Mansour MR, He S, Li Z, Lobbardi R, Abraham BJ, Hug C, Rahman S, Leon TE, Kuang YY, Zimmerman MW, Blonquist T, Gjini E, Gutierrez A, Tang Q, Garcia-Perez L, Pike-Overzet K, Anders L, Berezovskaya A, Zhou Y, Zon LI, Neuberg D, Fielding AK, Staal FJT, Langenau DM, Sanda T, Young RA, Look AT. 2018. JDP2: An oncogenic bZIP transcription factor in T cell acute lymphoblastic leukemia. The Journal of experimental medicine. 215(7):1929-1945. Pubmed: 29941549 DOI:10.1084/jem.20170484


A substantial subset of patients with T cell acute lymphoblastic leukemia (T-ALL) develops resistance to steroids and succumbs to their disease. encodes a bZIP protein that has been implicated as a T-ALL oncogene from insertional mutagenesis studies in mice, but its role in human T-ALL pathogenesis has remained obscure. Here we show that is aberrantly expressed in a subset of T-ALL patients and is associated with poor survival. JDP2 is required for T-ALL cell survival, as its depletion by short hairpin RNA knockdown leads to apoptosis. Mechanistically, JDP2 regulates prosurvival signaling through direct transcriptional regulation of Furthermore, is one of few oncogenes capable of initiating T-ALL in transgenic zebrafish. Notably, thymocytes from transgenic zebrafish express high levels of and demonstrate resistance to steroids in vivo. These studies establish as a novel oncogene in high-risk T-ALL and implicate overexpression of as a mechanism of steroid resistance in -overexpressing cells.
© 2018 Mansour et al.

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The Zon laboratory aims to dissect how assaults to the hematopoietic system cause severe diseases such as leukemias, lymphomas, and anemias. They investigate hematopoietic development and disease using chemical screens, genetic screens, and analysis of novel transgenic lines in zebrafish.

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