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© Oxford University Press 2007.
IN THIS ISSUE
Androgen Deprivation Therapy and the Risk of Cardiovascular DeathAndrogen deprivation therapy (ADT) may increase the risk of coronary artery disease. Tsai et al. (p. 1516) investigated the relationship between ADT use and the risk of death from cardiovascular causes in patients with localized prostate cancer. Among patients 65 years or older treated with radical prostatectomy, ADT use was associated with a statistically significant increase in the risk of death from cardiovascular causes. The 5-year cumulative incidence of cardiovascular death was 5.5% among patients receiving ADT and 2.0% among those who did not. Among patients who received other prostate cancer therapies, ADT use was also associated with an increased cumulative incidence of death from cardiovascular causes, but the increase was not statistically significant. The authors conclude that cardiovascular evaluation and intervention are advisable before initiating ADT.
In an editorial, Seidenfeld et al. (p. 1498) note that, in light of the association between ADT use and risk of cardiovascular death, the recommendation that patients should consider getting a cardiovascular evaluation before adding ADT to their treatment regimen makes sense for now. However, patients and clinicians need risk estimates that are based on randomized trials rather than retrospective analyses.
Risk of Invasive Cancer in the WHI Dietary Modification Trial
The Women's Health Initiative Dietary Modification Randomized Controlled Trial previously assessed the effects of a low-fat diet on the risks of breast cancer, colorectal cancer, and cardiovascular disease. Prentice et al. (p. 1534) examined the effects of the dietary modification on the risks of invasive ovarian and endometrial cancer and on the risk of overall invasive cancer. During 1993–98, more than 48,000 postmenopausal women were randomly assigned to a dietary modification intervention or their usual diet and followed for an average of 8.1 years. The risk for ovarian cancer was similar during the first 4 years, but it was reduced in the intervention group during the subsequent 4.1 years (0.38 cases versus 0.64 cases per 1,000 person-years). The risk of endometrial cancer was similar in the two groups, whereas a lower overall invasive cancer risk in the intervention group was suggested. The authors conclude that a low-fat diet may lower the risk of ovarian cancer in postmenopausal women.
Genetic Variants in Chromosome 8q24 and Prostate Cancer Risk
Genetic markers at human chromosome 8q24 have been linked to an increased risk of prostate cancer. Zheng et al. (p. 1525) evaluated associations between 18 single-nucleotide polymorphisms in a 1-Mb interval at 8q24 and the risk of prostate cancer among 1,563 patients and 576 control subjects of European American ancestry. They identified three independent loci at 8q24 that are associated with an increased risk of prostate cancer. An analysis of loci 1 and 2 indicated that 35% of the control subjects carried risk genotypes at one or both of these loci.
In an editorial, Savage and Greene (p. 1499) review other recently published genetic association studies involving this chromosome region and prostate cancer risk. They discuss how institutional policies that support data sharing in large genetic association studies have accelerated the pace of genomic research and discovery.
The Value of PSA Velocity in Prostate Cancer Screening
Prostate-specific antigen velocity (PSAV), the change in serum PSA level over time, has been used extensively in prostate cancer screening, but its value remains controversial. Etzioni et al. (p. 1510) review the current literature and enumerate a series of statistical considerations that should be made when evaluating and interpreting studies of PSAV. They outline several limitations of using PSAV in prostate cancer screening and show that this measure of PSA change may lead to confusion between disease aggressiveness and time from disease onset to detection. Studies documenting the association between PSAV and prostate cancer-specific survival do not necessarily prove that PSAV will be a valuable tool in prostate cancer screening, they write. Proof of the utility of PSAV will require a systematic evaluation of both the benefits and the costs of adding this measure of PSA change to established PSA screening practices.
Association Between Allergies and Brain Cancer Risk
A history of atopic conditions—asthma, eczema, or allergy—has been associated with a reduced risk of glioma in epidemiologic studies. Associations between meningioma, another type of brain tumor, and atopic disease have been less consistent. To further investigate the association, Linos et al. (p. 1544) carried out a meta-analysis of case–control and cohort studies. Eight observational studies were identified that included 3,450 patients with glioma and 1,070 with meningioma. Individuals with a history of an atopic condition had a 30–40% lower risk of glioma of those with no such history; no association was seen for meningioma. There was no evidence of bias caused by proxy reporting and no indication that publication bias explains the results. The authors suggest that, if the association with glioma is causal, it may reflect a protective effect of heightened immunity on intracranial tumor growth.
Targeting Tumor Endothelial Marker-8 with TEM8-Fc
Tumor endothelial marker-8 (TEM8) is an anthrax toxin receptor that is present in the cell membrane of tumor endothelial cells and appears to be specific for tumor angiogenesis. Duan et al. (p. 1551) developed an antibody-like molecule (TEM8-Fc) to target TEM8 in tumor cells. Treatment with TEM8-Fc led to a decrease in growth and metastasis of xenograft tumors derived from human cell lines in immune system–deficient mice. In vitro, TEM8 interacted with the M2 isoenzyme of pyruvate kinase (M2-PK), which has been previously shown to have a role in tumor growth and metastasis. The authors conclude that TEM8-Fc is a new antibody-like therapeutic agent for solid tumors that may act by binding to and inhibiting M2-PK activity.
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Del.icio.us What's this?
J Natl Cancer Inst 2007 99: 1551-1555.
J Natl Cancer Inst 2007 99: 1534-1543.
J Natl Cancer Inst 2007 99: 1516-1524.
J Natl Cancer Inst 2007 99: 1525-1533.
J Natl Cancer Inst 2007 99: 1544-1550.
J Natl Cancer Inst 2007 99: 1510-1515.
J Natl Cancer Inst 2007 99: 1498-1499.
J Natl Cancer Inst 2007 99: 1499-1501.
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