Evidence map›Paper›PMID 11467453›Full record

ReviewJournal of mammary gland biology and neoplasia2001

TGF-beta signaling in mammary gland development and tumorigenesis.

L M Wakefield, E Piek, E P Böttinger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 99 citations in OpenAlex.

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  14. Transforming growth factor beta1 (TGFβ1) polymorphisms and breast cancer risk.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
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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 2 institutions in 1 country.

L M WakefieldLaboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland, USA. wakefiel@dce41.nci.nih.gov
E Piek
E P Böttinger
National Cancer Institute · USAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ligands of the TGF-beta superfamily are unique in that they signal through transmembrane receptor serine-threonine kinases, rather than tyrosine kinases. The receptor complex couples to a signal transduction pathway involving a novel family of proteins, the Smads. On phosphorylation, Smads translocate to the nucleus where they modulate transcriptional responses. However, TGF-betas can also activate the mitogen-activated protein kinase (MAPK)4 pathway, and the different biological responses to TGF-beta depend to varying degrees on activation of either or both of these two pathways. The Smad pathway is a nexus for cross-talk with other signal transduction pathways and for modulation by many different interacting proteins. Despite compelling evidence that TGF-beta has tumor suppressor activity in the mammary gland, neither TGF-beta receptors nor Smads are genetically inactivated in human breast cancer, though receptor expression is reduced. Possible reasons are discussed in relation to the dual role of TGF-beta as tumor suppressor and oncogene.

Indexed as

AnimalsBreastFemaleHumansMammary Neoplasms, AnimalSignal TransductionTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID11467453
OpenAlexW2277013638

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.