C04993: ATR-Seckel Cancer Cells for Drug Discovery
Technical Details:
Advanced gene targeting methods were used to generate biallelic knock-in point mutations in human colorectal cancer cells that cause a loss of ATR function, but retain enough activity to permit viability. JHU researchers determined that progression of the cancer cell cycle after radiation treatment requires the ATR kinase.
Looking for Partners:
As ATR strongly contributed to clonogenic survival after radiation treatment, these data suggest that blocking ATR activity or activating p38 SAPK pathways might be useful strategies for the radiosensitization of check-point deficient cancer cells. This invention suggests ATR kinase is an anti-cancer target and provides a tool for novel drug discovery. These drugs could then be widely useful in combination therapy
