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CSHL team shows how loss of key protein promotes aggressive form of leukemia
Date:7/1/2010

f-renewing. But the team observed that cells with oncogenic Kras combined with a p53 deficiency did acquire the capacity to indefinitely self-renew, and transform into leukemia-initiating cells.

"Mice with one or the other mutation do develop T-cell malignancies, albeit ones with long latencies," Zhao says. "But we showed how suppression of p53 cooperates with oncogenic Kras to promote AML of the treatment-resistant type. Importantly, we found that loss of p53, independently of oncogenic Kras activation, promotes the proliferation of myeloid progenitors." It is the combination of p53 loss and activation of oncogenic Kras that confers upon these cells the ability to continually self-renew and thus give rise to aggressive AML.

"In this work, we discovered a new tumor-suppressing function of p53, distinct, for instance, from apoptosis, and somewhat related to senescence," said Zuber. "We showed that it has the ability to reinforce cell-fate and differentiation programs. In AML, p53 loss leads to cancer by disabling this reinforcement. The question we are now eager to answer is whether p53 has similar functions in other types of cancer."


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Contact: Peter Tarr
tarr@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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