Do blood vessels that feed tumors differ from other blood vessels? Fourteen years ago, experiments designed to answer that question led to the discovery of several genes that are more active in tumor-associated blood vessels than in normal blood vessels. New research now reveals the normal function of one of those genes and suggests it could be a good target for anticancer drug therapy.
The mystery of the gene, TEM5, began in 2000 with research conducted by Brad St. Croix, Ph.D., working in the laboratory of Bert Vogelstein, M.D., a Howard Hughes Medical Institute investigator and the Clayton Professor of Oncology, and Kenneth Kinzler, Ph.D., professor of oncology at the Johns Hopkins University School of Medicine. The researchers compared gene activity in normal blood vessels to those infiltrating colorectal tumors. Among other differences were nine genes that were highly active in the tumor-associated blood vessels, which the researchers dubbed tumor endothelial marker (TEM) 1 through 9. (Endothelial refers to the type of cell that makes up blood vessels.)
Nathans says that TEM5 might be a good target for cancer therapy because — although TEM5 is crucial for embryonic blood vessel development — mice do well if TEM5 is eliminated after birth. Nathans also suggests that temporarily disabling Wnt signaling in blood vessels might be used to improve drug treatment of brain diseases. Some potentially effective drugs cannot be used for treating brain diseases because they cannot cross the blood-brain barrier. Temporarily disabling that barrier might allow these drugs to gain access to the brain.
Source by : Science Daily News