Philadelphia -- The BRCA2 gene, linked to familial breast and ovarian cancers, plays an important and previously unsuspected role in human cell division, according to a new study by scientists at The Wistar Institute. When the BRCA2 protein is inactivated, their experiments showed, cells are dramatically delayed in their progress through mitosis, the cell-division stage of the cell cycle. The find opens an entirely new line of thinking for researchers working to understand how BRCA2 can cause cancer when mutated. With fresh insights may come more effective, more targeted treatments.
The same study also identified a new gene, dubbed BRAF35, and established that the BRAF35 protein associates closely with BRCA2 in a previously unknown complex. As with BRCA2, when the BRAF35 protein is inactivated, progress through mitosis is significantly delayed, raising the question of whether BRAF35, too, might be responsible for some cancers. Indeed, the BRAF35 gene maps to a location on chromosome 19 where anomalies have reported in many ovarian cancers.
A report on the study appears in the January 26 issue of Cell.
"This study helps us not only to better understand what BRCA2 is doing, but it also identifies a new gene, BRAF35, that may be involved in breast and ovarian cancers," says Wistar assistant professor Ramin Shiekhattar, Ph.D., senior author on the study. "It provides researchers with a number of new places to look for answers to our questions about these cancers."
Previous studies of BRCA2 had suggested that the gene was involved in DNA repair, not cell division. Shiekhattar's findings do not argue with those earlier observations, but offer an additional scientific framework within which to explore BRCA2 and its function.
"The complex in which we find BRCA2 and BRAF35 might serve a dual purpose for the cell," Shiekhattar notes. "It could be involved in both processes, DNA repair and cell cycle progression. Evolution often finds a way to use thes
Contact: Franklin Hoke
The Wistar Institute