News Release

Other highlights in the June 15 JNCI

Peer-Reviewed Publication

Journal of the National Cancer Institute

Study Examines Age-Related Prevalence of Anal Cancer Precursors in Homosexual Men

All age groups of sexually active, human immunodeficiency virus (HIV)-negative men who have sex with men have a high prevalence of anal cancer precursors, which may reflect their ongoing sexual exposure to human papillomavirus (HPV), and which may explain high rates of anal cancer, according to a new study.

HPV infection can cause anal and cervical cancers and their associated precancerous lesions. Knowledge of the age-related prevalence and natural history of cervical cancer precursors in women has guided the development of cervical cancer screening strategies for women. Similar information could help develop anal cancer screening strategies, particularly for men who have sex with men, a population in which anal cancer rates are high.

To determine the age-related prevalence of and risk factors for anal cancer precursors in men who have sex with men, Peter V. Chin-Hong, M.D., of the University of California, San Francisco, and colleagues obtained anal cytology and behavioral data from 1,262 HIV-negative men ages 18 to 89 in four U.S. cities: Boston, Denver, New York, and San Francisco.

The prevalence of low-grade and high-grade precancerous lesions was 15% and 5%, respectively, and did not change with age. This risk of low-grade lesions was associated with having more than five male anal sex partners, any use of "poppers" (alkyl nitrites used as recreational drugs) within the previous 6 months, use of injection drugs two or more times a month during the previous 6 months, older age at first anal intercourse, and infection with a greater number of HPV types. The risk of high-grade lesions was associated with any anal HPV infection and infection with an increasing number of HPV types.

Contact: Peter V. Chin-Hong, University of California, San Francisco, 415-502-9585, pvch@itsa.ucsf.edu

Consumption of Red and Processed Meat Associated With Increased Colorectal Cancer Risk

A new study has found that high levels of consumption of red and processed meat are associated with an increased risk of colorectal cancer, whereas high levels of fish consumption are associated with a decreased risk of the disease.

Elio Riboli, M.D., M.P.H., and Teresa Norat M.S., M.P.H., of the International Agency for Research on Cancer in Lyon, France, and colleagues used data from the European Prospective Investigation into Cancer and Nutrition (EPIC), a cohort of more than half a million Western Europeans, to examine the associations between intakes of red and processed meat, poultry, and fish and colorectal cancer risk.

During a mean follow-up of 4.8 years, 1,329 cases of colorectal cancer were documented. Among the study population, the risk of developing colorectal cancer over 10 years was 1.71% for subjects in the highest category of red and processed meat consumption compared with 1.28% for subjects in the lowest category. The risk of developing colorectal cancer was 1.86% among subjects in the lowest category of fish consumption compared with 1.28% among subjects in the highest category. There was no association between poultry consumption and colorectal cancer risk.

Contact: Nicolas Gaudin, Communications Office, International Agency for Research on Cancer, Lyon, France, com@iarc.fr

No Role for Iron Observed in Study of Colorectal Cancer in Women

A new study that used three different measures of iron status--genetic mutations, biochemical markers, and dietary intake--found no associations between iron and colorectal cancer risk in women.

Research has demonstrated that iron may be carcinogenic because of its ability to catalyze free radical formation, suppress the immune system, and fuel the growth of cancer cells. However, studies in humans that have examined the role of iron on the risk of developing colorectal cancer have had conflicting results, which may in part be the result of using different methods of measuring an individual's exposure to iron. Andrew T. Chan, M.D., M.P.H., of Massachusetts General Hospital in Boston, and colleagues used a comprehensive approach to assess the dietary iron intake and genetic and biochemical biomarkers of total body iron in a prospective, nested case–control study of women participating in the Nurses' Health Study.

None of the three markers of iron status--genetic, biochemical, or dietary--was associated with the risk of colorectal adenoma, the polyps that are precursors to most colorectal cancers. The authors conclude that their findings do not support a substantial role for iron in the development of colorectal adenoma.

Contact: Sue McGreevey, Public Affairs Office, Massachusetts General Hospital, 617-724-2764, smcgreevey@partners.org

Study Questions Performance of Microarray Data in Prediction of Breast Cancer Treatment Outcomes

Results of a new study call into question the ability of a model developed from microarray data to accurately predict outcomes from tamoxifen treatment in breast cancer patients.

Data from microarray studies have been used to develop predictive models for treatment outcome in breast cancers. One recent study identified two genes--HOXB13 and IL17BR--whose gene expression could be used to predict response to tamoxifen treatment in women with estrogen receptor-positive breast cancer. James F. Reid, of the Fondazione Istituto FIRC di Oncologia Molecolare in Milan, Italy, and colleagues attempted to validate this predictive model using an independent cohort of 58 patients with resectable estrogen receptor-positive breast cancer. They assessed the expression of the HOXB13 and IL17BR genes and the association between their expression and outcome by use of four statistical tests.

The authors could not validate the performance of the two-gene predictor with their cohort of samples nor could they develop a model with good predictive accuracy using the available independent microarray datasets. They conclude that treatment-response predictive models have poor performance with the small sample sizes of patients and the informative genes currently available.

In an editorial, Richard Simon, D.Sc., of the National Cancer Institute, provides possible explanations for the inconsistencies in the results of the two studies and makes recommendations about how these types of studies could be improved.

Contacts:

  • Article: James F. Reid, Fondazione Istituto FIRC di Oncologia Molecolare, +39-02.574.303.209, james.reid@ifom-ieo-campus.it
  • Editorial: National Cancer Institute Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov

    Study Identifies Gene That May Suppress Renal Tumors

    A new study has found evidence that the gene responsible for Birt-Hogg-Dubé (BHD) syndrome, a genetic disease characterized by the development of benign lesions in hair follicles and pulmonary cysts, may be a tumor suppressor gene that predisposes a person to renal tumors when both copies of the gene are inactivated.

    BHD syndrome is caused by a mutation in at least one copy of the BHD gene. People with BHD syndrome were found to have a sevenfold higher risk of renal cancer compared with the general population. Cathy D. Vocke, Ph.D., of the National Cancer Institute, and colleagues hypothesized that BHD may also be a tumor suppressor gene. They examined the BHD gene in 77 renal tumors from 12 patients with germline BHD mutations. They found evidence that most tumors from these patients had a mutation in their second copy of the BHD gene. They conclude that their results support a role for BHD as a tumor suppressor gene.

    Contact: National Cancer Institute Press Office, 301-496-6641, NCIPressOfficers@mail.nih.gov

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    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/.


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