JAK/STAT pathway dysregulation in tumors: a Drosophila perspective

Marc Amoyel, Abigail M Anderson, Erika A Bach

Research output: Contribution to journalArticle (Academic Journal)peer-review

48 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)96-103
Number of pages8
JournalSeminars in Cell and Developmental Biology
Publication statusPublished - Apr 2014


  • Animals
  • Cell Transformation, Neoplastic
  • Drosophila
  • Drosophila Proteins
  • Humans
  • Janus Kinases
  • Neoplasms
  • STAT Transcription Factors
  • Signal Transduction
  • Transcription Factors


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