoma. A Swedish nationwide, population-based, case-control study was conducted in 1995-1997. All patients were prospectively and uniformly documented and classified shortly after diagnosis. In all, 189 and 262 patients with oesophageal and cardia adenocarcinoma, respectively, and 820 population-based control subjects were interviewed. These patients together constituted 85% of eligible cases occurring in Sweden. Odds ratios (OR) with 95% confidence intervals (CI) were calculated by multivariable logistic regression with adjustment for plausible confounders. Regular users of chewing gum (P3 times/week for P6 months) were not at increased risk of oesophageal adenocarcinoma (OR 1.0, 95% CI 0.6-2.2), and no duration-response relation was observed (P = 0.38). No association between regular gum chewing and cardia adenocarcinoma was found (OR 1.0, 95% CI 0.6-1.7), irrespective of duration of use (P = 0.56). In conclusion, with regard to risk of oesophageal or cardia adenocarcinoma, gum chewing seems harmless.
Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 580, 69120, Heidelberg, Germany. m.mousavi@dkfz.de
The observed increased risks of gastric cancer among first-generation immigrants compared to those in Swedes suggest the role of childhood environmental exposure in the risk of this disease.
The association between exposure to ETS and the risk of lung cancer in life-time non-smoking women was investigated by means of a hospital based case-control study in Moscow, Russia. The main importance of our study is that it was conducted on a population with a specific smoking pattern from which no information is available on health effects of ETS. A total of 189 incident cases of histologically confirmed lung cancer were identified in 2 principal cancer treatment hospitals in Moscow. A total of 358 female oncology patients from the same hospitals were selected as controls. The controls matched by the hospitals to the cases were similarly restricted to never-smokers. Women diagnosed with cancer of the upper respiratory organs were ineligible for selection as controls. Personal interviews of cases and controls were conducted in the hospital wards, using a closed-form structured questionnaire. An elevated risk of lung cancer was observed in women whose husbands smoked. The odds ratio (OR) adjusted by age and education for husband's smoking was 1.53 (95% CI, 1.06-2.21). Smoking by other members of the family, by colleague's, or by fathers in the women's childhood do not affect the risk of lung cancer. The risk is higher for women whose husbands smoke "papirosy" (OR 2.12; 95% CI, 1.32-3.40), a special Russian type of cigarettes with a long mouthpiece, and usually very high levels of tar (> 30 mg/cig) and nicotine (> 1.8 mg/cig). Our study suggests that the association between exposure to ETS of the spouse and risk of lung cancer in non-smoking women is somewhat stronger for squamous-cell carcinoma (OR, 1.94; 95% CI, 0.99-3.81) than for adenocarcinoma (OR, 1.52; 95% CI, 0.96-2.39).
The impact of inflammatory bowel disease (IBD) on colorectal cancer (CRC) prognosis, taking into account other comorbidities, is not clear. We studied the overall mortality in CRC patients with a history of ulcerative colitis (UC) or Crohn's disease (CD) compared with non-IBD-CRC patients.
Data on all CRC and IBD patients diagnosed with CRC between 1977 and 2009 were retrieved from Danish medical registries. One-year and 5-year overall mortality were evaluated with the Kaplan-Meier method and with Cox regression, adjusting for year of CRC diagnosis, sex, Duke's stage, age at CRC diagnosis, and Charlson Comorbidity Index score.
We identified 653 CRC patients diagnosed with UC, 238 patients with CD, and 107,024 CRC patients without IBD. The patients with IBD were younger at diagnosis than patients without IBD. The Duke's stage distribution was similar for UC-CRC patients and non-IBD-CRC patients. The CD-CRC patients had a lower frequency of Duke's A and B stage tumors (36% versus 42%), a higher frequency of Duke's C stage tumors (31% versus 27%) and Duke's D-stage tumors (23% versus 21%), and a similar frequency of unknown stage tumors (10%) compared with non-IBD-CRC patients. After 5-years of follow-up, 59% of the UC and the non-UC-CRC patients had died compared with 62% of the patients with CD and 56% of the non-CD-CRC patients. The 5-year adjusted mortality rate ratios for patients with UC or CD were 1.14 (95% confidence interval, 1.03-1.27) and 1.26 (95% confidence interval, 1.07-1.49), respectively, compared with patients without IBD.
A history of IBD in patients with CRC may be associated with increased mortality.
Little is known about genetic risk factors for colorectal cancer. We assessed the association between polymorphisms in two genes involved in DNA repair of oxidative stress, GPX and OGG1, and risk of colorectal carcinoma or adenomas. We studied 166 cases with adenocarcinoma, 974 with adenomas and 397 controls recruited from the Norwegian cohort NORCCAP. No associations were found between the polymorphism GPX Pro198Leu and risk of colorectal adenomas or carcinomas. Carriers of the variant allele OGG1 Ser326Cys polymorphism had a lowered risk of colorectal cancer, OR=0.56 (95% confidence interval 0.33-0.95), while no association were found with risk of adenomas. This indicates that a low repair capacity of oxidative DNA damage may not be a risk factor for development of colorectal adenomas or carcinoma.
The importance of genetic factors in the etiology of esophageal cancer is uncertain. We addressed the question of heredity in a population-based, nationwide case-control study conducted in Sweden during 1995 through 1997. The study involved 189 patients with esophageal adenocarcinoma, 262 with cardia adenocarcinoma, 167 with esophageal squamous cell carcinoma, and, for comparison, 820 control subjects. Familial occurrence of cancer was explored at face-to-face interviews. Logistic regression, with multivariate adjustment for potential confounders, was used to calculate odds ratios (ORs), which estimated relative risk. Occurrence of esophageal cancer among first-degree relatives did not increase the risk of adenocarcinoma or squamous cell carcinoma of the esophagus. Neither were there any significant associations with familial occurrence of gastric cancer or other gastrointestinal tumors. The risk of cardia adenocarcinoma was moderately increased among persons with first-degree relatives with gastric cancer (OR, 1.6; 95% confidence interval, 1.0-2.6). Familial occurrence of any cancer was not associated with increased risks of any of the three studied tumors. In conclusion, heredity does not seem to contribute importantly to the occurrence of esophageal cancer of any histological type. A weak association between familial gastric cancer and the risk of cardia cancer may represent a genetic link.
