Evidence map›Paper›PMID 19117985›Full record

ArticleCancer research2009

TGFBI deficiency predisposes mice to spontaneous tumor development.

Ye Zhang, Gengyun Wen, Genze Shao, Cuidong Wang, Chyuansheng Lin, Hongbo Fang, Adayabalam S Balajee, Govind Bhagat, Tom K Hei, Yongliang Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  7. Review
  8. Chromosomal instability as an architect of the cancer stemness landscape.Frontiers in cell and developmental biology · 2024
    Review
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  10. Article
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  17. Annals of translational medicine · 2021
    Article
  18. Article
  19. Article
  20. Article

11 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

10 authors at 5 institutions in 2 countries.

Ye ZhangCenter for Radiological Research, Herbert Irving Comprehensive Cancer Center, and Department of Clinical Pathology, Columbia University, New York, NY 10032, USA.
Gengyun Wen
Genze Shao
Cuidong Wang
Chyuansheng Lin
Hongbo Fang
Adayabalam S Balajee
Govind Bhagat
Tom K Hei
Yongliang Zhao
Chinese Academy of Medical Sciences & Peking Union Medical College · CNColumbia University · USRockefeller University · USSylvester Comprehensive Cancer Center · USUniversity of Pennsylvania · US

Funding

MECHANISMS OF ARSENIC CARCINOGENESISR01ES011804 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HEI, TOM K. · 2002 to 2005
$1.5M
Role of TGFBI gene in cell proliferation and tumor progressionR01CA127120 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ZHAO, YONGLIANG · 2008 to 2011
$1.3M
NCI NIH HHS CA 127120NCI NIH HHS R01 CA127120NIEHS NIH HHS ES 11804NIEHS NIH HHS R01 ES011804
6 · The paper itself

Abstract

Loss of TGFBI, a secreted protein induced by transforming growth factor-beta, has been implicated in cell proliferation, tumor progression, and angiogenesis by in vitro studies. However, in vivo antitumor functions of TGFBI as well as the underlying molecular mechanism are not well understood. To these aims, we have generated a mouse model with disruption of TGFBI genomic locus. Mice lacking TGFBI show a retarded growth and are prone to spontaneous tumors and 7,12-dimethylbenz(a)anthracene-induced skin tumors. In relation to wild-type (WT) mouse embryonic fibroblasts (MEF), TGFBI(-/-) MEFs display increased frequencies of chromosomal aberration and micronuclei formation and exhibit an enhanced proliferation and early S-phase entry. Cyclin D1 is up-regulated in TGFBI(-/-) MEFs, which correlates with aberrant activation of transcription factor cyclic AMP-responsive element binding protein (CREB) identified by chromatin immunoprecipitation and luciferase reporter assays. TGFBI reconstitution in TGFBI(-/-) cells by either retroviral infection with WT TGFBI gene or supplement with recombinant mouse TGFBI protein in the culture medium leads to the suppression of CREB activation and cyclin D1 expression, and further inhibition of cell proliferation. Cyclin D1 up-regulation was also identified in most of the tumors arising from TGFBI(-/-) mice. Our studies provide the first evidence that TGFBI functions as a tumor suppressor in vivo.

Indexed as

9,10-Dimethyl-1,2-benzanthraceneAnimalsChromosome AberrationsCyclic AMP Response Element-Binding ProteinCyclin D1FemaleG1 PhaseGenes, bcl-1Genes, Tumor SuppressorGenetic Predisposition to DiseaseMiceMice, Inbred C57BLNeoplasms, ExperimentalPromoter Regions, GeneticRNA, MessengerS Phase9,10-Dimethyl-1,2-benzanthraceneCyclic AMP Response Element-Binding ProteinCyclin D1RNA, MessengerTgfb1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID19117985
PMCPMC2664305
OpenAlexW2140746826

What OpenQuestion holds

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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.