![Protecting Chromosomes from Stress]()
Cells constantly contend with endogenous sources of stress that can damage their DNA. Inability of the cell to repair this accumulating DNA damage can lead to chromosomal breaks and rearrangements that can lead to cancer. In the October 20 issue of Molecular Cell, Advaitha Madireddy, Ph.D., and Carl Schildkraut, Ph.D., offer insight into how so-called chromosomal fragile sites (CFS) respond to internal sources of stress. Drs. Madireddy, Schildkraut and colleagues identified a novel mechanism linking CFS instability to the Fanconi Anemia (FA) tumor-suppressor pathway. After studying FA-deficient cells, they found that this pathway protects fragile regions of the genome from endogenous DNA damage. These findings provide novel insights into the mechanisms by which chromosomes are protected from cellular stress—and how cancers can result when those protective mechanisms are disrupted. Dr. Madireddy is a Harry Eagle Scholar and Dr. Schildkraut is a professor of cell biology.
Posted on: Thursday, November 10, 2016