Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 lysine 27 trimethylation

@inproceedings{Lane2014TriplicationOA,
  title={Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 lysine 27 trimethylation},
  author={Andrew A. Lane and Bjoern Chapuy and Charles Y. Lin and Trevor R. Tivey and Hubo Li and Elizabeth C. Townsend and Diederik van Bodegom and Tovah A. Day and Shuo-Chieh Wu and Huiyun Liu and Akinori Yoda and Gabriela Alexe and Anna C. Schinzel and Timothy John Sullivan and S{\'e}bastien Malinge and Jordan E. Taylor and Kimberly Stegmaier and Jacob D. Jaffe and Michael Bustin and Geertruy Te Kronnie and Shai Izraeli and Marian H. Harris and Kristen E. Stevenson and Donna S Neuberg and Lewis B. Silverman and Stephen E. Sallan and James E. Bradner and William C. Hahn and John D. Crispino and David S Pellman and David M. Weinstock},
  booktitle={Nature Genetics},
  year={2014}
}
Down syndrome confers a 20-fold increased risk of B cell acute lymphoblastic leukemia (B-ALL), and polysomy 21 is the most frequent somatic aneuploidy among all B-ALLs. Yet the mechanistic links between chromosome 21 triplication and B-ALL remain undefined. Here we show that germline triplication of only 31 genes orthologous to human chromosome 21q22 confers mouse progenitor B cell self renewal in vitro, maturation defects in vivo and B-ALL with either the BCR-ABL fusion protein or CRLF2 with… CONTINUE READING
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