Hormonal, genetic, and environmental factors play major roles in the complex etiology of breast cancer. When treated continuously with 17␤-estradiol (E2), the ACI rat exhibits a genetically conferred propensity to develop mammary cancer. The susceptibility of the ACI rat to E2-induced mammary cancer appears to segregate as an incompletely dominant trait in crosses to the resistant Copenhagen (COP) strain. In both (ACI ϫ COP)F 2 and (COP ϫ ACI)F 2 populations, we find strong evidence for a major genetic determinant of susceptibility to E2-induced mammary cancer on distal rat chromosome 5. Our data are most consistent with a model in which the ACI allele of this locus, termed Emca1 (e strogen-induced m ammary ca ncer 1), acts in an incompletely dominant manner to increase both tumor incidence and tumor multiplicity as well as to reduce tumor latency in these populations. We also find evidence suggestive of a second locus, Emca2, on chromosome 18 in the (ACI ϫ COP)F 2 population. The ACI allele of Emca2 acts in a dominant manner to increase incidence and decrease latency. Together, Emca1 and Emca2 act independently to modify susceptibility to E2-induced mammary cancer.

Morbidly obese individuals have altered sense of taste and smell. Gastric bypass (GBP) alters taste but olfactory function has not been evaluated. Changes in these senses may influence dietary preferences following GBP. Our aim was to evaluate the effect of abdominal operation, specifically GBP, and weight loss on olfactory function. Fifty-five persons undergoing GBP and cholecystectomy and 40 persons undergoing cholecystectomy (CC) alone were administered the Cross Cultural Smell Identification Test (CC-SIT) preoperatively and 2 and 6 weeks postoperatively. Patients undergoing GBP underwent further tests at 3, 6, 9, and 12 months. Body mass index (BMI) was also assessed. Mean BMI was significantly greater preoperatively in the GBP group (50.6 ± 8.0 vs. 30.6 ± 7.3 kg/m(2), p < 0.05). Significantly more GBP patients had abnormal CC-SIT results preoperatively (12.7% vs. 5.0%). There were no significant differences in percentage of abnormal tests at 2 and 6 weeks within groups but remained lower in CC patients (2 weeks, GBP 6.2% vs. CC 5.7%; 6 weeks, GBP 9.8% vs. CC 3.2%, p < .05). BMI decreased in the GBP group at 12 months (50.6 ± 8.0 preoperatively to 31.9 ± 6.9 p < 0.05). Absolute olfactory dysfunction (AOD) was present at each interval up to 12 months after GBP. Only 22% of patients with AOD remained obese. GBP does not appear to influence olfactory function. AOD present in morbidly obese persons is not affected by weight loss. These findings support that olfactory dysfunction may be a contributing factor to the development of obesity.

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