One kind of leukemia sometimes masquerades as another, according to a study published online this week in the Journal of Experimental Medicine ( http://www.jem.org ).
Leukemia results when normal immune cells accumulate mutations that drive uncontrolled growth. T cell acute lymphoblastic leukemia (T-ALL) derives from immature T cells, whereas acute myeloid leukemia (AML) comes from myeloid cells.
Only 50% of adult T-ALL patients can be cured, and a team led by Adolfo Ferrando at Columbia University Institute for Cancer Genetics is trying to understand why.
Ferrando's group examined the genes expressed in tumors from T-ALL patients and found that half of the tumors expressed some genes normally found in stem cells and AML tumors. Many of these AML-like T-ALL tumors contained specific AML-associated mutations, and one quarter had mutations in ETV6, a gene involved in stem cell function—cells whose self-renewing capacity can propagate cancers. Additional work is needed to understand whether mutations in ETV6 influence the prognosis of patients with tumors in the gray zone between T-ALL and AML.
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The Journal of Experimental Medicine ( JEM ) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JEM content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jem.org .
Van Vlierberghe, P., et al. 2011. J. Exp. Med. doi:10.1084/jem.20112239
Journal of Experimental Medicine