Evidence map›Paper›PMID 27584724›Full record

ArticlePLoS biology2016

Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment.

Yoichiro Tamori, Emiko Suzuki, Wu-Min Deng

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2016. 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
6.4field-weighted citation impact, top 3% 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, 87 citations in OpenAlex.

  1. Article
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  7. Drosophila as a Model for Metastasis.Advances in experimental medicine and biology · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. A Window into Mammalian Basement Membrane Development: Insights from thebioRxiv : the preprint server for biology · 2023
    Article
  14. Article
  15. Human ERG oncoprotein repressesProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. The wing imaginal disc.Genetics · 2022
    Article
  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 3 institutions in 2 countries.

Yoichiro TamoriDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Emiko SuzukiStructural Biology Center, National Institute of Genetics and Department of Genetics, School of Life Science, The Graduate University for Advanced Studies (SOKENDAI), 1111 Yata, Mishima, Japan.
Wu-Min DengDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Florida State University · USNational Institute of Genetics · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

Notch signaling and germline-soma interactions in the Drosophila ovarian modelR01GM072562 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2006 to 2025
$5.6M
NIGMS NIH HHS R01 GM072562
6 · The paper itself

Abstract

Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this "tumor hotspot" where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism.

Indexed as

Tumor MicroenvironmentAnimalsCarcinogenesisDrosophila melanogasterDrosophila ProteinsEpithelial CellsGene Knockdown TechniquesImaginal DiscsJanus KinasesMicrotubulesNeoplasms, Glandular and EpithelialOrgan SpecificityProtein TransportRNA InterferenceSignal TransductionSTAT Transcription FactorsDrosophila Proteinshop protein, DrosophilaJanus KinasesSTAT Transcription FactorsTranscription FactorsTSG protein, Drosophila

Identifiers

PMID27584724
PMCPMC5008749
OpenAlexW2507894013

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.