Faculty Bibliography

Consider this. Our research at Cornell Medical Center has shown that a number of widely used chemical compounds, such as some pesticides and fuels, alter the production of hormones, much the same way as do known cancer-causing agents. Researchers at the U.S. National Toxicology Program have identified numerous such compounds that create mammary tumors in male rodents. Chances are very good that these substances cause cancer in humans. Every compound known to cause cancer in humans also produces cancer in animals, when adequately tested. And the compounds are not only present on Long Island; they're present everywhere. Because many of them are so widely available in the environment, it becomes very difficult to find anyone who is not exposed. To insist on proof of human harm before taking action treats people like lab rats. A recent report from the American Health Foundation about Long Island breast cancer, for example, found no difference in organochlorine residues in women with breast cancer and those without the disease who lived on Long Island and New York City. Unfortunately, there are three major problems with this approach. First, women with advanced disease may have undergone changes in metabolism that alter what remains in their bodies, especially fat- loving, organochlorine residues. Second, critical exposures to cancer- causing agents from early in life cannot be measured years later. Finally, women who have lived in the same area are likely to have undergone similar exposures, which lowers the chance of finding an effect from their environment. In fact, recent studies from Canada and Denmark that have taken samples from women more than a decade before cancer arises, and compared with women from different regions, have found that early exposures to higher levels of some organochlorine compounds do increase the risk of developing cancer

BACKGROUND AND OBJECTIVES: The ability to achieve clean margins with breast conserving therapy varies greatly even when the diagnosis of carcinoma is known beforehand. Although several reports reveal that the incidence of positive margins decreases after stereotaxic core biopsy of nonpalpable lesions and fine-needle aspiration biopsy of palpable lesions, the data on the results following mammotome biopsy (mmbx) is scanty. METHODS: Two hundred and ninety-eight biopsy specimens for mammographically indeterminate microcalcification from 1/97 through 3/30/98 were reviewed. Biopsies were performed using the biopsys method utilizing an 11-gauge multidirectional, vacuum-directed device. RESULTS: Ten percent (n = 31) of the mammotome biopsies were atypical and 9% (n = 27) were malignant. These 58 cases (19%) were recommended for surgical excision. The incidence of positive margins in this subset was determined. Of patients who underwent lumpectomy as their initial surgical procedure 69% had negative surgical margins. Seventy-seven percent of patients with carcinoma diagnosed by mammotome biopsy had definitive initial surgery with a single surgical procedure. CONCLUSIONS: Mmbx facilitates fewer surgical procedures to achieve negative margins, and thus provides a better cosmetic result.

The World Health Organization recently reported that breast cancer has become the most common cancer in women throughout the world. Known risk factors account for less than half of all cases of breast cancer, and inherited germ line mutations occur in at most only 10% of all cases. Cumulative exposure to estradiol and other hormones links many of the established risk factors for breast cancer. This paper reviews epidemiologic and toxicologic evidence on breast cancer risks and presents a comprehensive construct of risk factors intended to focus on the identification of those factors that can be controlled or modified. We attempt to provide a framework for interpreting the etiologic interplay of endogenous metabolic changes and environmental changes in the etiology of breast cancer. The construct we develop distinguishes between those risk factors that are directly causal, such as ionizing radiation and inherited germ cell defects, those vulnerability factors that extend the time period during which the breast undergoes development, and those contributing factors that increase total hormonal stimulation of the breast. Some hormonally active compounds, such as those in soy and broccoli and other phytoestrogen-containing foods, can be protective against breast cancer, while others, such as some environmental contaminants, appear to increase the risk of the disease by increasing levels of harmful hormones. Efforts to explain patterns of breast cancer should distinguish between these different risk factors. Identification of vulnerability and contributing risk factors can foster the development of public policy to reduce the burden of this prevalent cancer. Prudent precautionary principles suggest that reducing exposure to avoidable or modifiable risk factors should receive high priority from the public and private sectors