Evidence map›Paper›PMID 11042693›Full record

ArticleOncogene2000

Dual functions of E2F-1 in a transgenic mouse model of liver carcinogenesis.

E A Conner, E R Lemmer, M Omori, P J Wirth, V M Factor, S S Thorgeirsson

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

62 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. DNA methylation profile of liver of mice conceived byJournal of developmental origins of health and disease · 2022
    Article
  5. Review
  6. Mouse Models of Oncoimmunology in Hepatocellular Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Review
  7. Review
  8. Article
  9. Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

2 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

6 authors at 2 institutions in 1 country.

E A ConnerLaboratory of Experimental Carcinogenesis, Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, MD 20892, USA.
E R Lemmer
M Omori
P J Wirth
V M Factor
S S Thorgeirsson
National Cancer Institute · USNational Institutes of Health · US

Funding

TRANSGENIC MODELS FOR COOPERATION OF C-MYC AND GROWTH FACTORS IN TUMORIGENESISZ01BC005750 · BC · BASIC SCIENCES · PI THORGEIRSSON, SNORRI S · 1996 to 2002
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6 · The paper itself

Abstract

Deregulation of E2F transcriptional control has been implicated in oncogenic transformation. Consistent with this idea, we recently demonstrated that during hepatocarcinogenesis in c-myc/TGFalpha double transgenic mice, there is increased expression of E2F-1 and E2F-2, as well as induction of putative E2F target genes. Therefore, we generated transgenic mice expressing E2F-1 under the control of the albumin enhancer/promoter to test the hypothesis that E2F family members may contribute to liver tumor development. Overexpression of E2F-1 resulted in mild but persistent increases in cell proliferation and death during postnatal liver growth, and no increases in hepatic regenerative growth in response to partial hepatectomy. Nevertheless, from 2 months postnatally E2F-1 transgenic mice exhibited prominent hepatic histological abnormalities including preneoplastic foci adjacent to portal tracts and pericentral large cell dysplasia. From 6 to 8 months onward, there was an abrupt increase in the number of neoplastic nodules ('adenomas') with 100% incidence by 10 months. Some adenomas showed evidence of malignant transformation, and two of six mice killed at 12 months showed trabecular hepatocellular carcinoma. Endogenous c-myc was up-regulated in the early stages of E2F-1 hepatocarcinogenesis, whereas p53 was overexpressed in the tumors, suggesting that both E2F-1-mediated proliferation and apoptosis are operative but at different stages of hepatocarcinogenesis. In conclusion, E2F-1 overexpression in the liver causes dysplasia and tumors and suggests a cooperation between E2F-1 and c-myc oncogenes during liver oncogenesis.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsAlbuminsAnimalsApoptosisCell DivisionCell Transformation, NeoplasticCrosses, GeneticE2F1 Transcription FactorE2F2 Transcription FactorE2F Transcription FactorsEnhancer Elements, GeneticFemaleGene Expression Regulation, NeoplasticGenes, mycAlbuminsArid4a protein, mouseCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorE2F2 protein, humanE2F2 Transcription FactorE2F Transcription FactorsProto-Oncogene Proteins c-mycRetinoblastoma-Binding Protein 1Transcription Factor DP1Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID11042693
OpenAlexW2322812254

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.