Other highlights in the February 18 issue of JNCI

February 17, 2004

Two Studies Examine Aspirin for Cancer Prevention

Two studies in the February 18 issue of JNCI address the association between aspirin use and the risk of two different types of cancer.

In one study, Ellen T. Chang, Sc.D., of the Harvard School of Public Health, and colleagues examined the association between various pain relievers and the risk of Hodgkin's lymphoma. In a case-control study, participants were asked to report their average use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) and of acetaminophen over the previous 5 years. They found that the risk of Hodgkin's lymphoma was lower with regular aspirin use (2 or more tablets per week) than with non-regular aspirin use, and that there was no association between risk of Hodgkin's lymphoma and use of other non-aspirin NSAIDs, but the risk was higher with regular acetaminophen use.

"If aspirin use is indeed found to protect against Hodgkin's lymphoma, this relationship could afford insight into the pathogenesis of the disease and offer possible clues toward its prevention," the authors write.

In a second study, Chin Hur, M.D., of Massachusetts General Hospital, and colleagues examined the cost-effectiveness of aspirin as a chemoprevention strategy for esophageal cancer in patients with Barrett's esophagus. Patients with Barrett's esophagus are at an increased risk for esophageal cancer and, as such, often undergo periodic endoscopic screening. Aspirin use has been associated with a reduced risk of esophageal cancer, but the use of aspirin can cause bleeding and other harms.

Using a model analysis to compare the effectiveness and cost-effectiveness of aspirin for the chemoprevention of esophageal cancer in patients with Barrett's esophagus, Hur and colleagues found that aspirin therapy with or without endoscopic surveillance was both more effective (in terms of quality-adjusted life years) and cost less than no therapy or just endoscopic surveillance, respectively.

  • Aspirin and Hodgkin's lymphoma:
    Kevin Myron, Harvard School of Public Health, 617-432-3952, kmyron@hsph.harvard.edu
  • Aspirin and Barrett's esophagus:
    Sue McGreevey, Massachusetts General Hospital, 617-724-2764, smcgreevey@partners.org

    Tissue Microarray Analysis Yields Clues to Gene's Role in Cancer

    The loss of function of the tumor suppressor gene PML plays a role in the development of acute promyelocytic leukemia (APL). To investigate whether loss of PML function is involved in the development of other human cancers, Carmela Gurrieri and Pier Paolo Pandolfi, M.D., Ph.D., of Memorial Sloan-Kettering Cancer Center, and colleagues subjected tumor samples from patients with a wide variety of solid tumors to tumor tissue microarray analysis.

    They found that PML protein expression was reduced or abolished in many of the tumor types examined and that loss of PML protein was associated with tumor progression in prostate cancer, breast cancer, and central nervous system tumors. However, PML mRNA expression was not affected, and the PML gene was rarely mutated and was not subject to loss of heterozygosity. The authors present evidence that a proteasome-dependent mechanism may lead to PML destabilization in some cancer cells.

    Study Characterizes Gene Silencing in Precursor to Cervical Cancer

    Infection with high-risk human papillomavirus (HPV) types causes cervical cancer, and genetic and epigenetic processes drive the subsequent progression from premalignant cervical intraepithelial neoplasia (CIN) to invasive cervical cancer. Renske Steenbergen, Ph.D., of the Vrije Universiteit Medical Center in Amsterdam, and colleagues examined the role of the gene that encodes an adhesion molecule called tumor suppressor in lung cancer 1 (TSLC1) in this progression.

    They found that cervical carcinoma cell lines expressed less TSLC1 mRNA and had more TSLC1 promoter methylation than non-tumorigenic HPV-immortalized keratinocyte cell lines, and that overexpression of TSLC1 was associated with reduced anchorage-independent cell growth in vitro and the inhibition of tumor formation in mice. TSLC1 promoter hypermethylation was detected among high-grade CIN lesions and cervical squamous cell carcinomas, but not among cervical epithelial biopsy samples or low-grade CIN lesions.

    Titles of additional articles appearing in the February 18 JNCI:
    Note: The Journal of the National Cancer Institute is published by Oxford University Press and is not affiliated with the National Cancer Institute. Attribution to the Journal of the National Cancer Institute is requested in all news coverage. Visit the Journal online at http://jncicancerspectrum.oupjournals.org/.

    Journal of the National Cancer Institute

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