Evidence map›Paper›PMID 19564624›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

A "latent niche" mechanism for tumor initiation.

Marie McGovern, Roumen Voutev, John Maciejowski, Ann K Corsi, E Jane Albert Hubbard

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

60 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Analysis of the C. elegans Germline Stem Cell Pool.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Biology of theGenetics · 2019
    Review
  16. Molecular control of the female germline stem cell niche size in Drosophila.Cellular and molecular life sciences : CMLS · 2019
    Review
  17. Article
  18. Article
  19. Functional Interactions BetweenG3 (Bethesda, Md.) · 2018
    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

5 authors at 2 institutions in 1 country.

Marie McGovernDepartment of Pathology, Helen and Martin Kimmel Center for Stem Cell Biology, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA.
Roumen Voutev
John Maciejowski
Ann K Corsi
E Jane Albert Hubbard
New York University · USUniversity of America · US

Funding

CONTROL ONSET OF MEIOSIS IN C. ELEGANSR01GM061706 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUBBARD, E. JANE ALBERT · 2000 to 2018
$5.4M
Transcriptional regulation of mesoderm developmentR15DE018519 · NIDCR · CATHOLIC UNIVERSITY OF AMERICA · PI CORSI, ANN K · 2007 to 2017
$644k
NIDCR NIH HHS R15 DE018519NIDCR NIH HHS R15DE018519NIGMS NIH HHS R01 GM061706NIGMS NIH HHS R01GM61706
6 · The paper itself

Abstract

Stem cells, their niches, and their relationship to cancer are under intense investigation. Because tumors and metastases acquire self-renewing capacity, mechanisms for their establishment may involve cell-cell interactions similar to those between stem cells and stem cell niches. On the basis of our studies in Caenorhabditis elegans, we introduce the concept of a "latent niche" as a differentiated cell type that does not normally contact stem cells nor act as a niche but that can, under certain conditions, promote the ectopic self-renewal, proliferation, or survival of competent cells that it inappropriately contacts. Here, we show that ectopic germ-line stem cell proliferation in C. elegans is driven by a latent niche mechanism and that the molecular basis for this mechanism is inappropriate Notch activation. Furthermore, we show that continuous Notch signaling is required to maintain ectopic germ-line proliferation. We highlight the latent niche concept by distinguishing it from a normal stem cell niche, a premetastatic niche and an ectopic niche. One of the important distinguishing features of this mechanism for tumor initiation is that it could operate in the absence of genetic changes to the tumor cell or the tumor-promoting cell. We propose that a latent niche mechanism may underlie tumorigenesis and metastasis in humans.

Indexed as

Models, BiologicalAnimalsCaenorhabditis elegansCell DifferentiationCell ProliferationGerm CellsNeoplasmsPlasmidsReceptors, NotchRNA InterferenceSignal TransductionReceptors, Notch

Identifiers

PMID19564624
PMCPMC2710656
OpenAlexW2030336584

What OpenQuestion holds

Textmetadata
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.