Chronic lymphocytic leukemia (CLL) appears as the most common leukemia in the U.S. with little or no development in its treatment since quite a few years. In a major breakthrough, scientists witnessed three most common chromosome changes taking place in CLL. These alterations probably disrupt a molecular network which comprises various vital genes and have a strong impact on the outcome of the disease.
The molecular network may include genes on chromosome 13, chromosome 11 and chromosome 17. It also has the crucial tumor-suppressor gene TP53, the supposedly critical molecule known as ZAP-70 and two sets of regulatory molecules called microRNA. Those with a 13q deletion reportedly have a better prognosis than patients with the 11q or 17p deletion. However, the precise reason as to why the loss of chromosome 13 results in a better prognosis is apparently not known. In the present research, investigators were possibly able to highlight the molecular mechanism behind the impact of deletions on patient outcome.
Scientists assert that the loss of chromosome 13q interrupts a biochemical network which is involved in two families of microRNA and the TP53 tumor-suppressor gene. This interruption probably gives rise to greater activity of two genes BCL2 and MCL1 and restricts cancer cells from dying. The investigation apparently sheds light on the way CLL develops and identifies novel molecular targets for designing new treatments. Dr. Carlo M. Croce, professor of molecular virology, immunology and medical genetics, and director of the Human Cancer Genetics program at the OSUCCC and colleagues believe that the research findings empower physicians to detect CLL patients in need of closer follow-up or earlier treatment.
The research was published in the Journal of the American Medical Association (JAMA).