The St Jude researchers report that TEL2 cooperates with MYC to increase the chance that a certain mutation will occur in precancerous B lymphocytes, permitting these cells to become cancerous. This mutation inactivates the function of p53, a gene that orchestrates the ability of abnormal lymphocytes to commit suicide – ridding the body of potentially cancerous cells.
These findings help explain the interlocking roles of MYC, TEL2, and p53 in the development of B lymphoma.
“The study’s findings strongly suggest that physicians should look for TEL2 activity in a patient’s B-cells as part of the diagnosis of B-cell lymphoma,” said Dr Gerard Grosveld, chair of St Jude genetics and tumor cell biology. “TEL2 should also be considered a potential target for novel drugs to treat this disease.”
“TEL2 should be considered a new diagnostic marker, especially in patients who don’t have the classic genetic mutations that physicians normally use to diagnose the disease,” commented Dr Monica Cardone, a postdoctoral student in Grosveld’s laboratory who did much of the work on this project.
“It will also be very 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.”