Despite some limitations, these methods provide useful information on breast cancer risk for women who plan to participate in an annual mammographic screening program.

H. pylori treatment reduces the prevalence of precancerous gastric lesions and may reduce gastric cancer incidence, but further data are needed to prove the latter point. Long-term vitamin or garlic supplementation had no beneficial effects on the prevalence of precancerous gastric lesions or on gastric cancer incidence.

In the Shandong Intervention Trial, 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions, whereas 7.3 years of oral supplementation with garlic extract and oil (garlic treatment) or vitamin C, vitamin E, and selenium (vitamin treatment) did not. Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 randomly assigned subjects in this masked factorial placebo-controlled trial. Conditional logistic regression was used to estimate the odds of gastric cancer incidence, and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality. All statistical tests were two-sided. Gastric cancer was diagnosed in 3.0% of subjects who received H pylori treatment and in 4.6% of those who received placebo (odds ratio = 0.61, 95% confidence interval = 0.38 to 0.96, P = .032). Gastric cancer deaths occurred among 1.5% of subjects assigned H pylori treatment and among 2.1% of those assigned placebo (hazard ratio [HR] of death = 0.67, 95% CI = 0.36 to 1.28). Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality. Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer, a secondary endpoint (HR = 0.51, 95% CI = 0.30 to 0.87; P = .014).

The CARE model usually gave higher risk estimates for African American women than the Breast Cancer Risk Assessment Tool and is recommended for counseling African American women regarding their risk of breast cancer.

Background: To improve the discriminatory power of the Gail model for predicting absolute risk of invasive breast cancer, we previously developed a relative risk model that incorporated mammographic density (DENSITY) from data on white women in the Breast Cancer Detection Demonstration Project (BCDDP). That model also included the variables age at birth of fi rst live child (AGEFLB), number of aff ected mother or sisters (NUMREL), number of previous benign breast biopsy examinations (NBIOPS), and weight (WEIGHT). In this study, we developed the corresponding model for absolute risk. ( 1 ) used data from the Breast Cancer Detection Demonstration Project (BCDDP) to develop a model for the absolute risk of breast cancer for women in a given age interval. This model, known as the Gail model, included age at menarche (AGEMEN), age at birth of fi rst live child (AGEFLB), number of previous benign breast biopsy examinations (NBIOPS), and number of fi rst-degree relatives (mother or sisters) with breast cancer (NUMREL). We call these standard risk factors. This model was recalibrated to data from National Cancer Institute's (NCI's) Surveillance, Epidemiology, and End Results (SEER) program ( 2 ) , and the resulting model, called Gail model 2, is available at http://www.cancer.gov/bcrisktool/ . This model has been used to design prevention trials, such as the Breast Cancer

Breast cancer projections varied considerably by type of HL therapy, time since HL diagnosis, and age at end of follow-up. These estimates are applicable to HL survivors treated with regimens of the past and can be used to counsel such patients and plan management and preventive strategies. Projections should be used with caution, however, in patients treated with more recent approaches, including limited-field radiotherapy and/or ovary-sparing chemotherapy.

A B S T R A C T PurposeGiven the high incidence of colorectal cancer (CRC), and the availability of procedures that can detect disease and remove precancerous lesions, there is a need for a model that estimates the probability of developing CRC across various age intervals and risk factor profiles. MethodsThe development of separate CRC absolute risk models for men and women included estimating relative risks and attributable risk parameters from population-based case-control data separately for proximal, distal, and rectal cancer and combining these estimates with baseline age-specific cancer hazard rates based on Surveillance, Epidemiology, and End Results (SEER) incidence rates and competing mortality risks. ResultsFor men, the model included a cancer-negative sigmoidoscopy/colonoscopy in the last 10 years, polyp history in the last 10 years, history of CRC in first-degree relatives, aspirin and nonsteroidal anti-inflammatory drug (NSAID) use, cigarette smoking, body mass index (BMI), current leisuretime vigorous activity, and vegetable consumption. For women, the model included sigmoidoscopy/colonoscopy, polyp history, history of CRC in first-degree relatives, aspirin and NSAID use, BMI, leisure-time vigorous activity, vegetable consumption, hormone-replacement therapy (HRT), and estrogen exposure on the basis of menopausal status. For men and women, relative risks differed slightly by tumor site. A validation study in independent data indicates that the models for men and women are well calibrated. ConclusionWe developed absolute risk prediction models for CRC from population-based data, and a simple questionnaire suitable for self-administration. This model is potentially useful for counseling, for designing research intervention studies, and for other applications.

We followed 145 men with chronic hepatitis B virus (HBV) hepatitis for 10 years to determine whether exposure to aflatoxin, or concomitant exposure to hepatitis C virus (HCV), or family history of hepatocellular carcinoma (HCC) increased the risk of developing HCC. We collected 8 monthly urine samples before beginning follow-up and pooled them to detect aflatoxin metabolite M1 (AFM1). AFM1 was detected in 78 (54%) of the subjects. The risk of HCC was increased 3.3-fold (with a 95% confidence interval of 1.2-8.7) in those with detectable AFM1 (above 3.6 ng/L). This relative risk was adjusted for age and for HCV status. Hepatocellular carcinoma (HCC) is the second most common cause of death from cancer in China, where the mortality rate was 18 per 100,000 person-years in 1990 through 1992. 1 Infection with hepatitis B virus (HBV) and exposure to aflatoxin are both important risk factors for HCC. Ross et al. 2 studied 18,244 men aged 45 to 64 who lived in Shanghai between 1986 and 1989. In a sample of 140 controls who were age-matched to HCC cases, it was found that 15 (11%) were hepatitis B surface antigen (HBsAg)-positive, and 53 (38%) had detectable urinary aflatoxin metabolites or DNAadducts. A later analysis of 50 HCC cases and 267 agematched controls from this study 3 showed that compared with men without HBsAg or urinary aflatoxin biomarkers, relative risks were 7.3 with 95% a confidence interval (2.2, 24) for those only with HBsAg, 3.4 (1.1, 10) for those only with aflatoxin biomarkers, and 59 (17, 212) for those with both. Based on such data, Ross et al. 2 and Qian et al. 3 suggested that reduction of exposure to aflatoxin might prevent a considerable fraction of the HCC in this population.The previous cohort represented the general male population of Shanghai. We chose instead to follow prospectively a representative group of 145 carriers of HBsAg with a history of chronic hepatitis. These men were being cared for at the Medical Oncology Department of the Qidong Liver Cancer Institute/Hospital, Qidong, Jiangsu Province, China. HCC rates are very high in Qidong. The purpose of the study was to determine whether exposure to aflatoxin increased the risk of HCC or of fatal cirrhosis over a 10-year period in patients with HBV hepatitis. A positive finding would suggest that measures to reduce exposure to aflatoxin might also be beneficial to men with chronic HBV hepatitis and could be evaluated in treatment protocols. Because we collected monthly urine samples for 8 months before beginning follow-up, we were able to pool the samples to obtain estimates of long-term average urinary aflatoxin M1 (AFM1) concentrations, and the assay could detect concentrations of AFM1 as low as 3.6 ng/L. These data also give information on the added risks of HCC in men with chronic HBV hepatitis from exposure to hepatitis C virus (HCV) and from a family history of HCC. PATIENTS AND METHODSPopulation-based sampling was used to obtain a representative study cohort. In an earlier study of the prevalence of HBV infection sponsored by...