The genetic basis and cell of origin of mixed phenotype acute leukaemia View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-10

AUTHORS

Thomas B. Alexander, Zhaohui Gu, Ilaria Iacobucci, Kirsten Dickerson, John K. Choi, Beisi Xu, Debbie Payne-Turner, Hiroki Yoshihara, Mignon L. Loh, John Horan, Barbara Buldini, Giuseppe Basso, Sarah Elitzur, Valerie de Haas, C. Michel Zwaan, Allen Yeoh, Dirk Reinhardt, Daisuke Tomizawa, Nobutaka Kiyokawa, Tim Lammens, Barbara De Moerloose, Daniel Catchpoole, Hiroki Hori, Anthony Moorman, Andrew S. Moore, Ondrej Hrusak, Soheil Meshinchi, Etan Orgel, Meenakshi Devidas, Michael Borowitz, Brent Wood, Nyla A. Heerema, Andrew Carrol, Yung-Li Yang, Malcolm A. Smith, Tanja M. Davidsen, Leandro C. Hermida, Patee Gesuwan, Marco A. Marra, Yussanne Ma, Andrew J. Mungall, Richard A. Moore, Steven J. M. Jones, Marcus Valentine, Laura J. Janke, Jeffrey E. Rubnitz, Ching-Hon Pui, Liang Ding, Yu Liu, Jinghui Zhang, Kim E. Nichols, James R. Downing, Xueyuan Cao, Lei Shi, Stanley Pounds, Scott Newman, Deqing Pei, Jaime M. Guidry Auvil, Daniela S. Gerhard, Stephen P. Hunger, Hiroto Inaba, Charles G. Mullighan

ABSTRACT

Mixed phenotype acute leukaemia (MPAL) is a high-risk subtype of leukaemia with myeloid and lymphoid features, limited genetic characterization, and a lack of consensus regarding appropriate therapy. Here we show that the two principal subtypes of MPAL, T/myeloid (T/M) and B/myeloid (B/M), are genetically distinct. Rearrangement of ZNF384 is common in B/M MPAL, and biallelic WT1 alterations are common in T/M MPAL, which shares genomic features with early T-cell precursor acute lymphoblastic leukaemia. We show that the intratumoral immunophenotypic heterogeneity characteristic of MPAL is independent of somatic genetic variation, that founding lesions arise in primitive haematopoietic progenitors, and that individual phenotypic subpopulations can reconstitute the immunophenotypic diversity in vivo. These findings indicate that the cell of origin and founding lesions, rather than an accumulation of distinct genomic alterations, prime tumour cells for lineage promiscuity. Moreover, these findings position MPAL in the spectrum of immature leukaemias and provide a genetically informed framework for future clinical trials of potential treatments for MPAL. More... »

PAGES

373-379

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41586-018-0436-0

    DOI

    http://dx.doi.org/10.1038/s41586-018-0436-0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1106931798

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30209392


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