One kind of leukemia sometimes masquerades as another, according to a study published online this week in the Journal of Experimental Medicine (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.
Innovative triplet therapy shows encouraging results in advanced chronic myeloid leukemia