Drug limited type to kill cancer cells with DNA repair defects could treat leukemia -
A team of scientists led by Associate Research Professor Motomi Osato and Professor Yoshiaki Ito science cancer Institute of Singapore (Singapore CSI) at the national University of Singapore (NUS) found that a drug originally designed to kill a limited type of cancer cells with DNA repair defects could be used to treat leukemia and other cancers.
The new study suggests that treatment with poly (ADP-ribose) polymerase (PARP) inhibitors and standard chemotherapy drugs might be more effective in the fight against leukemia. In the same study, the researchers found that inactivation of genes RunX cause DNA repair defects and promotes the development of leukemia and other cancers. The study was published online in the leading journal Cell Reports last month.
Unlike other cancers that are most commonly seen in the elderly, leukemia is known for its high prevalence among young people. There has been little progress in the treatment of leukemia. Chemotherapy with or without transplantation of hematopoietic stem cells remains the current standard of care, resulting in a rate of about 50 percent recovery. The genes of the RUNX family are among the most commonly inactivated genes in leukemia and other cancers. Previous studies, RUNX1 is one of the most frequently mutated genes in leukemia and RUNX3 is involved in the development of the disease.
In this study, the research team also showed the link between genes RunX family and the path of human rare congenital disease called Fanconi anemia for the first time. The disease is caused by mutations in one of the 15 genes responsible for repair of a specific type of DNA damage. In the early stages of this study, the researchers found that deficiency RUNX resulted in an inability to produce blood cells and a massive expansion of abnormal hematopoietic cells. They recognized that these clinical manifestations are symptoms of Fanconi anemia and began to investigate the functions of RunX in this DNA repair pathway.
Other research has shown that RunX proteins play an essential and central role in the way of Fanconi anemia by facilitating the recruitment of a protein involved in the repair of DNA damage called FANCD2 to DNA damage sites. This unknown relationship between RUNX and Fanconi anemia prompted the research team to test the possibility that PARP inhibitors, a drug originally designed to kill a limited type of cancer cells to repair defects DNA, could be applied in the treatment of leukemia and cancers with RUNX alterations. These types of cancer were previously not thought to have DNA repair defects. Researchers have shown that the drug was effective in the treatment of leukemia and other cancers in cell culture experiments.
Dr. Osato said, "Common sense is often a veil that prevents us from understanding the truth. PARP inhibitors have been with us for some time, but nobody has made their application for leukemia. Our study has highlighted the possibility of more effective treatment using combination therapy with PARP inhibitors that can potentially be extended to other types of common cancers. "
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