Evidence map›Paper›PMID 20087440›Full record

ReviewInternational journal of biological sciences2010

Smad4-mediated TGF-beta signaling in tumorigenesis.

Guan Yang, Xiao Yang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.1field-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

88 citing papers in PubMed, 143 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Clinical and Molecular Characterization ofInternational journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Research progress on the dermatomyositis specific autoantibodies and malignancy associated dermatomyositis.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  11. Review
  12. Review
  13. Mutation spectrum associated with metastasis of advanced cholangiocarcinoma.The Journal of international medical research · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

28 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution.

Guan YangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, AMMS, Beijing, P.R. China.
Xiao Yang
State Key Laboratory of Proteomics

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-beta (TGF-beta) family members exert their function via specific type I and type II serine/threonine kinase receptors and intracellular Smad transcription factors, including the common mediator Smad4. The dual effects of TGF-beta signaling on tumor initiation and progression are cell-specific and yet to be determined under distinct contexts. A number of genetically manipulated mouse models with alterations in the TGF-beta pathway genes, particularly the pivotal Smad4, revealed that these genes play crucial functions in maintaining tissue homeostasis and suppressing tumorigenesis. Loss of Smad4 plays a causal role in initiating squamous cell carcinomas of skin and upper digestive tract as well as adenocarcinomas of gastrointestinal tract. However, for some cancers like pancreatic and cholangiocellular carcinomas, Smad4 deficiency does not initiate the tumorigenesis but acts as a promoter to accelerate or synergize the development and progression of cancers that are started by other oncogenic pathways. Intriguingly, emerging evidences from mouse models have highlighted the important roles of non-cell autonomous effects of Smad4-mediated TGF-beta signaling in the inhibition of oncogenesis. All these data have greatly deepened our understanding of molecular mechanisms of cell-autonomous and non-cell autonomous effect of Smad4-mediated TGF-beta signaling in suppressing carcinogenesis, which may facilitate the development of successful therapies targeting TGF-beta signaling for the treatment of human cancers.

Indexed as

AnimalsHumansNeoplasmsSignal TransductionSmad4 ProteinTransforming Growth Factor betaSmad4 ProteinTransforming Growth Factor betamouse modelSmad4TGF-βtumorigenesis

Identifiers

PMID20087440
PMCPMC2808050
OpenAlexW2123018511

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.