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Genes, chromosomes & cancer v.56 no.4, 2017년, pp.278 - 284   SCI SCIE SCOPUS
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Ph‐like acute lymphoblastic leukemia with a novel PAX5‐KIDINS220 fusion transcript

Sakamoto, Kenichi (Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan ) ; Imamura, Toshihiko (Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan ) ; Kanayama, Takuyo (Department of Pediatrics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Japan ) ; Yano, Mio (Department of Pediatrics, National Hospital Organization Maizuru Medical Center, Japan ) ; Asai, Daisuke (Department of Pediatrics, Japanese Red Cross Kyoto Daini Hospital, Japan ) ; Deguchi, Takao (Department of Pediatrics, Mie University, Japan ) ; Hashii, Yoshiko (Department of Pediatrics, Osaka University, Japan ) ; Tanizawa, Akihiko (Department of Pediatrics, University of Fukui, Japan ) ; Ohshima, Yusei (Department of Pediatrics, University of ) ; Kiyokawa, Nobutaka ; Horibe, Keizo ; Sato, Atsushi ;
  • 초록  

    Although “paired box 5” ( PAX5 )‐related fusion genes are well documented in childhood B‐cell precursor acute lymphoblastic leukemia (ALL), these types of fusion with the exception of PAX5‐JAK2 are rarely seen in patients with gene expression profiles similar to those of BCR‐ABL1 (Philadelphia)‐positive ALL (Ph‐like ALL). We report a novel fusion of the genes PAX5 and “kinase D‐interacting substrate of 220 kDa” ( KIDINS220 , also known as ARMS ) in a Ph‐like ALL. As PAX5 is a master regulator of B‐lymphocyte differentiation, PAX5 rearrangements induce a differentiation block in B lymphocytes. KIDINS220 is a mediator of multiple receptor signaling pathways, interacts with both T‐ and B‐cell receptors, and is necessary for sustained extracellular signal‐regulated kinase (ERK) signaling. Although functional studies are needed, the PAX5‐KIDINS220 fusion protein might not only inhibit wild‐type PAX5 function, but also promote sustained activation of the ERK signaling pathway through upregulation of KIDINS220. ⓒ 2016 Wiley Periodicals, Inc.


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