If a woman has a negative Pap test along with a negative test for cervical cancer-causing human papillomavirus (HPV) DNA, that may be an indication that she does not need to be screened as often for cervical cancer as women who have positive results, suggests a study in the January 1 issue of the Journal of the National Cancer Institute.
Mark E. Sherman, M.D., of the National Cancer Institute, and his colleagues examined the risk of cervical intraepithelial neoplasia 3 (CIN3) or cervical cancer among more than 20,000 women who received simultaneous screening with a Pap test and an HPV DNA test. They found that women with negative Pap and HPV baseline tests were at low risk for CIN3 or cancer in the subsequent 45 months. In contrast, women with a positive HPV test and a negative Pap test remain at risk and should continue routine screening, they say. They note that further evaluation of the role of HPV testing alone or in combination with Pap testing for cervical cancer screening is the focus of ongoing clinical trials.
Contact: NCI Office of Communications, 301-496-6641; fax: 301-496-0846, ncipressofficers@mail.nih.gov
Researchers Recommend Ways to Improve Analyses of DNA Microarray Data
DNA microarrays are increasingly being used for analyzing gene expression in human cancers. However, converting the thousands of data points from these microarrays into clear interpretable information has been challenging. In a commentary in the January 1 issue of the Journal of the National Cancer Institute, Richard Simon, D.Sc., of the National Cancer Institute, and his colleagues discuss the validity and effectiveness of methods for designing DNA microarray experiments and analyzing microarray data. They say that investigators should be aware of the potential pitfalls of using DNA microarray data if gene expression profiles are to be used to build predictors of patient prognosis.
Contact: NCI Office of Communications, 301-496-6641; fax: 301-496-0846, ncipressofficers@mail.nih.gov
Study Identifies Mechanism of Oltipraz Chemoprevention
The chemopreventive drug oltipraz is thought to exert its protective effects through the induction of glutathione-S-transferase (GST), which in turn detoxifies many chemical carcinogens. To identify the molecular signals that stimulate this induction, Keon Wook Kang and Sang Geon Kim, Ph.D., of Seoul National University, and their colleagues investigated the role of the CCAAT/enhancer binding protein (C/EBP) in oltipraz induction of GSTA2 (alpha form) and identified enhancer elements responsible for this induction in rat liver cells. The authors found that oltipraz activates C/EBPß, whose nuclear translocation activates the C/EBP binding site in the GSTA2 gene. They also found that the phosphatidylinositol 3-kinase pathway regulates nuclear translocation of C/EBPß.
Journal
JNCI Journal of the National Cancer Institute