Rad9 Inactivation Increase Efficacy Of Radiation In Cancer Therapy

Filed in archive Drugs, Vaccines and Therapeutics , Genomics, Proteomics and Bioinformatics on February 20, 2006

This entry is submitted by Gloria Gamat, via Creative Reporter.To make cancer cells easier to kill with ionizing radiation, a protein called mammalian Rad9 should be inactivated, based on a research study at Washington University School of Medicine in St. Louis.

Rad9 which is especially active in telomeres (the protective ends of chromosomes) was first thought of as a "watchman" that checks for DNA damage but is actually a "repairman" that fixes dangerous breaks in the DNA double helix.

"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," says senior 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 revealed that Rad9 proteins interact with chromosomes' telomeres, which are special structures at the ends of chromosomes that protect them from fusion or degradation. Specifically, Rad9 proteins were shown to interact with proteins called telomere binding proteins. When the scientists inactivated Rad9 in human cells, they saw damage to chromosomes and end-to-end fusion at telomeres.

The study's findings place Rad9 at an important juncture: its function is vital to the health of cells, and this makes it a key vulnerability to exploit for cancer therapy.

Read more from WUSTL. Photo shows chromosomal damage resulting in end-to-end fusion (bottom photo), courtesy of WUSTL.

About Gloria Gamat: Gloria is a Chemist and a single mom. Gloria also blogs about motherhood at EMothersOnline and about life and travel in the Philippines at The Philippine Culture Blog and at Pinoy Travel Blog respectively.