From OncoLog, June 2005, Vol. 50, No. 6
In Brief
Breast Cancer Gene May Be Vaccine Target
A gene that appears to help regulate normal embryonic development somehow becomes overexpressed in breast cancer cells, according to a new study conducted by Laszlo Radvanyi, Ph.D., associate professor of breast and melanoma medical oncology at M. D. Anderson, and scientists at Sanofi Pasteur’s Cancer Vaccine Program in Toronto, Canada. The study was recently published in the August 2, 2005, issue of the Proceedings of the National Academy of Sciences. Researchers hope to use the cancer-specific protein to train the immune system to specifically attack breast cancer cells.
“There is a tremendous need for new molecular targets to treat breast cancer,” Dr. Radvanyi says. “There are very few bona fide targets that are exquisitely specific for breast cancer. We believe this is one of them.”
While doing a large-scale genetic screen, Radvanyi and his collaborators zeroed in on the gene, called TRPS-1, which is found at high levels in all forms of breast cancer. After identifying TRPS-1, they showed that T-cells trained to detect TRPS-1 would attack and kill breast cancer cells containing the protein in laboratory experiments. “This immune response against breast cancer is exciting because our protein expression analysis showed that TRPS-1 appears to be overexpressed only in cancers and not in normal tissue, making an immune response potentially very specific for the tumor only,” Dr. Radvanyi says.
Researchers will next try to understand what the protein’s targets are inside the cell. “If we understand its targets, in addition to vaccines targeting TRPS-1, we might also be able to design inhibitors that disrupt its action, which could be clinically important given its early appearance in breast cancer,” Dr. Radvanyi says.
Potential “Weak Link” Between Virus and Liver Cancer Discovered
Researchers at M. D. Anderson have uncovered a crucial molecular link between a viral infection and development of a common and fatal form of liver cancer. In the process, they have identified a possible way to treat this disease as well as a number of other cancers.
In findings reported in Molecular Cell, Mien-Chie Hung, Ph.D., professor and chair of the Department of Molecular and Cellular Oncology, and his team traced the pathway by which the hepatitis B virus leads to the development of hepatocellular carcinoma. They found that it “turns off” the enzyme GSK-3ß, which acts to suppress tumor formation and inhibit the spread of cancer.
GSK-3ß could prove to be the Achilles' heel for liver cancer and other tumors—including breast, colon, kidney, and stomach cancers—that use a similar “pathway” to cancer development, the researchers say.
“This study identified a novel mechanism for how hepatitis B primes liver cells to turn cancerous, and what we found has potential relevance for other cancers as well,” says Dr. Hung. “We think it may be possible in the near future to develop novel therapeutic approaches for treatment of . . . cancers, including development of gene therapy and a small molecule that will activate GSK-3ß.” Dr. Hung collaborated with researchers from Baylor College of Medicine in Houston as well as Germany, Taiwan, and China.For more information on this topic or for questions about M. D. Anderson’s treatments, programs, or services, call askMDAnderson at (877) MDA-6789.
TOPHome/Current Issue | Previous Issues | Articles by Topic | Patient Education
About Oncolog | Contact OncoLog
Sign Up for E-mail Alerts
©2008 The University of Texas M. D. Anderson Cancer Center
1515 Holcombe Blvd., Houston, TX 77030
1-877-MDA-6789 (USA) / 1-713-792-3245
Patient Referral Legal Statements Privacy Policy