Other highlights in the July 19 JNCI

DNA In Urine May Detect Bladder Cancer

Bladder cancer can be detected using a test that examines nine genes from DNA found in a patient's urine, a study reports.

David Sidransky, M.D., of the Johns Hopkins School of Medicine in Baltimore, Md., and colleagues tested the tumor DNA and the urine DNA of 15 patients with bladder cancer and 25 controls to identify biomarkers for this cancer. They then used these markers to see if they could detect bladder cancer in 160 patients and 69 controls.

The authors found that the genetic patterns in urine DNA matched those in tumor DNA. In this way, they were able to use DNA samples from urine as a noninvasive method to identify genetic markers for patients with bladder cancer.

They write that larger, long-term follow-up "will be required in future studies to define the impact of this technology on early detection, prognosis, and disease monitoring before clinical application."

Contact: Valerie Mehl, mehlva@jhmi.edu

High Pesticide Exposure Raises Risk of Liver Cancer

DDT exposure may increase a person's chance of developing liver cancer, a study shows.

Katherine A. McGlynn, Ph.D., of the National Cancer Institute in Rockville, Md., and colleagues identified 168 patients with liver cancer and 385 controls among participants in the Nutritional Intervention Trials in Linxian, China. They measured the subjects' pre-diagnostic serum levels of DDT and of product the DDT breaks down into, called DDE.

High levels of DDT in blood serum plasma were associated with an increased risk of developing liver cancer, particularly among individuals with low DDE levels. The authors suggest that direct DDT exposure may increase a person's risk of developing liver cancer or that some individuals may be more susceptible to the effects of DDT because of a decreased ability to break down DDT into DDE.

Contact: NCI Press Officers, 301-496-6641, NCIPressOfficers@mail.nih.gov

Growth Factor Halts Lung Cancer Metastasis

A growth factor may inhibit lung tumor metastasis by stopping blood vessel growth caused by VEGF-A, and breaking down HIF-1a, two proteins linked to cancer growth.

Min-Liang Kuo, Ph.D., of National Taiwan University in Taipei, and colleagues studied the effect of growth factor CTGF on human lung cancer in mice. Data showed that CTGF breast down HIF1 which leads to repression of VEGF-A. This results in inhibition of lung tumor angiogenesis and metastasis.

In an accompanying editorial, Adriana Albini, Ph.D., of the National Cancer Research Institute in Genova, Italy, and colleagues write, "Targeting the tumor microenvironment, in addition to the tumor cells and/or endothelial cells themselves, may permit important improvements to clinical outcomes in the future."

Contacts:
Article: Min-Liang Kuo, toxkml@ha.mc.ntu.edu.tw Editorial: Adriana Albini, Adriana.albini@istge.it

Study Says Mouse Breast Stem Cells Are Similar to Aggressive Human Breast Cancer

A study by Geoffrey Lindeman, M.D., Ph.D., Jane Visvader, Ph.D., and colleagues at the Walter and Eliza Hall Institute in Melbourne, Australia, in collaboration with the BC Cancer Agency in Vancouver, Canada, finds that mouse mammary stem cells express receptor patterns similar to those of aggressive (or basal) human breast cancer, in which the stem cells did not express estrogen and progesterone receptors but did express another receptor. In contrast, mouse mammary cells that were not stem cells (luminal cells), expressed estrogen and progesterone receptors, similar to less aggressive types of breast cancer.

In an accompanying editorial, William F. Anderson, M.D., and Rayna Matsuno of the National Cancer Institute in Bethesda, Md., discuss the importance of Lindeman's findings. They write, "These data provide opportunity for reflection and change. At a minimum, breast cancer can no longer be viewed as a single biologic entity. […] If breast cancer consists of a mixture of at least two main types, we need a stratified rather than a unified approach for breast cancer research, prevention, and treatment."

Contact: Article: Brad Allan, Walter and Eliza Hall Institute of Medical Research, 61-3-9345-2345, allan@wehi.edu.au, or Nicole Adams, BC Cancer Agency, 604-877-6272, nadams@bccancer.bc.ca Editorial: NCI Press Officers, 301-496-6641, NCIPressOfficers@mail.nih.gov

Genetic Variation Not Linked To Breast Cancer Risk in New Study

Women with two copies of a genetic variation called STK15 F31I do not have an increased risk of breast cancer, a new study suggests. However, a meta-analysis of related studies produced inconsistent results. The study, led by Julian Peto, who heads the Cancer Research UK Epidemiology Group at the London School of Hygiene and Tropical Medicine, an colleagues at the Institute of Cancer Research in London, examined 507 patients with two primary breast cancers and 875 controls for the STK15 F31I genetic variation. They did not find an association between the genetic variation and breast cancer risk. They suggest that conflicting results obtained from their meta-analysis may be due to publication bias or population differences.

Contact: Julian Peto, 44-207-927-2455, julian.peto@lshtm.ac.uk

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Also in the July 18 JNCI: • Dietary Modifications May Not Benefit Cancer Patients: http://www.eurekalert.org/emb_releases/2006-07/jotn-dmm071306.php

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.oxfordjournals.org/.


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