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Fox Chase Cancer Center study: Novel DNA-repair gene mutation can cause resistance to cancer drugs

he mismatch. If this fails, the system halts the cell's replication cycle and causes the new cell to die--literally, to pop out of its skin in a process called apoptosis.

In addition to helping cells circumvent DNA damage that might otherwise lead to cancer, the mismatch-repair system also plays a critical role in allowing anticancer drugs known as alkylating agents to kill cancer cells. These agents are the oldest and most widely used chemotherapy drugs. They work by damaging the DNA of cancer cells and triggering the mismatch-repair system to interrupt the reproductive cycle and cause apoptosis.

"Our finding that the defective MED1 enzyme produces resistance to these drugs is consistent with previous observations in cell culture models, which show that reduced mismatch-repair proteins cause tolerance or resistance to alkylating agents," Bellacosa explained. "However, it appears that small amounts of DNA damage can be dealt with effectively by reduced levels of these proteins while an effective response to anticancer drugs requires normal amounts."

The experiments by Bellacosa and his colleagues suggest that colorectal tumors with the MED1 deficiency may resist treatment not only with alkylating agents but also with other drugs used against colorectal cancer, such as irinotecan. The research used cell cultures of mouse cell lines, including mice in which the Med1 gene has been inactivated.

"Clinical validation of these hypotheses may have significant implications for treatment selection," Bellacosa and his co-authors conclude. "Additional understanding of the mechanisms of MED1 and mismatch-repair inactivation may suggest methods to overcome drug resistance."


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Contact: Karen Carter Mallet
k_carter@fccc.edu
215-728-2700
Fox Chase Cancer Center
10-Nov-2003


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