生物
淋巴细胞白血病
祖细胞
祖细胞
癌症研究
计算生物学
白血病
遗传学
免疫学
干细胞
作者
Zhaohui Gu,Michelle L. Churchman,Kathryn G. Roberts,Ian Moore,Xin Zhou,Joy Nakitandwe,Kohei Hagiwara,S. William Pelletier,Sébastien Gingras,Hartmut Berns,Debbie Payne-Turner,Ashley Hill,Ilaria Iacobucci,Lei Shi,Stanley Pounds,Cheng Cheng,Deqing Pei,Chunxu Qu,Scott Newman,Meenakshi Devidas
出处
期刊:Nature Genetics
[Nature Portfolio]
日期:2019-01-07
卷期号:51 (2): 296-307
被引量:616
标识
DOI:10.1038/s41588-018-0315-5
摘要
Recent genomic studies have identified chromosomal rearrangements defining new subtypes of B-progenitor acute lymphoblastic leukemia (B-ALL), however many cases lack a known initiating genetic alteration. Using integrated genomic analysis of 1,988 childhood and adult cases, we describe a revised taxonomy of B-ALL incorporating 23 subtypes defined by chromosomal rearrangements, sequence mutations or heterogeneous genomic alterations, many of which show marked variation in prevalence according to age. Two subtypes have frequent alterations of the B lymphoid transcription-factor gene PAX5. One, PAX5alt (7.4%), has diverse PAX5 alterations (rearrangements, intragenic amplifications or mutations); a second subtype is defined by PAX5 p.Pro80Arg and biallelic PAX5 alterations. We show that p.Pro80Arg impairs B lymphoid development and promotes the development of B-ALL with biallelic Pax5 alteration in vivo. These results demonstrate the utility of transcriptome sequencing to classify B-ALL and reinforce the central role of PAX5 as a checkpoint in B lymphoid maturation and leukemogenesis.
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