Evidence map›Paper›PMID 11175353›Full record

ArticleOncogene2000

The H19 endodermal enhancer is required for Igf2 activation and tumor formation in experimental liver carcinogenesis.

M Vernucci, F Cerrato, N Besnard, S Casola, P V Pedone, C B Bruni, A Riccio

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. The emerging role of Nemo-like kinase (NLK) in the regulation of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The H19 locus acts in vivo as a tumor suppressor.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

7 authors at 3 institutions in 1 country.

M VernucciCentro di Endocrinologia ed Oncologia Sperimentale 'G Salvatore', CNR; Dipartimento di Biologia e Patologia Cellulare e Molecolare 'L Califano', Università di Napoli 'Federico II', Napoli, Italy.
F Cerrato
N Besnard
S Casola
P V Pedone
C B Bruni
A Riccio
University of Naples Federico II · ITInstitute for Experimental Endocrinology and Oncology · ITCentro di Riferimento Oncologico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of the linked but reciprocally imprinted Igf2 and H19 genes is activated in adult liver in the course of tumor development. By in situ hybridization analysis we have shown that both the Igf2 and H19 RNAs are expressed in the majority of the neoplastic nodules, and that hepatocellular carcinomas are developed in an experimental model of liver carcinogenesis. H19 is also highly activated in smaller and less distinct hyperplastic regions. The few neoplastic areas showing Igf2 but no H19 RNA display loss of the maternally inherited allele at the Igf2/H19 locus. These data are compatible with the existence of a common activation mechanism of these two genes during liver carcinogenesis and with a stronger H19 induction in the pre-neoplastic lesions. By using mice carrying a deletion of the H19 endodermal enhancer, we show that this regulatory element is necessary for the activation of the Igf2 and H19 genes upon induction of liver carcinogenesis. Furthermore, multiple sites of the H19 endodermal enhancer region become hypersensitive to DNase I when the carcinogenesis process is induced. Lastly, liver tumors developed in mice paternally inheriting the H19 enhancer deletion are found to have marked growth delays, increased frequency of apoptotic nuclei, and lack of Igf2 mRNA expression, thus indicating that this regulatory element plays a major role in the progression of liver carcinogenesis, since it is required for the activation of the anti-apoptotic Igf2 gene.

Indexed as

AnimalsApoptosisChromatinDeoxyribonucleasesEndodermEnhancer Elements, GeneticFemaleGene Expression Regulation, NeoplasticGenetic LinkageGenomic ImprintingIn Situ HybridizationInsulin-Like Growth Factor IILiverLiver Neoplasms, ExperimentalMaleMiceChromatinDeoxyribonucleasesH19 long non-coding RNAInsulin-Like Growth Factor IIRNA, Long NoncodingRNA, MessengerRNA, Untranslated

Identifiers

PMID11175353
OpenAlexW2325632885

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.