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Little Known DNA Repair Enzyme May Be A Tumor Suppressor Gene

s were different from normal cells, they found that the cells' chromosomes showed not only a dramatic ten-fold increase in the incidence of swapping and fusing of genes and other genetic material between chromosomes, but also an increase in the number of chromosomes compared to normal cells.

The high frequency of DNA rearrangements in Rev3L/p53-deficient cells suggests that pol zeta in normal cells is responsible for preventing double-stranded breaks in chromosomes. When pol zeta is absent, it leads to a massive amount of double-stranded breaks, some of which are repaired correctly and others that are repaired incorrectly by being fused to other genes or chromosomes.

These findings have significant implications for human cancer research, as such a high degree of chromosomal instability is a characteristic of cancer cells. Further, the human Rev3L gene is located in a segment of chromosome 6 which is home for multiple tumor suppressor genes and a slew of human cancers, including a number of leukemias and lymphomas. This segment is associated with chromosomal instabilities in this particular region of chromosome 6.

"Although it requires further investigation, we believe that mutations in this part of chromosome 6 could occur during the development of some cancers and this may have prognostic and therapeutic implications. We are now investigating this hypothesis by selectively deleting the Rev3L gene in adult mouse cells to study how the loss of DNA polymerase zeta influences the development and progression of spontaneous cancers," the researchers explained.

This work was supported by a grant from the National Cancer Institute, National Institutes of Health to Dr. Wood. In addition to Drs. Wittschieben and Wood, others involved in this study include Shalini C. Reshmi, Ph.D., and Susan M. Gollin, Ph.D., University of Pittsburgh Graduate School of Public Health.

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