Evidence map›Paper›PMID 17875704›Full record

ArticleCancer research2007

Transforming growth factor-beta can suppress tumorigenesis through effects on the putative cancer stem or early progenitor cell and committed progeny in a breast cancer xenograft model.

Binwu Tang, Naomi Yoo, Mary Vu, Mizuko Mamura, Jeong-Seok Nam, Akira Ooshima, Zhijun Du, Pierre-Yves Desprez, Miriam R Anver, Aleksandra M Michalowska and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.7field-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

58 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. The Outcome of TGFβ Antagonism in Metastatic Breast Cancer ModelsClinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  15. Article
  16. TGF-β Family Signaling in Tumor Suppression and Cancer Progression.Cold Spring Harbor perspectives in biology · 2017
    Review
  17. Targeting TGF-β Signaling for Therapeutic Gain.Cold Spring Harbor perspectives in biology · 2017
    Review
  18. Article
  19. Review
  20. Review
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

13 authors at 4 institutions in 1 country.

Binwu TangLaboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892, USA.
Naomi Yoo
Mary Vu
Mizuko Mamura
Jeong-Seok Nam
Akira Ooshima
Zhijun Du
Pierre-Yves Desprez
Miriam R Anver
Aleksandra M Michalowska
Joanna Shih
W Tony Parks
Lalage M Wakefield
National Cancer Institute · USBaylor College of Medicine · USCalifornia Pacific Medical Center · USUniversity of Washington · US

Funding

TGF-betas in breast cancer progressionZ01BC005785 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WAKEFIELD, LALAGE · 1996 to 2008
$1.9M
Intramural NIH HHS Z01 BC005785NCI NIH HHS N01-CO-12400
6 · The paper itself

Abstract

The transforming growth factor-beta (TGF-beta) pathway has tumor-suppressor activity in many epithelial tissues. Because TGF-beta is a potent inhibitor of epithelial cell proliferation, it has been widely assumed that this property underlies the tumor-suppressor effect. Here, we have used a xenograft model of breast cancer to show that endogenous TGF-beta has the potential to suppress tumorigenesis through a novel mechanism, involving effects at two distinct levels in the hierarchy of cellular progeny that make up the epithelial component of the tumor. First, TGF-beta reduces the size of the putative cancer stem or early progenitor cell population, and second it promotes differentiation of a more committed, but highly proliferative, progenitor cell population to an intrinsically less proliferative state. We further show that reduced expression of the type II TGF-beta receptor correlates with loss of luminal differentiation in a clinical breast cancer cohort, suggesting that this mechanism may be clinically relevant. At a molecular level, the induction of differentiation by TGF-beta involves down-regulation of Id1, and forced overexpression of Id1 can promote tumorigenesis despite persistence of the antiproliferative effect of TGF-beta. These data suggest new roles for the TGF-beta pathway in regulating tumor cell dynamics that are independent of direct effects on proliferation.

Indexed as

AnimalsBreast NeoplasmsCell DifferentiationCell Line, TumorDown-RegulationFemaleGene Expression ProfilingHumansInhibitor of Differentiation Protein 1MiceMice, NudeNeoplasm TransplantationNeoplastic Stem CellsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIID1 protein, humanInhibitor of Differentiation Protein 1Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor beta

Identifiers

PMID17875704
PMCPMC2427144
OpenAlexW2166049118

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.