JAK/STAT pathway dysregulation in tumors: A Drosophila perspective
Seminars in Cell & Developmental Biology, ISSN: 1084-9521, Vol: 28, Page: 96-103
2014
- 74Citations
- 103Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations74
- Citation Indexes74
- 74
- CrossRef61
- Captures103
- Readers103
- 103
- Mentions1
- References1
- Wikipedia1
Review Description
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.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1084952114000597; http://dx.doi.org/10.1016/j.semcdb.2014.03.023; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84901283763&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24685611; https://linkinghub.elsevier.com/retrieve/pii/S1084952114000597; http://linkinghub.elsevier.com/retrieve/pii/S1084952114000597; http://europepmc.org/abstract/med/24685611; http://europepmc.org/articles/PMC4037387
Elsevier BV
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