Jun J. Yang, PhD, highlights one of the ALL sessions at the 2017 annual meeting of the American Society of Hematology (ASH) in Atlanta, Georgia.

My lab presented our work today on GATA3 in acute lymphoblastic leukemia (Abstract 475).

Research has shown how the GATA3 gene spurs the development of a type of high-risk leukemia. We sequenced more than 5,000 pediatric ALL patients and found overexpression of GATA3 led to increased expression of a leukemia oncogene known as CRLF2. This oncogene is the defining molecular feature in nearly 50 percent of the high-risk leukemia know as Ph-like ALL.

We’ve been working on this project for the past few years and now we’re able to put the story together and share that with our colleagues here at ASH. The next step is to further examine the biology behind GATA3 and use that information to develop better therapies for Ph-like ALL.

In addition, there’s been other exciting progress in ALL research reported today. University of Southern California reported a study on clonal competition of ALL during therapy. This research could have an impact on discovery in the future using that technology (Abstract 480).

The Plenary Scientific Session talks look particularly interesting, especially the presentation on the interaction between DNMT3A and splicing factors in acute myeloid leukemia (Abstract 1).