Evidence map›Paper›PMID 25125747›Full record

ReviewTransactions of the American Clinical and Climatological Association2014

TGFBR1 and cancer susceptibility.

Boris Pasche, Michael J Pennison, Hugo Jimenez, Minghui Wang

Open access · greenAbstract readReview
In one paragraph

Review in Transactions of the American Clinical and Climatological Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. TRIM44 Promotes Endometrial Carcinoma Progression by Activating the FRS2 Signalling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  8. Up-Regulation ofCell journal · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. High Expression ofJournal of clinical medicine · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

4 authors.

Boris PascheWinston Salem, NC.
Michael J PennisonWinston Salem, NC.
Hugo JimenezWinston Salem, NC.
Minghui WangWinston Salem, NC.

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
INCIDENCE AND MOLECULAR SCREENING FOR HEREDITARY CANCERR01CA067941 · NCI · OHIO STATE UNIVERSITY · PI DE LA CHAPELLE, ALBERT · 2000 to 2004
$2.9M
TGF-beta polymorphisms and breast cancer in familiesR01CA112520 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PASCHE, BORIS · 2005 to 2013
$2.1M
TGFBR1 Signaling in Colorectal CancerR01CA137000 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PASCHE, BORIS · 2010 to 2014
$1.5M
TGF-beta pathway polymorphisms and colon cancer riskR01CA108741 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PASCHE, BORIS · 2006 to 2008
$804k
NATURAL HISTORY AND INCIDENCE OF HEREDITARY COLON CANCERU01CA067941 · NCI · UNIVERSITY OF HELSINKI · PI DE LA CHAPELLE, ALBERT · 1996 to 1999
–
NCI NIH HHS CA108741NCI NIH HHS CA112520NCI NIH HHS CA137000NCI NIH HHS CA16058NCI NIH HHS CA67941NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA067941NCI NIH HHS R01 CA108741NCI NIH HHS R01 CA112520NCI NIH HHS R01 CA137000NCI NIH HHS U01 CA067941
6 · The paper itself

Abstract

Transforming growth factor beta (TGF-β) is a potent inhibitor of cell growth. TGFBR1 6A is a polymorphism consisting of a 9-base pair in-frame deletion within exon 1 of the type I TGF-β receptor (TGFBR1), which results in a receptor with decreased TGF-β signaling capability. The discovery of an association between TGFBR1*6A and cancer susceptibility led to the hypothesis that hypomorphic variants of the TGF-β signaling pathway may predispose to the development of cancer. This hypothesis was tested in vivo with the development of a mouse model of Tgfbr1 haploinsufficiency. Tgfbr1 (+/-) mice developed twice as many intestinal tumors as Tgfbr1 (+/+). Tgfbr1 haploinsufficiency was also associated with early onset adenocarcinoma and increased tumor cell proliferation. A case control study identified two haplotypes associated with constitutively decreased TGFBR1 and substantially increased colorectal cancer risk indicating that TGFBR1 may act as a potent modifier of cancer risk.

Indexed as

AnimalsBiomarkers, TumorCell Transformation, NeoplasticGenetic Predisposition to DiseaseHumansMice, KnockoutNeoplasmsPhenotypeProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IRisk FactorsSignal TransductionTransforming Growth Factor betaBiomarkers, TumorProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanTgfbr1 protein, mouseTransforming Growth Factor beta

Identifiers

PMID25125747
PMCPMC4112675
OpenAlexW2288797421

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.