Evidence map›Paper›PMID 21461994›Full record

ReviewJournal of mammary gland biology and neoplasia2011

TGFBR1 signaling and breast cancer.

Lakisha Moore-Smith, Boris Pasche

Open access · greenAbstract readReview
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Keratin 80 Promotes Migration and Invasion of Non-Small Cell Lung Cancer Cells by Regulating the TGF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  15. Transforming growth factor-β in tumour development.Frontiers in molecular biosciences · 2022
    Review
  16. TRIM44 Promotes Endometrial Carcinoma Progression by Activating the FRS2 Signalling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  17. Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Lakisha Moore-SmithDivision of Hematology/Oncology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294-3300, USA.
Boris Pasche
University of Alabama at Birmingham · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
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
NCI NIH HHS CA 108741NCI NIH HHS CA 112520NCI NIH HHS CA 137000NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA108741NCI NIH HHS R01 CA112520NCI NIH HHS R01 CA137000NIAID NIH HHS T32 AI007051
6 · The paper itself

Abstract

Over the past decade mutations discovered in genes such as BRCA1, BRCA2, TP53 and PTEN, have emerged as high-penetrance susceptibility genes and are clinically relevant for determination of breast cancer risk. Genetic counseling and subsequent screening for mutations and gene rearrangement has improved patient outcome through early detection and prophylactic interventions in patients with familial breast cancer syndromes. However, these high-penetrance genes only account for a small fraction of the hereditary linked breast cancers. It is currently believed that low-penetrance susceptibility alleles and/or environmental factors may play an important role in the remaining cases. TGFBR1*6A (*6A) is a common hypomorphic variant of the type I TGF-β receptor gene (TGFBR1) that has been associated with risk for several forms of cancer, in particular breast cancer. Several epidemiological studies have suggested that patients who carry the *6A allele have an increased risk of breast cancer. Furthermore, functional analysis suggests that this mutation alters TGF-β signaling and promotes tumorigenesis. Although a decade of research has provided basic information in regards to the prevalence of this mutation in several cancer types and populations the molecular underpinning of its functional effects are poorly understood. A better understanding of the molecular mechanism of TGFBR1 signaling in breast cancer may have an impact on breast cancer risk assessment and breast cancer prevention.

Indexed as

AllelesAnimalsBreast NeoplasmsFemaleHumansMutationProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, human

Identifiers

PMID21461994
PMCPMC4753062
OpenAlexW2063076260

What OpenQuestion holds

Textmetadata
LicenceTDM
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.