Certain genes are turned off early, before clinical signs of the disease appear in the development of chronic leukemia, a new study, led by researchers at the Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute, has shown.
The researchers examined cancer cells from patients with chronic lymphocytic leukemia (CLL) and from a new strain of mice that develops a very similar disease.
The findings suggest that changes called epigenetic alterations, which silence a gene's ability to make its protein, might serve as markers for detecting CLL early and for monitoring its progression.
The researchers said that the findings also point to a strategy for treating the disease earlier using drugs that reverse such changes, and further confirm the value of the mouse model for studying CLL causes and treatment.
The study showed that a gene called FOXD3 likely plays a key role in CLL, and that the gene is silenced early, followed by the silencing of other genes.
"Our data suggest that the silencing of FOXD3 might represent a very early gene involved in the initiation of CLL that we can potentially target for re-expression with specific drugs," says study leader Dr. John C. Byrd, professor of internal medicine, and director of the hematologic malignancies program at the James Cancer Hospital and Solove Research Institute and a CLL specialist.
"Next, we need to learn whether therapy to reverse this silencing can delay or prevent CLL progression," he added.
The findings are published online in the Proceedings of the National Academy of Sciences Early Edition.