© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 16, 1347,
August 18, 1999
© 1999 Oxford University Press
IN THIS ISSUE |
Although several risk factors for breast cancer have been identified, researchers continue to investigate potential causes. Bonnet et al. (p. 1376) have examined 100 invasive breast cancers for the presence of Epstein-Barr virus (EBV), which has been associated with Burkitt's lymphoma, nasopharyngeal carcinoma and, more recently, other malignancies. By use of the polymerase chain reaction, they found evidence of EBV DNA in 51 of the 100 tumors. Because the virus was only detected in 10% of samples of healthy tissue adjacent to the tumors, infection appears to be largely specific to the tumor itself. The researchers also found evidence that viral genes were being expressed by infected tumor cells. EBV infection was detected most frequently in breast tumors with poor prognostic characteristics.
In an accompanying editorial, Magrath and Bhatia (p. 1349) further discuss the findings of Bonnet and colleagues in the context of other investigators' results on EBV and breast cancer, the biology of EBV, and EBV's role in other cancers.
Breast Cancer Metastasis Gene?
Deletion of a major portion or all of one copy of a gene—known as loss of heterozygosity, or LOH—may provide clues to the future behavior of a tumor. O'Connell et al. (p. 1391) compared the frequency of LOH at four sites on chromosome 14 in breast tumors from women with and without axillary lymph-node metastases. In contrast to their expectation, the researchers found that LOH at two sites occurred at higher frequency in tumors from women without metastases than in tumors from women with metastases. This finding suggests the presence of a metastasis-related gene that may promote rather than suppress the spread of breast cancer. The authors state that isolation of the gene may eventually lead to better diagnosis and treatment of breast cancer.
This finding suggests the presence of a metastasis-related gene that may promote rather than suppress the spread of breast cancer.
In an accompanying editorial, Welch and Rinker-Schaeffer present guidelines for selecting markers of cancer metastasis. They stress the need to distinguish between markers of tumor growth and markers of metastasis.
Why People Smoke
Cigarette smoking is the largest preventable cause of cancer and other diseases in the United States, and it is increasing in the rest of the world. Bergen and Caporaso (p. 1365) summarize and evaluate published literature on the determinants of current and persistent smoking in individuals and in populations. They focus in particular on the biochemistry and pharmacology of smoking, related psychiatric disorders (nicotine dependence being the most common psychiatric diagnosis in the U.S.), and genetic susceptibility. The authors conclude that, although genetic factors explain much of the variability in individual likelihood of smoking, future studies of this complex behavior must also take into account factors related to the demographic and social environment, as well as other psychiatric conditions.
. . . [A]lthough genetic factors explain much of the variability in individual likelihood of smoking, future studies . . . must also take into account factors related to the demographic and social environment. . . .
Prostaglandin Synthesis and Prostate Cancer
Prostaglandins are involved in the regulation of several important physiologic and pathologic processes. Recent evidence suggests that they could be involved in tumor progression. In the first in vivo exploration of this hypothesis, Tremblay et al. (p. 1398) have studied the expression of the prostaglandin G/H synthase-2 enzyme in prostatic adenocarcinomas of the dog, the only nonhuman species that frequently develops spontaneous prostate cancer. The investigators found that prostaglandin G/H synthase-2 was not detectable in normal prostates, but was expressed in epithelial tumor cells in 18 (75%) of 24 adenocarcinomas. The authors conclude that the expression of this enzyme in a majority of spontaneous prostatic adenocarcinomas suggests that it may be involved in the development of canine prostate cancer.
"The induction of prostaglandin G/H synthase-2 in a majority of canine prostatic adenocarcinomas provides a novel element in our understanding of prostate cancer in dogs."
—Tremblay et al.
Breast Density, Family History, and Cancer Risk
Women with a family history of breast cancer are at increased risk of the disease. To determine whether this risk is increased by having mammographically dense breasts, Boyd et al. (p. 1404) analyzed data from a nested case-control study based on the Canadian National Breast Cancer Screening Study. The investigators report that mammographic density may be strongly associated with risk of breast cancer in women with a family history of the disease. According to the authors, recent evidence from other studies shows that mammographic density may be modified by dietary and hormonal interventions. How these complex relationships may contribute to prevention remains to be elucidated.
Health Insurance, Race, and Stage of Cancer at Diagnosis
To determine whether health insurance coverage might be a factor in previously observed racial differences in the stage at which cancer is diagnosed, Roetzheim et al. (p. 1409) examined data on all patients with incident cases of melanoma or colorectal, breast, or prostate cancer in Florida in 1994. They found that patients who were uninsured were more likely diagnosed with these cancers at late-stage than patients with commercial indemnity insurance. Patients insured by Medicaid were more likely diagnosed with late-stage breast cancer and melanoma. Racial differences in stage at diagnosis, however, were not explained by insurance coverage or the socioeconomic status of the patients.
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