Other highlights in the August 18 JNCI

08/12/04

Chromosomal Regions Containing Possible Prostate Cancer Susceptibility Genes Identified

A new study has identified five chromosomal regions that are likely to harbor prostate cancer susceptibility genes.

Prostate cancer is the second leading cause of cancer death among men in the United States. Family history is one of the most well-established risk factors for the disease, but no genes that confer prostate cancer susceptibility have been found to date.

In an analysis of 426 families with histories of prostate cancer, Jeffrey M. Trent, Ph.D., of the Translational Genomics Research Institute in Phoenix, and Jianfeng Xu, M.D., Dr.PH., of Wake Forest University School of Medicine in Winston-Salem, N.C., and colleagues found evidence of a prostate cancer susceptibility gene on the long arm of chromosome 17. In addition, four other regions that might hold susceptibility genes were identified among specific subsets of families. Further fine mapping studies will be needed to identify any prostate cancer susceptibility genes in these regions, the authors say.

Contacts:

  • Wake Forest University: Karen Richardson (krchrdsn@wfubmc.edu) or Shannon Koontz (shkoontz@wfubmc.edu), 336-716-4587
  • TGen: Galen Perry, Director of Communications, 602-343-8423, gperry@tgen.org

    Gene Mutation Associated With Lower Risk of Prostate Cancer Found

    Men who carry a specific mutation in the MIC-1 gene may have a lower risk of developing prostate cancer than men who do not have the mutation, according to a new study. Henrik Grönberg, Ph.D., of Umeĺ University in Umeĺ, Sweden, and colleagues had hypothesized that variations in the MIC-1 gene, which is thought to play an important role in the inflammatory response to infection, could be associated with the risk of prostate cancer.

    Contact: Henrik Grönberg, Umeĺ University, 46-90-785-1982 or 46-90-785-6888, henrik.gronberg@oc.umu.se

    Gene Hypermethylation May Help Predict Neuroblastoma Prognosis

    Neuroblastoma is the most common extracranial solid cancer diagnosed in infants and children, but there are few predictors for the disease's prognosis. In a new study of neuroblastoma cell lines and tumor samples, Manel Esteller, M.D., Ph.D., of the Spanish National Cancer Centre in Madrid, and colleagues found that by looking at the hypermethylation status--an indicator of whether a gene is turned on or off--of the promoters of several tumor suppressor genes, they could group tumors by their potential for malignancy. This method may be able to help distinguish clinically relevant groups of neuroblastomas, according to the authors.

    Contact: Miguel Alaminos, Spanish National Cancer Centre, 34-95-822-8146 or 34-95-824-4034, malaminos@histolii.ugr.es

    Study Identifies Possible New Target for Anticancer Drug Development

    Expression of the enzyme heparanase is associated with the invasive, angiogenic, and metastatic potential of a variety of malignant tumors, and with poor survival of cancer patients. In a new study, Israel Vlodavsky, Ph.D., of the Bruce Rappaport Faculty of Medicine in Haifa, Israel, and colleagues of the Hadassah Medical Center in Jerusalem found that silencing the heparanase gene in mouse tumors resulted in less vascularization and metastasis and extended the survival of the mice. The authors conclude that heparanase gene silencing could be a potential target for anticancer drug development.

    Contact: Israel Vlodavsky, Bruce Rappaport Faculty of Medicine (Technion, Haifa), 972-4-829-5410, vlodavsk@cc.huji.ac.il

    Researchers Study Molecular Mechanisms Involved in Medullary Thyroid Carcinoma

    In a new study of medullary thyroid carcinoma in mice, Brigitte M. Pützer, M.D., Ph.D., of the University of Rostock in Rostock, Germany, and colleagues found that disruption of oncogenic RET signaling is associated with decreased cell viability and cell proliferation in vivo, which indicates that RET stimulates cell proliferation and inhibits apoptosis. The authors suggest that RET signaling should be investigated further as a target for new therapies for the disease.

    Contact: Grit Haberer, University of Rostock, 49-381-494-5066, grit.haberer@med.uni-rostock.de

    Also in the August 18 JNCI:

  • Intervention Studies That Use Cancer Patients from High-Risk Clinics May Be Subject to Bias: http://www.eurekalert.org/emb_releases/2004-08/jotn-ist081204.php

    Source: Eurekalert & others

    Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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