Journal
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Volume 28, Issue -, Pages 96-103Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2014.03.023
Keywords
JAK/STAT; Upd; Dome; Hop; Stat92E; Chinmo; Socs36E; dPIAS; PRC1; ESCRT; Ras; Scribbled; Notch; Imaginal discs; Melanotic tumors; Tum-l; T42; Myeloproliferative neoplasms; Carcinoma
Categories
Funding
- NIH [T32 CA009161, R01 GM085075]
- NYSTEM [C028132]
- Hirschl Trust
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Sustained activation of the JAK/STAT pathway is causal to human cancers. This pathway is less complex in Drosophila, and its dysregulation has been linked to several tumor models in this organism. Here, we discuss models of metastatic epithelial and hematopoietic tumors that are causally linked to dysregulation of JAK/STAT signaling in Drosophila. First, we focus on cancer models in imaginal discs where ectopic expression of the JAK/STAT pathway ligand Unpaired downstream of distinct tumor suppressors has emerged as an unexpected mediator of neoplastic transformation. We also discuss the collaboration between STAT and oncogenic Ras in epithelial transformation. Second, we examine hematopoietic tumors, where mutations that cause hyperactive JAK/STAT signaling are necessary and sufficient for fly leukemia. We highlight the important contributions that genetic screens in Drosophila have made to understanding the JAK/STAT pathway, its developmental roles, and how its function is co-opted during tumorigenesis. (C) 2014 Elsevier Ltd. All rights reserved.
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