New findings in DNA repair may lead to cancer inhibitors

Plazma Inferno!

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Science has known for quite some time how a cellular DNA repair protein is directed to lesions in DNA through modifications on histone proteins that are bound tightly to DNA. Cancer cells divide very quickly and experience a high load of damage to DNA. Without quick and efficient repair systems, these cells will inevitably die. Cancer cells are extremely dependent on DNA repair mechanisms and the new molecular mechanism the team found works as a very attractive target for cancer therapy.
The research team led by Professor Anja Groth at the University of Copenhagen worked closely with Dinshaw Patel at Memorial Sloan-Kettering Cancer Center in New York. The team located a detailed crystal structure of the TONSL protein bound to the histone protein, which they show is what directs TONSL to lesions on the DNA. This single structure communicates to researchers exactly how the protein works and allows them a wonderful opportunity to design a molecule that can bind to TONSL and stop it from locating the DNA that has been damaged. An inhibitor molecule such as this one may be used in cancer treatment because blocking TONSL function may be able to help promote cancer cells to accumulate DNA damage and eventually die off. The team of researchers has put together a team of experts in medicinal chemistry and rational drug design to develop small molecule inhibitors.