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© Oxford University Press 2007.
IN THIS ISSUE
Evidence on Use of PET in Lung Cancer Diagnosis and StagingTumor imaging with 18fluorodeoxyglucose positron emission tomography, or PET, has the potential to improve the clinical management of patients with lung cancer. Ung et al. (p. 1753) identified studies that have provided evidence about the use of PET in lung cancer diagnosis and staging. Their systematic review indicates that PET has high sensitivity and reasonable specificity for distinguishing between benign and malignant lesions and that it is better than computed tomography for staging mediastinal tumors in non–small-cell lung cancer. PET also appears to have good accuracy in staging patients with small-cell lung cancer. The authors underscore the need for cytologic or histologic confirmation of mediastinal lymph node involvement to avoid denying patients potentially curative surgery due to false positive mediastinal images. Future research is needed to determine not only if PET should be integrated into the standard staging and diagnosis of lung cancer but also how PET would be incorporated into a diagnostic algorithm.
In an editorial, Giaccone (p. 1741) notes that recent improvements in imaging technology will need to be considered to be able to formulate the most appropriate guidelines and recommendations for the use of PET in lung cancer.
Invasive Breast Cancer Risk Models in African American Women
The National Cancer Institutes Breast Cancer Risk Assessment Tool, also known as the Gail model, is widely used for counseling individuals and determining eligibility for breast cancer prevention trials, but its validity for projecting risk in African American women is uncertain. Gail et al. (p. 1782) developed a model for projecting the risk of invasive cancer in African American women using data from the Women's Contraceptive and Reproductive Experiences (CARE) study. The number of cancers predicted for African American women by the CARE model was higher than that predicted by the Breast Cancer Risk Assessment Tool and agreed well with the number of cancers observed among African American women in the Women's Health Initiative. The authors conclude that the CARE model is recommended over the Breast Cancer Risk Assessment Tool for counseling African American women about their breast cancer risk.
Tumor Microenvironment and Efficacy of Oncolytic Virus Therapy
Oncolytic viruses have tumor-killing properties in experimental models, but they have not shown efficacy in patients. Host immune responses combined with changes in the tumor vasculature in response to ongoing tumor cell destruction may limit the therapeutic effectiveness of oncolytic viruses. Kurozumi et al. (p. 1768) used a rat glioma model to investigate oncolytic virus therapy–induced changes in tumor blood vessels and the impact of modulating the tumor vasculature with an angiogenesis inhibitor, cRGD peptide, on the efficacy of oncolytic virus therapy. Treatment of rat gliomas with an oncolytic virus increased tumor vessel leakage, tumor inflammation, and leukocyte infiltration (a marker of the host immune response). Pretreatment of rat gliomas with the angiogenesis inhibitor reduced all three responses and enhanced the anticancer efficacy of oncolytic virus treatment by increasing its propagation in tumors.
In an editorial, Rhim and Tosato (p. 1739) discuss the impact of the tumor microenvironment on the growth and survival of tumor cells and whether other antiangiogenic therapies may improve the efficacy of oncolytic virus therapy in patients.
Carbohydrates, Insulin Levels, and Prostate Tumor Growth
Recent studies have shown that obesity is an important adverse prognostic factor in prostate cancer, but the mechanism of this association is unknown. Venkateswaran et al. (p. 1793) assigned mice that had been engrafted with human prostate cancer cells to one of two diets of equal caloric value but different carbohydrate content. Mice fed the high-carbohydrate diet weighed more and showed higher serum insulin and insulin-like growth factor levels than mice fed the low-carbohydrate diet. The tumors of mice on the high-carbohydrate diet exhibited faster growth that was associated with evidence of increased insulin-mediated signaling in the tumors. The authors suggest that additional research is needed to determine whether diets that are associated with reductions in insulin levels may have benefits for prostate cancer patients.
Distinct Etiology of HPV16-Associated Head and Neck Cancers
Alcohol consumption, smoking, and infection with human papillomavirus type 16 (HPV16) are risk factors for head and neck squamous cell carcinoma (HNSCC), but the relationships among these factors has been unclear. Applebaum et al. (p. 1801) investigated the smoking and drinking habits of patients with HNSCC and matched control subjects and tested their blood for the presence of antibodies signifying prior HPV16 infection. Regression models were used to analyze the relationships among the three variables as risk factors for HNSCC. Smoking and alcohol consumption did not add to the risk of HNSCC in patients who were infected with HPV16, suggesting that the etiologies of HPV16-related HNSCC and smoking and alcohol- related HNSCC are distinct.
Breast Cancer Risk Among Male BRCA1, BRCA2 Mutation Carriers
Men who carry germline mutations in the BRCA2 gene are known to have a higher risk of developing breast cancer than men in the general population, but it is unclear whether the same holds true for men with germline mutations in the BRCA1 gene. Tai et al. (p. 1811) evaluated the risk of developing breast carcinoma for male BRCA1 and BRCA2 mutation carriers in the U.S. population based on data from 1,939 families that included 97 male members with breast cancer. At all ages, the cumulative risk of male breast cancer was higher in both BRCA1 and BRCA2 mutation carriers than in noncarriers. The relative risk of developing breast cancer was highest for men in their 30s and 40s and decreased with increasing age. Both the relative and cumulative risks of breast cancer were higher for male BRCA2 mutation carriers than for male BRCA1 mutation carriers.
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J Natl Cancer Inst 2007 99: 1811-1814.
J Natl Cancer Inst 2007 99: 1782-1792.
J Natl Cancer Inst 2007 99: 1768-1781.
J Natl Cancer Inst 2007 99: 1793-1800.
J Natl Cancer Inst 2007 99: 1753-1767.
J Natl Cancer Inst 2007 99: 1801-1810.
J Natl Cancer Inst 2007 99: 1739-1741.
J Natl Cancer Inst 2007 99: 1741-1743.
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