Cancer cells have a remarkable ability to survive treatments that damage their DNA. One reason is that they rely on sophisticated repair systems that can fix genetic damage that would otherwise kill them. Among the most important of these systems is homologous recombination, a highly accurate DNA repair process that depends on proteins such as RAD51 and CHK1.
Cancer therapies known as PARP inhibitors were designed to exploit weaknesses in DNA repair. While these drugs have been successful against certain tumors, many cancers eventually adapt. By restoring their DNA repair capabilities, they become resistant to treatment and continue growing.
Now, researchers led by Director Kyungjae Myung at the Center for Genomic Integrity within the Institute for Basic Science (IBS), working with Joo-Yong Lee of Chungnam University, have identified a potential way to overcome that resistance. Instead of targeting genetic mutations, the team found a method for destabilizing the machinery cancer cells use to repair DNA.
Targeting DNA Repair Proteins
DNA repair proteins inside cells are constantly being produced and removed to maintain a healthy balance. The researchers discovered that disrupting this balance can leave cancer cells unable to cope with DNA damage.
