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Switching Off Protein Could Play Key Role In Success Of Radiation Therapy For Cancer

Switching off a mammalian protein called Rad9 could hold the key to killing cancer cells easily with ionizing radiation, according to new research at Washington University School of Medicine in St. Louis. Rad9 was previously thought // to be a "watchman" for DNA, but it is now fund to be a "repairman" for DNA that fixes any breaks in the master molecule.

That is why reserachers are now looking at Rad9 with renewed interest. Turning off the protein could make the radiation treatments more effective, the reserachers say in the study, which appears online in the journal Molecular and Cellular Biology. "Our study suggests that if we could inactivate Rad9 in tumor cells, we would be able to kill them with a very low dose of radiation and gain a therapeutic advantage," observed lead author Tej K. Pandita, Ph.D., associate professor of radiation oncology and on the faculty of the Siteman Cancer Center at Washington University School of Medicine and Barnes-Jewish Hospital. The study found that Rad9 proteins interact with telomeres in the chromosomes. These telomeres are special structures located at the ends of chromosomes and protect them from fusion or degradation. "We saw that Rad9 stabilizes telomeres, and because we aren't yet sure how it does it, we will continue to study how Rad9 influences the telomere structure," Pandita said. "We speculate that without Rad9, some of the other proteins associated with the telomeric structure become delocalized, exposing the DNA at the ends of chromosomes." The reserachers are also looking at ways to identify people with mutations in Rad9, since they definitely expose people to the risk of developing cancer, "If Rad9 isn't functioning properly in cells, it can lead to genomic instability and result in the malignant transformation of cells," Pandita commented. "In fact, fusions at the telomeric ends of chromosomes like those seen in the absence of Rad9 appear frequently in tumor tissues." Main Article: Pandita RK, Sha
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