Overexpression of a gene called uPA delayed tumor progression and decreased tumors' ability to create new blood vessels and proliferate, according to a new study.
Jaime M. Merchan, M.D., Vikas Sukhatme, M.D., Ph.D., and colleagues inserted two genes – tPA and uPA – into mammary cancer cells. These genes encode for enzymes that activate plasminogen, an enzyme that helps break down blood clots.
Mice inserted with the mammary cells overexpressing tPA and uPA showed increased inhibition of tumor growth and metastasis in the lungs. When mammary cancer cells carried uPA genes with mutations that inhibited the activity of its enzymes, the tumors grew faster than tumors overexpressing active uPA. The authors suggest that uPA expression delays tumor progression and decreases angiogenesis and proliferation.
In an accompanying editorial, Giovanna Tosato, M.D., and Mahashi Narazaki, Ph.D., from the National Cancer Institute in Bethesda, Md., point to the clinical observation that link high tumor expression of uPA with poor prognosis and discuss differences between the experimental mouse model and human cancer. They write, "the study by Merchan et al…raises important unresolved questions relative to the role of PAs in cancer progression."
Merchan and Sukhatme completed this research at the Mayo College of Medicine in Rochester, Minn., and Beth Israel Deaconess Medical Center and Harvard Medical School in Boston, Mass. Merchan now works at the University of Miami.
Contacts:
Article: William Kaufhold, University of Miami, 305-243-5184, kkaufhold@med.miami.edu
Editorial: NCI Press Officers, 301-496-6641, NCIPressOfficers@mail.nih.gov
Cost Effectiveness for Mammography Screening Guidelines Estimated
Choosing efficient mammography screening policies requires evaluating the cost effectiveness of screening programs and understanding their impact on patients' quality of life, a new study reports.
Natasha K. Stout, Ph.D., at the Harvard School of Public Health in Boston, and colleagues created a model to simulate mammography outcomes in the United States between 1990 and 2000 for women aged 40 and older. They estimated the costs and cost effectiveness for screening as practiced in the 1990s, as well as no screening and 64 different screening scenarios.
The authors observed that actual screening practices in the 1990s, which were a mixture of frequent and infrequent screening, have added substantially to the quantity and quality of life of women in the United States at an additional $62.5 million compared to the cost of no screening. They found that many other screening practices could add ever more to women's quantity and quality of life for lower costs than actual practices.
The authors write, "Because many of the alternative screening scenarios examined in our analysis were more effective and less costly than the actual screening patterns from 1990 through 2000, it is likely that current screening programs can be improved."
Contact: Todd Datz, Harvard School of Public Health, 617-432-5531, tdatz@hsph.harvard.edu
Imatinib Fights Prostate Cancer By Targeting Endothelial Cells
Imatinib, a molecule that inhibits a growth factor commonly expressed by tumor cells, can counter prostate cancer by targeting a molecule (PDGF-R) located on tumor-associated endothelial cells rather than the tumor cells themselves. Isaiah J. Fidler, D.V.M, Ph.D., at the University of Texas M.D. Anderson Cancer Center in Houston, and colleagues implanted multidrug-resistant prostate cancer cells in mice, who were then randomly assigned to receive treatment with the anticancer drug paclitaxel, imatinib, imatinib and paclitaxel or water (control). Treatment with imatinib or with imatinib plus paclitaxel resulted in prostate bone tumor regression and inhibited lymph node metastasis.
Contact: Laura Sussman, 713-745-2457, lsussman@mdanderson.org
Review Describes COX-2 Independent Targets of Some NSAIDs with Anti-Cancer Activity
Nonsteroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of developing cancer by inhibiting the activity of an enzyme called COX-2. A review by Sabine Groesch, Ph.D., of the Institut fuer Klinische Pharmakolgie in Frankfurt, Germany, and colleagues discusses additional COX-2 independent molecular targets of some NSAIDs and how this class of drugs may work as anti-cancer agents.
Contact: Dr. Gerd Geisslinger, 0049-69-63017619, geisslinger@em.uni-frankfurt.de
Also in the June 6 JNCI:
HPV Testing Finds Precancerous Lesions at a Higher Rate than Conventional Pap Smears: http://www.eurekalert.org/emb_releases/2006-06/jotn-htf060106.php
Study Says Lung Cancer Overdiagnosis a Result of Screening: http://www.eurekalert.org/emb_releases/2006-06/jotn-ssl060106.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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JNCI Journal of the National Cancer Institute