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Potential Breakthrough in Acute Leukemia (AML) Research

by Civilian Exposure

 

In a recent release from researchers in Oregon and LLS.org, a potential breakthrough may be in the making concerning the understanding of the proliferation of acute leukemia (AML).

Published recently in Cancer Research, the journal published by the American Association of Cancer Research (AACR), a recent study at Oregon Health & Sciences University (OHSU) “has resulted in the identification of an important gene mutation in an adult patient with AML. This is the first time that the mutation of the anaplastic lymphoma kinase (ALK) gene has been seen in an AML patient. It is a mutation that is already known to be present in solid tumors and is treatable with ALK inhibitors. Therefore, this represents a potential new target for therapy for patients with AML, a blood cancer for which the standard of care has not changed for more than 30 years.”

The utilization of advanced genome-sequencing technologies is showing signs of promise in the fight to identify driver mutations in diseases such as AML.  It also creates opportunities for scientists to tests drugs that might be effective in targeting and inhibiting the abnormal genes.

“Genetic lesions involving ALK have been seen recurrently in a number of different types of solid tumors, but to my knowledge, ALK mutations have not previously been implicated as a major contributor to leukemia,” said Jeffrey Tyner, PhD, an assistant professor in the Department of Cell, Developmental, and Cancer Biology at the Knight Cancer Institute at Oregon Health & Science University. “The discovery of new mutant versions of ALK that may contribute to the development of leukemia and can be therapeutically targeted suggests new treatment options for patients with leukemia with ALK mutations.”

This discovery is encouraging news for patients with AML and other leukemias.

Read more about this development here: http://llsorg.prod.acquia-sites.com/news/leukemias-with-alk-mutations-identified-may-respond-to-alk-inhibitors

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