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Background: Incidence rates have risen rapidly for esophageal adenocarcinoma and moderately for gastric cardia adenocarcinoma, while rates have remained stable for esophageal squamous cell carcinoma and have declined steadily for noncardia gastric adenocarcinoma. We examined anthropometric risk factors in a population-based case-control study of esophageal and gastric cancers in Connecticut, New Jersey, and western Washington. Methods: Healthy control subjects (n = 695) and case patients with esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma (n = 589) were frequency-matched to case patients with adenocarcinomas of esophagus or gastric cardia (n = 554) by 5-year age groups, sex, and race (New Jersey only). Classification of cases by tumor site of origin and histology was determined by review of pathology materials and hospital records. Data were collected using in-person structured interviews. Associations with obesity, measured by body mass index (BMI), were estimated by odds ratios (ORs). All ORs were adjusted for geographic location, age, sex, race, cigarette smoking, and proxy response status. Results: The ORs for esophageal adenocarcinoma rose with increasing adult BMI. The magnitude of association with BMI was greater among the younger age groups and among nonsmokers. The ORs for gastric cardia adenocarcinoma rose moderately with increasing BMI. Adult BMI was not associated with risk of esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma. Conclusions: Increasing prevalence of obesity in the United States population may have contributed to the upward trends in esophageal and gastric cardia adenocarcinomas. [J Natl Cancer Inst 1998;90:150-5]

Background: The consumption of alcoholic beverages is a strong risk factor for cancers of the oral cavity and pharynx (oral cancers). Alcohol dehydrogenase type 3 ([ADH.sub.3]) metabolizes ethanol to acetaldehyde, a carcinogen. We evaluated whether individuals homozygous for the fast-metabolizing [ADH.sup.1][sub.3] allele ([ADH.sup.1-1][sub.3]) have a greater risk of developing oral cancer in the presence of alcoholic beverage consumption than those with the slow-metabolizing [ADH.sup.2][sub.3] allele ([ADH.sup.1-2][sub.3] and [ADH.sup.2-2][sub.3]). Methods: As part of a population-based study of oral cancer conducted in Puerto Rico, the [ADH.sub.3] genotypes of 137 patients with histologically confirmed oral cancer and of 146 control subjects (i.e., individuals with no history of oral cancer) were determined by molecular genetic analysis of oral epithelial cell samples. Risks were estimated by use of multiple logistic regression analyses. Results: Compared with nondrinkers with the [ADH.sup.1-1][sub.3] genotype, consumers of at least 57 alcoholic drinks per week with the [ADH.sup.1-1][sub.3], [ADH.sup.1-2][sub.3], and [ADH.sup.2-2][sub.3] genotypes had 40.1-fold (95% confidence interval [CI] = 5.4-296.0), 7.0-fold (95% CI = 1.4-35.0), and 4.4-fold (95% CI = 0.6-33.0) increased risks of oral cancer, respectively; the risk associated with the [ADH.sup.1-1][sub.3] genotype, compared with the [ADH.sup.1-2][sub.3] and [ADH.sup.2-2][sub.3] genotypes combined, was 5.3 (95% CI = 1.0-28.8) among such drinkers. Considering all levels of alcohol consumption, the risk of oral cancer per additional alcoholic drink per week increased 3.6% (95% CI = 1.9%-5.4%) for subjects with the [ADH.sup.1-1][sub.3] genotype and 2.0% (95% CI = 0.9%-3.0%) for subjects with the [ADH.sup.1-2][sub.3] or [ADH.sup.2-2][sub.3] genotype (two-sided P = .04). Conclusions: The [ADH.sup.1-1][sub.3] genotype appears to substantially increase the risk of ethanolrelated oral cancer, thus providing further evidence for the carcinogenicity of acetaldehyde. [J. Natl Cancer Inst 1997;89:1698-1705]

Background: Incidence rates for adenocarcinomas of the esophagus and gastric cardia have risen steeply over the last few decades. To determine risk factors for these tumors, we conducted a multicenter, population-based, case-control study. Methods: The study included 554 subjects newly diagnosed with esophageal or gastric cardia adenocarcinomas, 589 subjects newly diagnosed with esophageal squamous cell carcinoma or other gastric adenocarcinomas, and 695 control subjects. Estimates of risk (odds ratios [ORs] and corresponding 95% confidence intervals [CIs]) were calculated for the four tumor types separately and for esophageal and gastric cardia adenocarcinomas combined. Results: Risk of esophageal and gastric cardia adenocarcinomas combined was increased among current cigarette smokers (OR = 2.4; 95% = 1.7-3.4), with little reduction observed until 30 years after smoking cessation; this risk rose with increasing intensity and duration of smoking. Risk of these tumors was not related to beer (OR = 0.8; 95% CI = 0.6-1.1) or liquor (OR = 1.1; 95% CI = 0.8-1.4) consumption, but it was reduced for drinking wine (OR = 0.6; 95% CI = 0.5-0.8). Similar ORs were obtained for the development of noncardia gastric adenocarcinomas in relation to tobacco and alcohol use, but higher ORs were obtained for the development of esophageal squamous cell carcinomas. For all four tumor types, risks were higher among those with low income or education. Conclusions: Smoking is a major risk factor for esophageal and gastric cardia adenocarcinomas, accounting for approximately 40% of cases. Implications: Because of the long lag time before risk of these tumors is reduced among exsmokers, smoking may affect early stage carcinogenesis. The increase in smoking prevalence during the first two thirds of this century may be reflected in the rising incidence of these tumors in the past few decades among older individuals. The recent decrease in smoking may not yet have had an impact. [J Natl Cancer Inst 1997;89:1277-84]

Background: Cancer incidence rates have been reported to be increasing in the United States, although trends vary according to form of cancer. Purpose: We identify the cancers accounting for the rising incidence, quantify the changes that have occurred from the mid-1970s to the early 1990s, and contrast incidence and mortality trends to provide clues to the determinants of the temporal patterns. Methods: Sex-, race-, and age-specific and age-adjusted incidence rates for the 5-year periods 1987-1991 versus 1975-1979 were calculated for 28 cancers among men and 30 cancers among women using data from the Surveillance, Epidemiology, and End Results (SEER) Program of cancer registration covering about 10% of the U.S. population. Similar rates were computed using national mortality data. Cancers were ranked according to the change in incidence rates over the two periods. Results: Age-adjusted incidence rates for all cancers combined increased by 18.6% among males and 12.4% among females from 1975-1979 to 1987-1991, due largely to rising rates for prostate cancer among men and for breast and lung cancers among women. National mortality rates for all cancers combined rose less steeply, 3% and 6% among men and women, respectively, driven mostly by continuing increases in lung cancer mortality, while death rates for the majority of the cancers were steady or declining. Total cancer incidence rose at all ages, but with different tumors responsible for the increases at different ages: leukemia and brain/nervous system cancer among children; testicular cancer, nonmelanoma skin cancer (largely Kaposi's sarcoma), non-Hodgkin's lymphoma, and melanoma among young and middle-aged adults; and prostate, breast, and lung cancers among older individuals. In contrast, mortality rates for all cancers combined declined among both males and females under age 55 years, increasing only among older persons. Conclusions: Trends in cancer incidence and mortality differ. For most cancers, incidence rates are rising, while mortality rates are generally stable or declining. Implications: Much of the recent increase in cancer incidence can be explained by known factors. Improved action appears to account for most of the increases in breast cancer among women and prostate cancer among men. On the other hand, cigarette smoking is the major determinant of the rise in lung cancer among women, acquired immunodeficiency syndrome has led to increases in non-Hodgkin's lymphoma and Kaposi's sarcoma among young and middle-aged men, and sunlight exposure patterns have affected the trends in melanoma. Some trends remain unexplained, however, and may reflect changing exposures to carcinogens yet to be identified and clarified.

Background: Renal cell cancer, although still relatively uncommon, has been increasing in incidence in the United States and other countries around the world. Purpose: Since previous studies have suggested an association with high intake of meat, we sought to further examine the role of diet in renal cell cancer risk. Methods: Patients with histologically confirmed renal cell cancer that had been diagnosed between July 1, 1988, and December 31, 1990, were identified through the Minnesota Cancer Surveillance System, a statewide cancer registry. The patients eligible for inclusion in this study were white residents of Minnesota between 20 and 79 years of age. Control subjects were selected from the general population of Minnesota residents; subjects under age 65 were selected by use of a random-digit-dialing method and those 65 years or older were sampled from the Health Care Financing Administration riles. Population-based control subjects were frequency-matched to cases by sex and 5-year age groups. A total of 690 patients and 707 control subjects were interviewed. Patients and control subjects were similar in distribution by sex, age, and educational level. Usual adult dietary intakes were assessed by questionnaire, and odds ratios were calculated by logistic regression analyses. Results: Significantly increased risks of renal cell cancer were observed with increasing consumption of several food groups, including red meat (P for trend = .05), high-protein foods (P = .01), and staple (grains, breads, and potatoes) foods (P = .009). When examined by macronutrient status, risks increased monotonically with the amount of protein intake, from 1.2 (95% confidence interval [CI] = 0.7-1.9) to 1.4 (95% CI = 0.8-2.5) and 1.9 (95% CI = 1.0-3.6) (P for trend = .03) in the second, third, and fourth quartiles of intake, respectively, after adjustment for age, sex, caloric intake, body mass index, and cigarette smoking. No significant or consistent associations were detected with the intake of other dietary nutrients or beverages. Conclusion: Although an independent effect of dietary protein has not been previously associated with renal cell cancer, high protein consumption has been related to development of other chronic renal conditions that may predispose an individual to this cancer. Implication: These findings should prompt further study of dietary protein and its potential contribution to the origins of renal cell cancer. [J Natl Cancer Inst 86:1131-1139, 1994]

Background: Studies in laboratory animals have suggested inhibitory effects of green tea on the induction of some cancers, notably, esophageal cancer. However, only a few epidemiologic studies have evaluated green tea as a potential inhibitor of human esophageal cancer. Purpose: Our purpose was to evaluate the relationship between green tea consumption and the risk of esophageal cancer. Methods: This esophageal cancer study was part of a larger multicenter, case-control study that included three other gastrointestinal sites (pancreas, colon, and rectum). Medical records of patients aged 30-74 years old who were diagnosed with esophageal cancer from October 1, 1990, through January 31, 1993, were identified from the Shanghai Cancer Registry, which covers 6.8 million people in the urban area of Shanghai, People's Republic of China. During the ascertainment period, records of 1016 eligible cases of esophageal cancer were identified. Control subject records were selected by frequency matching in accordance with the age-sex distribution of the four gastrointestinal cancers ascertained by the cancer registry during 1986-1987. Patient interviews were then conducted using a structured, standardized questionnaire to obtain information on demographic characteristics, residential history, height and weight, diet, smoking, alcohol and tea drinking, medical history, family history of cancer, occupation, physical activity, and reproductive history. Results: Of the 902 patients interviewed, 734 (81.4%) had their disease pathologically confirmed. There were 1552 control subjects interviewed, including 240 alternates. All analyses of tea effects were conducted separately among men and women and all were adjusted for age. After further adjustment for other known confounders, a protective effect of green tea drinking on esophageal cancer was observed among women (odds ratio [OR] = 0.50; 95% confidence interval [CI] = 0.30-0.83), and this risk decreased (P for trend [000 [less than or equal to].O1) as tea consumption increased. Among men, the ORs were also below 1.00, although not statistically significant. ORs for green tea intake were estimated among those persons who neither smoked nor drank alcohol. In this subset, statistically significant decreases in risk among tea drinkers were observed for both men (OR = 0.43; 95% CI = 0.22-0.86; P for trend = .05) and women (OR = 0.40; 95% CI= 0.20-0.77; P for trend

Background: The exceptionally high rate of second primary cancers among patients with oral and pharyngeal cancers is well recognized, yet there has been limited epidemiologic study of risk factors for second tumors. Purpose: To evaluate the relation of smoking and alcohol consumption to the development of second cancers among this high-risk patient group, we conducted a nested case-control study. Methods: A total of 1090 patients enrolled in a 1984-1985 population-based, case-control study of oral cancer in four areas of the United States were followed through June 1989 for the occurrence of second primary cancers. Information on tobacco and alcohol consumption was obtained from the original interviews and was updated by follow-up interviews obtained for 80 case patients with second cancers and 189 sex-, study area-, and survival-matched cancer patients free of second cancers (control subjects). Results: Tobacco smoking and alcohol drinking each contributed to risk of second cancers, with the effects of smoking more pronounced than those of alcohol. The odds ratios (ORs) for smoking (adjusted for alcohol) rose with duration intensity of smoking and were strongest for tumors of the aerodigestive tract (oral cavity, pharynx, esophagus, larynx, and lungs), with ORs reaching 4.7 (95% confidence interval [CI] = 1.4-16) among smokers of 40 or more cigarettes per day for 20 or more years. Current smokers as of the baseline survey experienced a fourfold increased risk of a second aerodigestive tract cancer relative to nonsmokers and former smokers. No reduction in risk was associated with cessation of smoking or drinking at or after the index diagnosis, although the short median interval (27 months) between tumor diagnoses limited observation of the effects due to recent cessation. Risk was significantly reduced, however, 5 years after smoking cessation. Among drinkers, second cancer risk was greatest for beer intake, with an OR for a second aerodigestive tract cancer for a second aerodigestive tract cancer of 3.8 (95% CI = 1.2-12) for 15 or more beers per week. Conclusions: Oral and pharyngeal cancer patients with the highest intakes of tobacco and alcohol are the ones most prone to develop second primary cancers. Implications: Avoidance of tobacco smoking and alcohol drinking is the most desirable way not only to prevent primary oral cancers, but also the reduce risk of second cancers of the aerodigestive system. [J Natl Cancer Inst 86:131-137, 1994]

Background: A number of vitamins and minerals have been shown to influence carcinogenesis in experimental animals. In humans, epidemiologic evidence suggests that intake of fruits and vegetables may reduce risk of esophageal and other cancers. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian, China, have persistently low intake of multiple nutrients and exhibit one of the world's highest rates of esophageal/gastric cardia cancer, with an exceptionally high risk of esophageal dysplasia. Purpose: To determine whether supplementation with multiple vitamins and minerals may reduce esophageal/gastric cardia cancer among persons with esophageal dysplasia, we conducted a 6-year prospective intervention trial in Linxian. Methods: Mortality and cancer incidence were ascertained from May 1985 through May 1991 for 3318 persons with cytologic evidence of esophageal dysplasia who were randomly assigned to receive, throughout that period, daily supplementation with 14 vitamins and 12 minerals or placebo. Doses were typically two to three times U.S. Recommended Daily Allowances. Compliance was assessed by counting unused pills monthly for all trial participants and by assaying nutrient levels in blood collected from samples of individuals randomly selected without replacement every 3 months throughout the trial. Cancers were identified through routine surveillance and by special cytology and endoscopy screenings after 2 1/2 years and 6 years. Results: A total of 324 deaths occurred during the 6-year intervention period: 167 occurred in the control (placebo) group and 157 occurred in the supplement group. Cancer was the leading cause of death (54% of all deaths); 18% were due to cerebrovascular diseases and 29% to other causes. Cumulative esophageal/gastric cardia death rates were 8% lower (relative risk [RR] = 0.92; 95% confidence interval [CI] = 0.67-1.28) among individuals receiving supplements rather than placebo, a nonsignificant (P>.10) difference. Risk of total mortality was 7% lower (RR = 0.93; 95% CI = 0.75-1.16; P>.10), total cancer 4% lower (RR = 0.96; 95% CI = 0.71-1.29; P>.10), cerebrovascular disease 38% lower (RR = 0.62; 95% CI = 0.37-1.06; P = .08), and other diseases 12% higher (RR = 1.12; 95% CI = 0.74-1.69; P>.10) among the treated group. Cumulative cancer incidence rates were nearly the same in the two groups. Conclusions: No substantial short-term beneficial effect on incidence or mortality for this type of cancer occurred following daily supplementation with multiple vitamins and minerals among adults with precancerous lesions of the esophagus. Implications. Although no statistically significant short-term benefits were observed, longer follow-up should be more informative about the effectiveness of this 6-year supplementation on cancer and other diseases among individuals with esophageal dysplasia. [J Natl Cancer Inst 85:1492-1498, 1993]

Background: Epidemiologic evidence indicates that diets high in fruits and vegetables are associated with a reduced risk of several cancers, including cancers of the esophagus and stomach. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian County, China, have one of the world's highest rates of esophageal/gastric cardia cancer and a persistently low intake of several micronutrients. Purpose: We sought to determine if dietary supplementation with specific vitamins and minerals can lower mortality from or incidence of cancer as well as mortality from other diseases in Linxian. Methods: Individuals of ages 40-69 were recruited in 1985 from four Linxian communes. Mortality and cancer incidence during March 1986-May 1991 were ascertained for 29584 adults who received daily vitamin and mineral supplementation throughout this period. The subjects were randomly assigned to intervention groups according to a one-half replicate of a [2.sup.4] factorial experimental design. This design enabled testing for the effects of four combinations of nutrients: (A) retinol and zinc; (B) riboflavin and niacin; (C) vitamin C and molybdenum; and (D) beta carotene, vitamin e, and selenium. Doses ranged from one to two times U.S. Recommended Daily Allowances. Results: A total of 2127 deaths occurred among trial participants during the intervention period. Cancer was the leading cause of death, with 32% of all deaths due to esophageal or stomach cancer, followed by cerebrovascular disease (25%). Significantly (P = .03) lower total mortality (relative risk [RR] = 0.91; 95% confidence interval [CI] = 0.84-0.99) occurred among those receiving supplementation with beta carotene, vitamin E, and selenium. The reduction was mainly due to lower cancer rates (RR = 0.87; 95% CI = 0.75-1.00), especially stomach cancer (RR = 0.79; 95% CI = 0.64-0.99), with the reduced risk beginning to arise about 1-2 years after the start of supplementation with these vitamins and minerals. No significant effects on mortality rates from all causes were found for supplementation with retinol and zinc, riboflavin and niacin, or vitamin C and molybdenum. Patters of cancer incidence, on the basis of 1298 cases, generally resembled those for cancer mortality. Conclusions: The findings indicate that vitamin and mineral supplementation of the diet of Linxian adults, particularly with the combination of beta carotene, vitamin E, and selenium, may effect a reduction in cancer risk, in this population. Implications: The results on their own are not definitive, but the promising findings should stimulate further research to clarify the potential benefits of micronutrient supplements. [J Natl Cancer Inst 85-1483-1492, 1993]

Background: In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear. Purpose: The purpose of this study was to explore reasons for the higher incidence of oral cancer among Blacks than Whites. Methods: We used data from a large, population-based case-control study of oral cancer risk factors conducted in four areas of the United States. On the basis of interviews that ascertained characteristics of 1065 oral cancer patients (871 Whites and 194 Blacks) and 1182 controls (979 Whites and 203 Blacks), we examined racial differences in exposure prevalences and relative risks for a number of known etiologic factors, including tobacco and alcohol consumption, diet, and socioeconomic and other variables. To evaluate the extent to which the major risk factors explained the excess risk of oral cancer among Blacks, population-attributable risks were calculated. Results: Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking ([is greater than or equal to] 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher (P = .01) percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. With regard to other potential etiologic factors, protective effects provided by higher dietary intake of fruits and vitamin C were more pronounced for Whites, while Blacks more often tended to be in socio-demographic and medical or dental health categories associated with increased risk. Conclusions: These analyses provide evidence that various environmental or lifestyle determinants of oral cancer may contribute to the higher oral cancer rates in Blacks than in Whites in the United States, but that patterns and risks associated with alcohol consumption, particularly among current smokers, are the most important contributors to the excess risk in Blacks. Implications: These findings suggest that the key to prevention of oral and pharyngeal cancers among both Blacks and Whites is reduced intake of alcoholic beverages and, because of strong interactive effects, the cessation of smoking. [J Natl Cancer Inst 85:465-473, 1993]

Background: Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. Purpose: Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomack cancer. Methods: A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. Results: Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. Conclusions: The finding provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis. [J Natl Cancer Intl 84:1261-1266, 1992]

Background: Nasopharyngeal carcinoma (NPC) is a relatively uncommon cancer in the United States. Its etiology among White Americans is not well known, but cigarette smoking has been implicated in some epidemiologic studies. Purpose: The purpose of this study was to investigate the roles of cigarette use and alcohol consumption as risk factors for NPA in the United States. Methods: We conducted a case-control study using data from the National Mortality Followback Survey based on information from death certificates. In this study, we compared use of cigarettes and alcohol by 204 White American men and women who died of NPC with that by 408 who died of causes unrelated to cigarette smoking and alcohol use. Results: Risk of NPC increased in proportion to the amount and duration of smoking (with a more than threefold increase among persons smoking heavily) and declined following cessation of smoking. After controlling for smoking, we found an 80% excess risk of NPC among persons whose intake of alcohol was heavy. Conclusion: Use of cigarettes and consumption of alcohol were found to be statistically significant risk factors for NPC. The findings are among the strongest to date indicating that use of cigarettes and perhaps alcohol may contribute to the etiology of these relatively rare cancers among Whites in the United States. [J Natl Cancer Inst 84:619-622, 1992]