Molecular Network That Influences Development Of CLL Revealed By Study

January 28, 2011

BlankMolecular Network That Influences Development Of Chronic Lymphocytic

Leukemia Revealed By Study

26 Jan 2011

A study shows for the first time that the three most common chromosome changes

seen in chronic lymphocytic leukemia disrupt a molecular network that includes

several important genes and strongly influences the outcome of the disease.

The research was led by investigators at the Ohio State University Comprehensive

Cancer Center - Arthur G. Cancer Hospital and J. Solove Research

Institute (OSUCCC - ) and at University of Texas M.D. Cancer

Center, working in collaboration with investigators at seven other centers in

Italy and the United States. The findings were published recently in the Journal

of the American Medical Association (JAMA).

The network involves genes on chromosome 13, chromosome 11 and chromosome 17,

along with the important tumor-suppressor gene TP53, the prognostically

important molecule called ZAP-70 and two sets of regulatory molecules called

microRNA.

" Our findings might allow doctors to better identify which CLL patients need

closer follow-up or earlier treatment, " says first author Dr. Muller Fabbri, a

research scientist at the OSUCCC - . " Moreover, our study provides

important new information about how CLL develops and identifies new molecular

targets for the development of new treatments. "

CLL is the most common leukemia in the U.S., where 15,000 new cases were

expected in 2010, along with 4,400 deaths from the disease.

The disease has an extremely variable clinical outcome, Fabbri notes. While most

patients have a slowly progressing form of the disease that requires little or

no treatment for many years, others have aggressive disease that requires

immediate therapy.

Chromosome damage is common in CLL, and it often involves the loss of pieces of

chromosome 13. The loss of pieces of chromosomes 11 and 17 may also occur. More

specifically, these changes are called the 13q deletion, and the 11q and 17p

deletions.

" Patients with a 13q deletion generally have a better prognosis than patients

with the 11q or 17p deletion, " Muller says. " But we don't know why the loss of

part of chromosome 13 results in a better prognosis. Our discovery helps unravel

this mystery. It identifies a molecular mechanism that explains why these

deletions affect patient outcome. "

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