Genomic analyses identify recurrent MEF2D fusions in acute lymphoblastic leukaemia

Zhaohui Gu(St. Jude Children's Research Hospital), Michelle L. Churchman(St. Jude Children's Research Hospital), Kathryn G. Roberts(St. Jude Children's Research Hospital), Yongjin Li(St. Jude Children's Research Hospital), Yu Liu(St. Jude Children's Research Hospital), Richard C. Harvey(University of New Mexico), Kelly McCastlain(St. Jude Children's Research Hospital), Shalini C. Reshmi(Nationwide Children's Hospital), Debbie Payne-Turner(St. Jude Children's Research Hospital), Ilaria Iacobucci(St. Jude Children's Research Hospital), Ying Shao(St. Jude Children's Research Hospital), I‐Ming Chen(University of New Mexico), Marcus Valentine(St. Jude Children's Research Hospital), Deqing Pei(St. Jude Children's Research Hospital), Karen Mungall(BC Cancer Agency), Andrew J. Mungall(BC Cancer Agency), Yussanne Ma(BC Cancer Agency), Richard A. Moore(BC Cancer Agency), Marco A. Marra(BC Cancer Agency), Eileen Stonerock(Nationwide Children's Hospital), Julie M. Gastier-Foster(Nationwide Children's Hospital), Meenakshi Devidas(University of Florida Health), Yunfeng Dai(University of Florida Health), Brent L. Wood(University of Washington), Michael J. Borowitz(Johns Hopkins University), Eric E. Larsen(New England Cancer Specialists), Kelly W. Maloney(Children's Hospital Colorado), Leonard A. Mattano(Bridge Pharma (United States)), Anne Angiolillo(Children's National), Wanda L. Salzer(United States Army Medical Research and Development Command), Michael J. Burke(Medical College of Wisconsin), Francesca Gianni(Ospedale Papa Giovanni XXIII), Orietta Spinelli(Ospedale Papa Giovanni XXIII), Jerald P. Radich(Fred Hutch Cancer Center), Mark D. Minden(University Health Network), Anthony V. Moorman(Newcastle University), Bella Patel(Institute of Cancer Research), Adele K. Fielding(Cancer Research UK), Jacob M. Rowe(Shaare Zedek Medical Center), Selina M. Luger(University of Pennsylvania), Ravi Bhatia(University of Alabama at Birmingham), Ibrahim Aldoss(University of Alabama at Birmingham), Stephen J. Forman(City of Hope), Jessica Kohlschmidt(Alliance for Clinical Trials in Oncology), Krzysztof Mrózek(The Ohio State University), Guido Marcucci(City of Hope), Clara D. Bloomfield(The Ohio State University), Wendy Stock(University of Chicago Medical Center), Steven M. Kornblau(The University of Texas MD Anderson Cancer Center), Hagop M. Kantarjian(The University of Texas MD Anderson Cancer Center), Marina Konopleva(The University of Texas MD Anderson Cancer Center), Elisabeth Paietta(Montefiore Medical Center), Cheryl L. Willman(University of New Mexico), Mignon L. Loh(UCSF Benioff Children's Hospital), Stephen P. Hunger(Children's Hospital of Philadelphia), Charles G. Mullighan(St. Jude Children's Research Hospital)
Nature Communications
November 8, 2016
Cited by 293Open Access
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Abstract

Chromosomal rearrangements are initiating events in acute lymphoblastic leukaemia (ALL). Here using RNA sequencing of 560 ALL cases, we identify rearrangements between MEF2D (myocyte enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL (B-ALL) cases with a distinct gene expression profile, the most common of which is MEF2D-BCL9. Examination of an extended cohort of 1,164 B-ALL cases identified 30 cases with MEF2D rearrangements, which include an additional fusion partner, FOXJ2; thus, MEF2D-rearranged cases comprise 5.3% of cases lacking recurring alterations. MEF2D-rearranged ALL is characterized by a distinct immunophenotype, DNA copy number alterations at the rearrangement sites, older diagnosis age and poor outcome. The rearrangements result in enhanced MEF2D transcriptional activity, lymphoid transformation, activation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment. Thus, MEF2D-rearranged ALL represents a distinct form of high-risk leukaemia, for which new therapeutic approaches should be considered.


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