Biomedical subjects
H A Weiss
Publications and source records attributed to H A Weiss.
Pregnancy characteristics and maternal risk of breast cancer.
In a population-based case-control study of parous women less than 45 years of age, we evaluated the relations of various pregnancy characteristics to maternal breast cancer risk. Cases (N = 1,239) diagnosed with in situ or invasive breast cancer from 1990 to 1992 in Atlanta, GA, Seattle/Puget Sound, WA, and five counties in central New Jersey, and population controls (N = 1,166) identified by random-digit dialing, were interviewed regarding the details of their pregnancies. We used logistic regression to estimate relative risks (RR) and 95% confidence intervals (CI) and to adjust for breast cancer risk factors. Women who reported nausea or vomiting in their first pregnancy had a slightly lower risk of breast cancer (RR = 0.87; 95% CI = 0.72-1.0). We found no strong or consistent associations for maternal risk related to gestational length, pregnancy weight gain, gestational diabetes, pregnancy hypertension, or gender of the offspring, although we found some evidence for reductions in risk for toxemia (RR = 0.81; 95% CI = 0.61-1.1) and specific sex (RR for female twins vs singletons = 0.48; 95% CI = 0.20-1.3) and timing characteristics of twinning. Overall, these data provide little support for the hypothesis that pregnancy hormone levels are associated with subsequent maternal risk of breast cancer in young women.
Dietary relationships with early onset (under age 45) breast cancer in a case-control study in the United States: influence of chemotherapy treatment.
Methodologic investigations have addressed selection and recall bias in case-control studies of diet and breast cancer, whereas the effect of disease progression and medical treatment on estimates of dietary intake has been largely overlooked. In a multicenter, population-based case-control study of breast cancer in the United States, 1,588 newly diagnosed cases and 1,451 controls completed a self-administered food-frequency questionnaire. Initial evaluation suggested increased risk related to high intakes of calories, carbohydrates, fat, and protein. All nutrient associations were diminished after adjustment for calories. Evaluation by stage of disease revealed no relation of calories to risk among women with in situ disease, but elevated risks among women with localized (odds ratio [OR] = 1.33, 95 percent confidence interval [CI] = 1.0-1.7 highest cflowest quartile) or regional and distant disease (OR = 1.79, CI = 1.3-2.4). Further evaluation showed that the increased risk associated with calories was restricted to cases who reported having been treated with chemotherapy (OR = 1.66, CI = 1.3-2.1). A gradient of increasing risk with time interval from diagnosis to interview suggested the chemotherapy regimen itself and not necessarily characteristics of tumors requiring this treatment was responsible for the observed increased risk. These results indicate that epidemiologic studies of diet and breast cancer, particularly among young women, should evaluate possible bias related to post-diagnosis influences.
Prenatal and perinatal risk factors for breast cancer in young women.
There is increasing interest in the role of early life exposures in breast carcinogenesis, especially estrogen exposure in utero. Estrogen levels during pregnancy may be higher in twin pregnancies and among older women and slightly lower among smokers. We analyzed early life risk factors in a population-based case-control study in the United States of 2,202 breast cancer cases and 2,009 controls under age 55 years. Twins were at an increased risk of breast cancer compared with singletons (relative risk = 1.62; 95% confidence interval = 1.0-2.7), particularly women with a twin brother (relative risk = 2.06), a finding consistent with the observation of high estrogen levels in dizygotic twin pregnancies. Little association was seen between maternal age at birth and breast cancer risk. We carried out further analyses for 534 cases and 497 controls under age 45 years, using data from a questionnaire completed by their mothers relating to the daughters' early life exposures. There was no evidence of an effect of smoking or diethylstilbestrol exposure during pregnancy on daughters' breast cancer risk. A reduced breast cancer risk was seen among women who had been breastfed (relative risk = 0.74; 95% confidence interval = 0.6-1.0). These findings indicate some effect of early life exposures on breast cancer risk, although the role of estrogen exposure may be less central than previously suggested.
Laterality of breast cancer in the United States.
Breast cancer laterality of over 250,000 cases from the Surveillance, Epidemiology, and End Results (SEER) program in the United States was studied in relation to gender, race, tumor stage, histology, age at diagnosis, year of diagnosis, estrogen receptor status, and marital status. The data, which include all invasive and in situ breast cancer cases in the SEER program during the years 1973-92, confirm results from other studies of an overall five percent excess of left-sided disease in women. The excess occurs for all races and stages of disease, and for invasive disease, the excess increases with age. There was no significant variation in the laterality of invasive disease over time, though for in situ tumors, the left-sided excess was significantly greater during the years 1978-82 than in other periods. No excess of left-sided breast cancer was observed among men. There is no evidence that detection bias plays a major role, and although the left breast is slightly larger, on average, than the right, there is little evidence that breast size is associated with breast cancer risk. The reason for the left-sided excess among women remains unclear.
Epidemiology of in situ and invasive breast cancer in women aged under 45.
The incidence of in situ breast cancer in the USA has increased rapidly in recent years, even among young women. A population-based case-control study of 1616 breast cancer cases aged under 45 in the USA was used to examine risk factors for in situ, local and regional/distant tumours. Almost 60% of in situ tumours were detected by routine mammograms compared with 18% of local tumours and 8% of regional/distant tumours. After adjustment for screening history and established risk factors, family history of breast cancer in a first-degree relative and African-American race were associated with an increased risk of all stages of breast cancer. The associations with nulliparity, a previous breast biopsy and body mass index were significantly stronger for in situ tumours than for local or regional/distant disease. Alcohol consumption was associated with an increasing trend in risk of regional/distant tumours but not of earlier stage tumours, indicating that alcohol may be involved in late-stage events. Analyses by histological type of in situ tumours suggested that both ductal and lobular carcinoma in situ were associated with most established breast cancer risk factors, and the magnitude of association tended to be greater for the ductal form.
Aspirin, non-steroidal anti-inflammatory drugs and protection from colorectal cancer: a review of the epidemiological evidence.
There is substantial experimental, clinical and epidemiological evidence that regular use of non-steroid anti-inflammatory drugs (NSAIDs), particularly aspirin, is associated with a reduced risk of colorectal cancer. The protective effect is thought to arise from inhibition of prostaglandin synthesis, although the precise mechanism remains unclear. Of the epidemiological studies carried out, all but one have found that regular use of NSAIDs reduces the risk of colorectal cancer by 30-50%. The consistency of this finding across studies and the magnitude of the reduced risk tend to support a causal association between NSAID use and reduced risk of colorectal cancer. Further, the protective effect increases with longer duration of use, and persists after controlling for other colorectal cancer risk factors. However, these observational studies are limited by inherent biases, potential confounding with other lifestyle factors, and sparse information on dose and duration of use. Only one randomized controlled trial has been carried out, and no reduction in risk was associated with intake of one aspirin per day, though this may be due to the short follow-up period and the low dose of aspirin taken. Further observational studies and randomized controlled trials are needed to confirm the association, to quantify the dosage required for a protective effect, and to identify those patients most likely to benefit.
Leukemia mortality after X-ray treatment for ankylosing spondylitis.
Leukemia mortality has been studied in 14,767 adult ankylosing spondylitis patients diagnosed between 1935 and 1957 in the United Kingdom, of whom 13,914 patients received X-ray treatment. By 1 January 1992, there were 60 leukemia deaths among the irradiated patients, almost treble that expected from national rates. Leukemia mortality was not increased among unirradiated patients. Among those irradiated, the ratio of observed to expected deaths for leukemia other than chronic lymphocytic leukemia was greatest in the period 1-5 years after the first treatment (ratio = 11.01, 95% confidence interval 5.26-20.98) and decreased to 1.87 (95% confidence interval 0.94-3.36) in the 25+ year period. There was no significant variation in this ratio with sex or age at first treatment. The ratio for chronic lymphocytic leukemia was slightly but not significantly raised (ratio = 1.44, 95% confidence interval 0.62-2.79). Most irradiated patients received all their exposure within a year. Based on a 1 in 15 random sample, the mean total marrow dose was 4.38 Gy. Doses were nonuniform, with heaviest doses to the lower spine. The risk for nonchronic lymphocytic leukemia was adequately described by a linear-exponential model that allowed for cell sterilization in heavily exposed parts of the marrow and time since exposure. Ten years after first exposure, the linear component of excess relative risk was 12.37 per Gy (95% confidence interval 2.25-52.07), and it was estimated that cell sterilization reduced the excess relative risk by 47% at 1 Gy (95% confidence interval 17%-79%). The average predicted relative risk in the period 1-25 years after exposure to a uniform dose of 1 Gy was 7.00.
Cancer mortality following X-ray treatment for ankylosing spondylitis.
Mortality has been studied in 15,577 ankylosing spondylitis (AS) patients diagnosed between 1935 and 1957 in the UK, of whom 14,556 received X-ray treatment. By January 1, 1992 over half of the cohort had died. Among the irradiated patients, cancer mortality was significantly greater than expected from the national rates for England and Wales, with a ratio of observed deaths to expected (relative risk, RR) of 1.30, and significant increases individually for leukaemia, non-Hodgkin's lymphoma, multiple myeloma and cancers of the oesophagus, colon, pancreas, lung, bones, connective and soft tissue, prostate, bladder and kidney. Among the unirradiated patients, cancer mortality was lower than expected from national rates (RR = 0.79). Among irradiated patients, the RRs for leukaemia, lung cancer, and all other neoplasms all decreased significantly with increasing time since first treatment following an initial increase. By 35 years after first treatment, the radiation-related excess for lung cancer had completely disappeared, while for other neoplasms the RR remained significantly raised, although at a lower level than in earlier periods. Most irradiated patients received several courses of treatment within a 5-year period. Based on a 1 in 15 random sample, the mean total body dose received in this period was 2.64 Gy, with the heaviest dose to the vertebrae. A linear dose-response model for all neoplasms except leukaemia gave an excess RR of 0.18 Gy-1 in the period 5-24.9 years after first treatment, which decreased significantly to 0.11 Gy-1 in the period more than 25 years after first treatment. There was no evidence that a linear-quadratic model fitted the data better than a linear model. There were significant dose-response relationships individually for cancers of the lung, oesophagus, colon, pancreas, prostate, bladder and kidney.
And still more on surgical training for specialists of all kinds.
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Oxidation of functional thiols by sulphoxides.
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