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International study suggests improved treatment alternative for lymphoid leukemia
Date:2/11/2013

cording to the National Cancer Institute, the overall survival rate for all ages of people with ALL is 66.4 percent and 90.8 percent for children under the age of 5 years.

During the onset of a disease like ALL, cancer signals among cells activate a protein called p53, which is often referred to as the "guardian of the genome." A repressor of tumor growth, p53 normally initiates a DNA repair program that is supposed to induce programmed cell death to stop or slow down tumor progression.

In the case of ALL, the researchers said the disease relies on the Gfi1 protein to get around p53's tumor repressing capabilities by essentially overriding p53. Gfi1 has an important role in the normal development of lymphoid cells. But analyses of ALL mouse models and primary human tumors showed that Gfi1 is overexpressed in the disease state.

When the researchers removed Gfi1 in established mouse lymphoid tumors, the leukemia regressed through p53-induced cell death. Next, to see if removal of Gfi1 would be effective in modeled human ALL, the research team inserted T-cell leukemia cells from human patients into mice. Inhibiting Gfi1 in this instance stopped the progression of human leukemia in the animals without any harmful effects.

The scientists are continuing their research to see if results of the current study will be translatable to human patients.


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Contact: Nick Miller
nicholas.miller@cchmc.org
513-803-6035
Cincinnati Children's Hospital Medical Center
Source:Eurekalert

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