© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 24, 1961,
December 20, 2000
© 2000 Oxford University Press
IN THIS ISSUE |
Most people who start smoking as adolescents continue smoking as adults, and reducing adolescent smoking is therefore a critical public health goal. School-based prevention programs have been thought to be important for achieving this goal. Peterson et al. (p. 1979) tested the effectiveness of current "best practices" in the Hutchinson Smoking Prevention Project, a group-randomized trial of a school-based, social-influences smoking prevention intervention spanning grades 3–12. A total of 8388 students from 40 school districts were enrolled in the trial as third graders and followed to 2 years after high school. Despite a state-of-the-art intervention that started early and ran through high school and despite the trial’s methodologic strengths, daily smoking prevalence at grade 12 and 2 years after high school was essentially the same for students in the experimental districts as for students in the control districts. The authors conclude that there is no evidence from this trial that a school-based, social-influences approach deters youth smoking.
In an accompanying editorial, Clayton et al. (p. 1964) point out that the failure of the social-influences approach may reflect the paucity of knowledge about why adolescents smoke. They note the need for a better understanding of the etiology of tobacco use and dependence and suggest that new theoretical models are needed that blend individual biologic and psychologic factors with those operating in the larger society and culture.
Tocopherols, Selenium, and Prostate Cancer
Observational studies have suggested that 
-tocopherol and selenium may protect against some forms of prostate cancer. However, the data are inconsistent, 
-tocopherol (the most common vitamin E in food) has never been studied, and effects of the nutrients on prostate cancer risk have never been assessed simultaneously. Helzlsouer et al. (p. 2018) addressed this question by analyzing levels of - and -tocopherol and selenium in blood and toenails sampled from male Maryland residents and by following the incidence of prostate cancer in the study group. The authors found that risk of prostate cancer was reduced fivefold in subjects with the highest levels of -tocopherol. Selenium showed a weaker but still protective effect that was most evident among subjects with the highest levels of -tocopherol. The authors caution that their results could have implications for a proposed prostate cancer chemoprevention trial of -tocopherol and selenium.
In an accompanying editorial, Giovannucci (p. 1966) places the Helzlsouer study in the context of related observational and laboratory studies of tocopherols. He points out that -tocopherol, the major tocopherol in currently available vitamin E supplements, is preferentially processed over -tocopherol by the liver and can displace it physiologically. The balance of the two forms in the body is potentially important, he says, and should be taken into account in the design of future studies.
"Little attention has been paid to the possibility that -tocopherol . . . might also be involved in the pathogenesis of prostate cancer."
—Helzlsouer et al.
HER2 Status and Response to Chemotherapy
Current treatments for invasive breast cancer include anthracycline-based regimens consisting of doxorubicin and cyclophosphamide (AC) and combination chemotherapy with cyclophosphamide, methotrexate, and 5-fluorouracil (CMF). Previous studies have suggested that HER2 could be a useful tumor marker for predicting the relative efficacy of these treatments. Paik et al. (p. 1991) conducted a retrospective study of tumor samples from 2034 patients within the National Surgical Adjuvant Breast and Bowel Project Protocol B-15 to evaluate whether HER2 expression could provide a rational basis for choosing between the AC and CMF regimens. The authors found that patients with HER2-positive tumors had better clinical outcomes when treated with anthracycline (doxorubicin)-based regimens than with CMF, while those with HER2-negative tumors benefited equally well from the treatments. Although these results did not reach statistical significance, the authors conclude that, in the context of other recent retrospective analyses, anthracycline-based regimens are generally preferred in HER2-positive patients.
Protecting Normal Cells From Chemotherapy
Many cancer chemotherapy agents target proliferating cells, so often both normal and cancer cells are killed. The differential sensitivities of normal and cancer cells to cell cycle inhibitors prompted Chen et al. (p. 1999) to investigate whether these inhibitors could protect normal cells from chemotherapeutic agents. They observed that nonlethal concentrations of staurosporine preferentially arrested normal cells in G0/G1 phase of the cell cycle by inhibiting the retinoblastoma protein pathway without affecting tumor cell proliferation. They treated normal and cancer cells with staurosporine, followed by a chemotherapeutic agent, doxorubicin or camptothecin. After this two-step treatment, tumor cells were selectively killed, but normal cells resumed proliferation after the drugs were removed. Thus, the authors propose that staurosporine-insensitive proliferating tumor cells can be specifically targeted with chemotherapeutic agents after normal cells are protected by the staurosporine-induced cell cycle arrest.
Explaining Racial Variation in Prostate Cancer
African-American men have a higher incidence of prostate cancer and more aggressive disease than white American men. Although disparities in health care access may contribute to these differences, Platz et al. (p. 2009) report that these differences were seen among men in the Health Professionals Follow-up Study, all of whom should have similar access to health care. Multivariate adjustment showed that differences in the distribution of known and suspected dietary and lifestyle risk factors for prostate cancer did not explain the higher disease risk among African-Americans. The authors analyzed several determinants of prostate epithelial cell growth in a subset of men in the study and found that the mean number of CAG repeats in the androgen receptor gene varied by race, as has been seen in other studies. However, they note that this factor is unlikely to be the sole explanation for racial differences in prostate cancer risk.
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