© 2005 Oxford University Press
IN THIS ISSUE
Effect of Antioxidant Vitamins on Second Primary Tumors
Epidemiologic studies have shown an association between low intake of antioxidant vitamins and increased cancer risk, although randomized trials have been equivocal. In this issue (p. 481), Bairati et al. report the results of a randomized trial to investigate the effect of supplementation with 
-tocopherol and 
-carotene on risk of second primary cancers in patients with head and neck cancer. Supplementation began on the first day of radiation therapy and continued for 3 years after radiation therapy ended. (The use of -carotene was discontinued partway through the trial, after which patients in the intervention arm received -tocopherol only.) Compared with placebo-treated patients, patients receiving -tocopherol had a statistically significantly higher rate of second primary cancers during the 3-year supplementation period but a lower rate after the supplementation ended. The reason for the difference over time is not clear, but the authors suggest caution in the use of high-dose -tocopherol supplementation for cancer chemoprevention.
In an editorial, Kim and Hong (p. 468) suggest that several questions must be addressed to improve the success of future chemoprevention trials: Are chemoprevention strategies worth pursuing? What agents are appropriate for testing? Which patient populations are appropriate to study? What type of chemoprevention approach should be pursued?
Menopausal Hormone Therapy After Breast Cancer
Von Schoultz and Rutqvist (p. 533) report results of two independent randomized clinical trials of patients with early-stage breast cancer that compared menopausal hormone therapy with no such treatment. They note that, although the designs of both studies were similar, one trial, the Stockholm trial, had the unique goal to minimize use of progestogen combined with estrogen. The other trial, the Hormonal Replacement Therapy After Breast Cancer—Is It Safe? (HABITS) was stopped after 2.1 years of follow-up because of a higher risk of breast cancer recurrence associated with menopausal hormone therapy than with no treatment. However, at 4.1 years of follow-up in the Stockholm trial, risk of breast cancer recurrence was not associated with menopausal hormone therapy. The authors conclude that the doses of estrogen and progestogen and treatment regimens may be related to the risk of breast cancer recurrence.
In an editorial, Chlebowski and Anderson (p. 471) point out that the results of these two trials provide additional evidence that use of combined estrogen and progestin is associated with a higher breast cancer risk than its nonuse. They urge that trials be designed to test specific agents that relieve estrogen-deficiency symptoms in breast cancer survivors, such as the use of estrogen alone in symptomatic women with a hysterectomy.
Erythropoietin Treatment for Cancer-Related Anemia
To determine the association between erythropoietin treatment and hematologic response, blood transfusion, adverse events, and overall survival, Bohlius et al. (p. 489) conducted a systematic review and a meta-analysis of the results of 27 randomized controlled trials published between 1993 and May 2002. The trials compared adult cancer patients treated with recombinant human erythropoietin with those not treated. The authors found that risk for blood transfusion was lower in treated patients, that patients with very low baseline hemoglobin levels were more likely to have a hematologic response than untreated patients, and that risk for thromboembolic events was similar between the groups. The authors conclude that erythropoietin treatment may reduce the risk for blood transfusions and improve hematologic response in cancer patients and that evidence that erythropoietin affects survival is inconclusive.
Trial of Maintenance Chemotherapy for NSCLC
Non–small-cell lung cancer is a leading cause of cancer mortality; more than 85% of NSCLC patients die within 2 years after receiving standard cisplatinbased chemotherapy. One possible strategy to improve survival is to prolong the duration of chemotherapy treatment by following the initial (induction) treatment with a second, maintenance regimen that involves a different drug. In this issue (p. 499), Westeel et al. report the results of a randomized trial in which NSCLC patients who responded to induction treatment with mitomycin–ifosfamide–cisplatin (MIC) were then randomly assigned to receive intravenous vinorelbine or no further treatment. There were no differences between the arms in progression-free or overall survival. Moreover, vinorelbine treatment was associated with higher toxicity in MIC-treated patients than was seen previously in chemotherapy-naïve patients.
Tumor Growth and Circadian Clock Gene Expression in Mice
The circadian clock regulates the approximate 24-hour cycles of many animals, including mammals. It has been reported that tumors grow faster in animals with a disrupted circadian clock, but the molecular mechanism is unclear. Filipski et al. (p. 507) compared the expression patterns of circadian clock and cell cycle genes in the livers and tumors of mice synchronized by normal light and dark schedules (normal circadian clock) or with schedules designed to simulate chronic jet lag in humans (disrupted circadian clock) and found that meal timing reversed the disrupted circadian clock gene expression patterns and slowed tumor growth in chronically jet-lagged mice. The authors conclude that altered light-dark or feeding schedules modified the expression of circadian clock genes and genes involved in carcinogenesis and tumor progression.
Dietary Patterns and the Risk of Pancreatic Cancer
To determine whether dietary patterns are associated with the risk of pancreatic cancer, Michaud et al. (p. 518) analyzed data from two large prospective cohort studies. They identified two major dietary patterns, "prudent" (characterized by high fruit and vegetable intake) and "western" (characterized by high meat and high fat intake), by factor analysis. In a pooled analysis of men and women, they found no association between either dietary pattern and the risk of pancreatic cancer. Stratifying by body mass index or physical activity did not change the association. They concluded that dietary patterns were not associated with the risk of pancreatic cancer in these two large cohort studies of men and women.
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