Evidence map›Paper›PMID 31568500›Full record

ArticlePLoS genetics2019

Cytoneme-mediated signaling essential for tumorigenesis.

Sol Fereres, Ryo Hatori, Makiko Hatori, Thomas B Kornberg

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Emerging Roles of Cytoneme-Mediated Signaling in Cancer.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Ovarian germline stem cell dedifferentiation is cytoneme dependent.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Airineme-Mediated Intercellular Communication.Results and problems in cell differentiation · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Regulatory mechanisms of cytoneme-based morphogen transport.Cellular and molecular life sciences : CMLS · 2022
    Review
  17. Article
  18. Article
  19. Cells · 2021
    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

4 authors at 1 institution in 1 country.

Sol FereresCardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States of America.
Ryo HatoriCardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States of America.ORCID 0000-0003-2224-5802
Makiko HatoriCardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States of America.ORCID 0000-0002-2742-479X
Thomas B KornbergCardiovascular Research Institute, University of California, San Francisco, San Francisco, California, United States of America.ORCID 0000-0002-6879-7066
University of California, San Francisco · US

Funding

MUTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007185 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI David J Erle, LAURENCE HUANG · 1985 to 2026
$24.6M
MOLECULAR AND CELLULAR BASIS OF CARDIOVASCULAR DISEASET32HL007731 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Brian L Black · 1992 to 2026
$12.4M
Tumor cytonemes, a new target for tumor suppressionR21CA205580 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KORNBERG, THOMAS B. · 2016 to 2017
$379k
NCI NIH HHS R21 CA205580NHLBI NIH HHS T32 HL007185NHLBI NIH HHS T32 HL007731
6 · The paper itself

Abstract

Communication between neoplastic cells and cells of their microenvironment is critical to cancer progression. To investigate the role of cytoneme-mediated signaling as a mechanism for distributing growth factor signaling proteins between tumor and tumor-associated cells, we analyzed EGFR and RET Drosophila tumor models and tested several genetic loss-of-function conditions that impair cytoneme-mediated signaling. Neuroglian, capricious, Irk2, SCAR, and diaphanous are genes that cytonemes require during normal development. Neuroglian and Capricious are cell adhesion proteins, Irk2 is a potassium channel, and SCAR and Diaphanous are actin-binding proteins, and the only process to which they are known to contribute jointly is cytoneme-mediated signaling. We observed that diminished function of any one of these genes suppressed tumor growth and increased organism survival. We also noted that EGFR-expressing tumor discs have abnormally extensive tracheation (respiratory tubes) and ectopically express Branchless (Bnl, a FGF) and FGFR. Bnl is a known inducer of tracheation that signals by a cytoneme-mediated process in other contexts, and we determined that exogenous over-expression of dominant negative FGFR suppressed tumor growth. Our results are consistent with the idea that cytonemes move signaling proteins between tumor and stromal cells and that cytoneme-mediated signaling is required for tumor growth and malignancy.

Indexed as

AnimalsCarcinogenesisCell Membrane StructuresCell Transformation, NeoplasticDrosophila melanogasterDrosophila ProteinsErbB ReceptorsImaginal DiscsIntercellular Signaling Peptides and ProteinsModels, AnimalNeoplasm MetastasisNeoplasmsPseudopodiaReceptors, Invertebrate PeptideSignal TransductionTumor MicroenvironmentDrosophila ProteinsEgfr protein, DrosophilaErbB ReceptorsIntercellular Signaling Peptides and ProteinsReceptors, Invertebrate Peptide

Identifiers

PMID31568500
PMCPMC6786653
OpenAlexW2977454722

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.