"By explaining how E1A works, we hope to develop novel strategies to make human immunological defenses against tumors, as well as chemotherapy and radiation therapy, more effective in combating cancer," said Dr. James Cook, chief of infectious diseases and a member of the UIC Cancer Center.
The latest study is published in the July 23 issue of the Proceedings of the National Academy of Sciences.
To date, Cook and his colleagues have tested the E1A gene in cancer cells from four species: hamsters, mice, rats and humans. In all four cases, E1A renders the malignancies susceptible to defender cells of the immune system.
"We believe that these observations may reveal a common Achilles heel of many types of cancer cells," Cook said.
According to Cook, the goal is to find ways to make standard treatments for cancer more effective. Although the disease may respond to the first course of chemotherapy or radiation, typically tumor cells become more resistant later on, when the cancer recurs or metastasizes. The reasons are not clear.
Possibly, series of mutations are acquired as the tumor grows, yielding a naturally selected population of cells capable of thwarting killing agents. The standard clinical course is to change the drug or radiation strategy, but that may not be feasible or useful.
As an alternative, based on the studies Cook is undertaking, physicians may one day be able to alter the resistant malignant tissue itself, making it vulnerable to therapy.
"E1A is helping us identify the set of cellular switches that need to be turned on or off to render cancer cells more sensitive to therapeutic injury," Cook said.