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The two genes TEL2 and MYC cooperate with each other to promote pediatric cases of the immune system cancer B-cell lymphoma, according to results of a study by St. Jude investigators.
B cell lymphoma is a cancer in which the antibody-producing cells (B lymphocytes) multiply uncontrollably and crowd out other blood cells.
The St. Jude researchers report that TEL2 cooperates with MYC to increase the chance that a certain mutation will occur in precancerous B lymphocytes that permits these cells to become cancerous. This mutation inactivates the function of p53, a gene that orchestrates the ability of abnormal lymphocytes to commit suicide—a process called apoptosis—and thus rids the body of potentially cancerous cells.
“The study’s findings strongly suggest that physicians should look for TEL2 upregulation in a patient’s B cells as part of the diagnosis of B cell lymphoma,” said Gerard Grosveld, PhD, Genetics and Tumor Cell Biology chair. Grosveld is senior author of the report on this work, which appears in the March issue of Molecular Cell Biology. “TEL2 promotes the development of lymphoma by enlarging the B lymphocyte population. This increases the likelihood that at least a few of the cells acquire a mutation eliminating p53 function just by chance. In the absence of p53, the cells remain alive and become cancerous,” he said.
“It will be interesting to study the effect of drugs that block TEL2 activity, since such an approach might one day represent an effective treatment for leukemia patients,” said Monica Cardone, PhD, the postdoctoral student in Grosveld’s laboratory who did much of the work on this project.
Other St. Jude authors of the report include Ayten Kandilci and Cintia Carella, both of Genetics and Tumor Cell Biology; Jonas Nilsson, PhD, and Jennifer Brennan, both of Biochemistry; Kelli Boyd, PhD, ARC; and John Cleveland, PhD, Biochemistry.
Last update: April 2005