Faculty Bibliography

The authors examined the relation between postmenopausal serum levels of testosterone and dehydroepiandrosterone sulfate (DHEAS) and subsequent risk of breast cancer in a case-control study nested within the New York University Women's Health Study cohort. A specific objective of their analysis was to examine whether androgens had an effect on breast cancer risk independent of their effect on the biologic availability of estrogen. A total of 130 cases of breast cancer were diagnosed prior to 1991 in a cohort of 7,054 postmenopausal women who had donated blood and completed questionnaires at a breast cancer screening clinic in New York City between 1985 and 1991. For each case, two controls were selected, matching the case on age at blood donation and length of storage of serum specimens. Biochemical analyses were performed on sera that had been stored at -80 degrees C since sampling. The present report includes a subset of 85 matched sets, for whom at least 6 months had elapsed between blood donation and diagnosis of the case. In univariate analysis, testosterone was positively associated with breast cancer risk (odds ratio (OR) for the highest quartile = 2.7, 95% confidence interval (CI) 1.1-6.8, p < 0.05, test for trend). However, after including % estradiol bound to sex hormone-binding globulin (SHBG) and total estradiol in the statistical model, the odds ratios associated with higher levels of testosterone were considerably reduced, and there was no longer a significant trend (OR for the highest quartile = 1.2, 95% CI 0.4-3.5). Conversely, breast cancer risk remained positively associated with total estradiol levels (OR for the highest quartile = 2.9, 95% CI 1.0-8.3) and negatively associated with % estradiol bound to SHBG (OR for the highest quartile = 0.05, 95% CI 0.01-0.19) after adjustment for serum testosterone levels. These results are consistent with the hypothesis that testosterone has an indirect effect on breast cancer risk, via its influence on the amount of bioavailable estrogen. No evidence was found of an association between DHEAS and risk of breast cancer in postmenopausal women

The relation between diet and female colorectal cancer was analyzed in a prospective study of 14,727 women aged 34-65 years, who were enrolled at mammographic screening clinics in New York and Florida from 1985 to 1991. They were followed through the end of 1994 (average 7.1 yrs) by a combination of direct contact through mail and telephone and record linkages with regional tumor registries, resulting in 100 incident cases of colorectal cancer. There was no overall positive or inverse association of colorectal cancer risk with intakes of total calories, total or subclasses of fat, carbohydrate, or dietary fiber, whereas there was an inverse association with total protein. Among major food groups, there was a progressive decline in risk of colorectal cancer with increasing intake of fish and shellfish (relative risk for 4th vs. 1st quartile = 0.49, 95% confidence interval = 0.27-0.89). A similar inverse association was also observed for consumption of dairy products, and this association was explained mainly by calcium, not by other nutrients, such as fat or protein. The results of the present study indicated that certain dietary components of fish or dairy products may protect against colorectal cancer, whereas the relations with red meat or total fat remained unclear

A standard nomenclature that concisely describes any disaster is currently lacking. This article describes a model taxonomy system. Instead of the term 'disaster,' a root word 'PICE,' 'potential injury-creating event,' is used. Descriptive modifiers to account for all possible scenarios surround this root word, as illustrated. [table: see text] A modifier is chosen from each column and a stage is assigned to each PICE. Column A describes the potential for additional casualties. Column B describes whether resources are overwhelmed and, if so, whether they must simply be augmented (disruptive) or they must first be reconstituted (paralytic). Column C describes the extent of geographic involvement. 'Stage' refers strictly to the likelihood that outside medical assistance will be needed. Stage 0 means there is little chance, stage I means there is a small chance (place outside help on 'alert'), stage II means there is a moderate chance (place on 'standby'), and stage III means local medical resources are clearly overwhelmed (immediately dispatch outside resources, commit personnel, prepare remote hospitals). For example, a multiple vehicle crash in a large city would be a 'static, controlled, local PICE, stage 0.' In conclusion, a new nomenclature for describing disasters is reported. A short phrase describes the incident and communicates the need for outside assistance. The model may be useful for disaster planning, management, and research

The purpose of this study was to compare the effects of glaucoma, at different stages of the disease process, on the two color-opponent system and on the luminance system. Discrimination thresholds were measured along the two equiluminant cardinal color axes (RG and YV) and along an achromatic luminance axis (LD) in 27 patients with open-angle glaucoma (OAG) and in 13 glaucoma suspects. Patients with OAG showed increased thresholds along all three axes. The threshold increases correlated significantly with the level of visual field loss. For glaucoma suspects, thresholds were also increased along all three axes. A subgroup of patients with OAG, those with pigmentary glaucoma, showed minimal increases in threshold along the RG axis. To further investigate this finding an additional 15 patients, seven with primary OAG and eight with pigmentary glaucoma were run in a two-alternative forced-choice experiment. For patients with pigmentary glaucoma, thresholds were increased less along the RG axis. The results of the study for OAG patients and glaucoma suspects are consistent with deficits in the two color-opponent systems, and in the luminance system

A positive association between postmenopausal serum levels of total estradiol, percentage of free estradiol, and percentage of estradiol not bound to sex hormone-binding globulin (SHBG) and breast cancer risk was recently reported by the New York University Women's Health Study (P. Toniolo et al., J. Natl. Cancer Inst., 87: 190-197, 1995). Data from this prospective study are used to assess whether the observed associations differ according to estrogen receptor (ER) status of the tumor. Between 1985 and 1991, 7063 postmenopausal women donated blood and completed questionnaires at a large breast cancer screening clinic in New York City. Before 1991, 130 cases of first primary breast cancer were identified by active follow-up of the cohort. For each case, two controls were selected, matching the case on age at first blood donation and length of storage of specimens. Biochemical analyses were performed on sera that had been stored at -80 degrees since sampling. ER information was abstracted from pathology reports. Separate statistical analyses were conducted of ER-positive, ER-negative, and ER-unknown groups (53, 23, and 54 matched sets, respectively). In each of the 3 groups, the mean estradiol and the mean percentage of free estradiol were greater (21-28% and 6-7%, respectively) in cases than in controls. Conversely, the mean percentage of estradiol bound to SHBG was 9-12% lower in cases than in controls. The logistic regression coefficients measuring the strength of the association between estradiol and its free and SHBG-bound fractions and breast cancer risk were similar in the ER-positive, ER-negative, and ER-unknown groups. These data suggest that in postmenopausal women, the association of endogenous estrogens with breast cancer risk is independent of the ER status of the tumor. This result is more compatible with the hypothesis of a progression from ER-positive to ER negative tumors than with the hypothesis that ER status identifies two distinct types of breast cancer

In this paper we discuss estimation of the reliability of an exposure variable in the presence of confounders measured without error. We give an explicit formula that shows how the exposure becomes less reliable as the degree of correlation between the exposure and confounders increases. We also discuss biases in the corresponding logistic regression estimates and methods for correction. Data from a matched case-control study of hormone levels and risk of breast cancer are used to illustrate the methods