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© Oxford University Press 2007.
IN THIS ISSUE
Health Claims of Tomatoes, Lycopene, and CancerHealth claims that describe the relationship between a food or food component and a disease—such as those based on reports of an association between tomato and/or lycopene intake and decreased risk of some types of cancer—require premarket approval by the U.S. Food and Drug Administration (FDA) to be included on labels of conventional foods and dietary supplements. Kavanaugh et al. (p. 1074) describe the FDA's evidence-based review of the scientific data on the relationship between tomato and/or lycopene intake and the risk for prostate and other cancers. The FDA found no credible evidence to support an association between lycopene intake and a reduced risk of prostate, lung, colorectal, gastric, breast, ovarian, endometrial, or pancreatic cancer. It also found no credible evidence that tomato consumption reduces the risk of lung, colorectal, breast, cervical, or endometrial cancer. The FDA found very limited evidence to support an association between tomato consumption and a reduced risk of prostate, ovarian, gastric, or pancreatic cancers.
In an editorial, Coates (p. 1059) discusses the importance of using evidence-based review principles to evaluate diet–health relationships and several issues concerning processes that FDA used to evaluate the strength of the available evidence. In a second editorial, Giovannucci (p. 1060) discusses how prostate-specific antigen screening may have influenced the results of the studies the FDA reviewed in this case.
Kaposi Sarcoma, Herpesvirus, and Immunosuppression
Infection by human herpesvirus 8 and immunosuppression have been identified as important factors in the development of Kaposi sarcoma, but whether this disease arises from the transformation and proliferation of a single cell or non-neoplastic proliferation of independent populations of cells has been difficult to resolve. Duprez et al. (p. 1086) approached this question by analyzing human herpesvirus DNA in Kaposi sarcoma lesions. Studying samples representing all clinical forms of the disease, the authors found that tumors in most patients arose from the expansion of multiple cells, although some lesions appeared to derive from a single cell based on the unique viral DNA detected. In patients with multiple lesions, analysis of the viral DNA indicated that individual lesions represented separate expansion from one or more cells. The authors conclude that Kaposi sarcoma lesions, especially in patients with advanced tumors, are reactive proliferations rather than true metastatic malignancies.
In an editorial, Gill (p. 1063) points out additional questions that need resolution if the pathogenesis of Kaposi sarcoma is to be understood. These include the possible roles of infected circulating endothelial precursor cells in the disease's development.
Microbubbles, Chemotherapy Delivery, and Tumor Imaging
Cancer drugs can be targeted to tumors by encapsulating them in micelles (nanoparticles formed by polymeric molecules) and releasing their contents with tumor-directed ultrasound, but this approach also requires a means of tumor imaging. Rapoport et al. (p. 1095) describe a method for delivering drugs in a different type of nanoparticle, called a nanobubble or microbubble. When nanobubbles containing the cancer drug doxorubicin were introduced into mice, they accumulated selectively in tumors and then coalesced to form larger microbubbles. The microbubbles generated echoes when exposed to ultrasound that allowed for tumor visualization. The resonance of the microbubbles in response to sound energy released the encapsulated drug and enhanced its entry into tumor cells. In mice treated with ultrasound, the microbubbles were more effective than micelles at inhibiting tumor growth. The authors suggest that using nanobubbles as both drug delivery and imaging agents for cancer therapy deserves further exploration.
HDAC1 Expression and Inhibition in Drug-Resistant Neuroblastoma
The low survival of patients treated for high-risk neuroblastoma may be due to drug resistance acquired during therapy, which is often caused by the loss of p53 function. To find other targets that might modulate drug resistance, Keshelava et al. (p. 1107) identified genes that were overexpressed in two drug-sensitive neuroblastoma cell lines compared with three multidrug-resistant neuroblastoma cell lines by genome-wide expression analysis. Knocking down expression of one of those genes, histone deacetylase 1 (HDAC1), made neuroblastoma cells more sensitive to chemotherapeutic agents. The histone deacetylase inhibitor depsipeptide enhanced the cytotoxicity of the four agents commonly used to treat neuroblastoma, independent of the p53 status of the neuroblastomas. The authors conclude that HDAC1 may be a therapeutic target in multidrug-resistant neuroblastoma.
Plasma Vitamin D Concentration and Risk of Colorectal Cancer
Low vitamin D status may play a role in colorectal carcinogenesis. To investigate this association, Wu et al. (p. 1120) analyzed data from the Health Professionals Follow-up Study and pooled the data with previous findings from the Nurses’ Health Study. In the Health Professionals Follow-up Study, 179 colorectal cancer patients were matched to 356 control subjects by age and month and year of blood collection. An association between higher plasma vitamin D concentration and lower risk of colorectal cancer was suggested, and a statistically significant association for reduced risk of colon cancer was observed. In the pooled analysis, higher plasma vitamin D concentration was associated with reduced risks of both colorectal and colon cancer. However, the number of rectal cancers was small and the results inconsistent. The authors conclude that the findings further support an association between vitamin D and colon cancer risk.
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J Natl Cancer Inst 2007 99: 1074-1085.
J Natl Cancer Inst 2007 99: 1120-1129.
J Natl Cancer Inst 2007 99: 1095-1106.
J Natl Cancer Inst 2007 99: 1107-1119.
J Natl Cancer Inst 2007 99: 1086-1094.
J Natl Cancer Inst 2007 99: 1060-1062.
J Natl Cancer Inst 2007 99: 1059.
J Natl Cancer Inst 2007 99: 1063.
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