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© Oxford University Press 2007.
IN THIS ISSUE
New Guidelines for Microarray Data Analysis and ReportingDNA microarray technology, which allows the expression of thousands of genes in a small biologic sample to be readily quantified, has recently found many applications in cancer research. However, questions have been raised about the validity of studies that analyze microarray data to better understand biologic mechanisms or to develop tools that predict clinical outcomes. Focusing on studies in which gene expression profiles were related to a clinical cancer outcome, Dupuy and Simon (p. 147) recorded common errors in recently published statistical analyses of microarray data. They then developed guidelines for the analysis of these data that are presented as a checklist of Dos and Don'ts.
Intensified Chemotherapy in Osteosarcoma Patients
Using modern chemotherapy with surgery, the 5-year survival rate of patients with localized high-grade osteosarcoma is 50–70%. However, several recently complete clinical trials found that increasing the number of chemotherapeutic agents or the length of treatment did not improve patient survival. Lewis et al. (p. 112) conducted a randomized clinical trial in which cisplatin and doxorubicin were given to osteosarcoma patients in the same total doses as in conventional treatment but over a shorter time period. This intensified treatment regimen improved histologic response compared with conventional treatment but did not lead to a statistically significant improvement in survival.
In an accompanying editorial, George (p. 98) discusses questions that must be addressed if response rate is to be properly used as an endpoint in a clinical trial.
Colorectal Adenomas After Cessation of Calcium Treatment
Calcium supplements reduce the risk of colorectal adenomas in people with a history of these tumors. To investigate whether the protective effect of calcium extends beyond the period of active supplementation, Grau et al. (p. 129) followed participants in a randomized trial of calcium supplementation for an average of 7 years after the end of randomized treatment. Subjects in the calcium group had a lower risk of adenomas than those in the placebo group during the first 5 years after treatment ended, but there was no difference in adenoma risk in the subsequent 5 years. The authors conclude that the protective effect of calcium supplementation extends for up to 5 years after active treatment.
In an editorial, Martínez and Jacobs (p. 99) discuss the public health implications of the results of this study and other calcium supplementation trials. They point out that, important as efforts at risk reduction are, it is also essential to increase rates of colorectal cancer screening.
Dietary Antioxidant Supplements and the Risk of Gastric Cancer
Gastric cancer is one of the most common malignancies worldwide, with nearly a million new cases per year. Responding to epidemiologic evidence that a diet rich in fresh fruit and vegetables may be protective, Plummer et al. (p. 137) tested the effect of daily supplementation with the antioxidants vitamin C, vitamin E, and beta-carotene on the progression and regression of pre-cancerous gastric lesions in a Venezuelan population at high risk for gastric cancer. Although 3 years of vitamin supplementation increased median plasma levels of all three vitamins, it had no effect on rates of progression or regression of pre-cancerous lesions.
In an accompanying editorial, Taylor (p. 101) summarizes the results of clinical trials that aimed to prevent gastric cancer and recommends some approaches that should be emphasized in future trials.
Allergies, Cancer, and the Risk of Non-Hodgkin Lymphoma
An association between allergies and cancer, including non-Hodgkin lymphoma (NHL), has been suspected. Melbye et al. (p. 158) investigated the association between allergy and NHL in a population-based case–control study and in a prospective study with prediagnostic blood specimens. In the first study, they found that having hay fever, but not other allergic conditions, was associated with a reduced risk of NHL. Specific IgE reactivity in serum, an indication of an allergic reaction, was associated with lower NHL risk. However, among case patients, specific IgE reactivity was inversely associated with NHL dissemination. In the second study, no association was found between NHL and specific IgE reactivity, except possibility immediately before diagnosis. The authors conclude that allergy may not be associated with NHL risk. The inverse association observed may arise because NHL suppresses the immunologic response to allergens.
Ki67 Expression in Tumors After Short-Term Endocrine Therapy
A change in tumor expression of the cell proliferation antigen Ki67 after short-term exposure to therapeutic agents is a marker of efficacy in breast cancer patients before they undergo surgery. To examine the prognostic value of Ki67 expression during endocrine therapy, Dowsett et al. (p. 167) measured the levels of Ki67 in tumor biopsy samples taken before and after 2 weeks of presurgical treatment with anastrozole or tamoxifen alone or in combination in 158 patients with hormone receptor–positive primary breast cancer. They found that higher Ki67 expression after 2 weeks of endocrine therapy was associated with lower recurrence-free survival, whereas higher Ki67 expression before therapy was not. The authors conclude that measurement of tumor Ki67 expression after short-term endocrine treatment may improve the prediction of recurrence-free survival.
Periodontal Disease and the Risk of Pancreatic Cancer
Previous studies have reported positive associations between tooth loss or periodontal disease and risk of pancreatic cancer. To further examine this association, Michaud et al. (p. 171) analyzed data from a prospective survey-based study of more than 50,000 male health professionals aged 40–75. After 16 years of follow-up, 216 men were diagnosed with pancreatic cancer. A history of periodontal disease was associated with an increased risk of pancreatic cancer, compared with no history of periodontal disease, even after adjusting for smoking history (overall, 61 vs. 25 cases per 100,000 person-years; never smokers, 61 vs. 19 cases per 100,000 person-years). The authors conclude that plausible biologic mechanisms may be involved but that confirmation of the association is necessary.
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J Natl Cancer Inst 2007 99: 101-103.
J Natl Cancer Inst 2007 99: 112-128.
J Natl Cancer Inst 2007 99: 129-136.
J Natl Cancer Inst 2007 99: 137-146.
J Natl Cancer Inst 2007 99: 147-157.
J Natl Cancer Inst 2007 99: 158-166.
J Natl Cancer Inst 2007 99: 167-170.
J Natl Cancer Inst 2007 99: 171-175.
J Natl Cancer Inst 2007 99: 98-99.
J Natl Cancer Inst 2007 99: 99-100.
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