Evidence map›Paper›PMID 24685611›Full record

ReviewSeminars in cell & developmental biology2014

JAK/STAT pathway dysregulation in tumors: a Drosophila perspective.

Marc Amoyel, Abigail M Anderson, Erika A Bach

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.5field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Frontiers in cellular and infection microbiology · 2026
    Article
  4. GαCell communication and signaling : CCS · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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  10. ThebioRxiv : the preprint server for biology · 2024
    Article
  11. Review
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  15. Review
  16. Article
  17. Article
  18. Article
  19. Cancer cachexia: lessons from Drosophila.Disease models & mechanisms · 2022
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Marc AmoyelDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, 550 First Avenue, MSB 497B, New York, NY 10016, USA.
Abigail M AndersonDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, 550 First Avenue, MSB 497B, New York, NY 10016, USA.
Erika A BachThe Helen L. and Martin S. Kimmel Center for Stem Cell Biology, New York University School of Medicine. Electronic address: erika.bach@nyu.edu.
New York University · US

Funding

TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
Eludicating the Molecular Mechanisms That Regulate Stem Cell Numbers in VivoR01GM085075 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BACH, ERIKA A · 2009 to 2023
$4.3M
JAK/STAT PATHWAY CONTROL OF CELL COMPETITION DURING DEVELOPMENT.R03HD069576 · NICHD · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BACH, ERIKA A · 2012 to 2014
$249k
NCI NIH HHS T32 CA009161NICHD NIH HHS R03 HD069576NIGMS NIH HHS R01 GM085075
6 · The paper itself

Abstract

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.

Indexed as

AnimalsCell Transformation, NeoplasticDrosophilaDrosophila ProteinsHumansJanus KinasesNeoplasmsSignal TransductionSTAT Transcription FactorsTranscription FactorsDrosophila Proteinshop protein, DrosophilaJanus KinasesSTAT Transcription FactorsTranscription FactorsCarcinomaChinmoDomedPIASESCRTHopImaginal discsJAK/STATMelanotic tumorsMyeloproliferative neoplasmsNotchPRC1RasScribbledSocs36EStat92ET42Tum-lUpd

Identifiers

PMID24685611
PMCPMC4037387
OpenAlexW2049429718

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.