Evidence map›Paper›PMID 25266280›Full record

ArticleHepatology (Baltimore, Md.)2015

Dysregulated serum response factor triggers formation of hepatocellular carcinoma.

Stefan Ohrnberger, Abhishek Thavamani, Albert Braeuning, Daniel B Lipka, Milen Kirilov, Robert Geffers, Stella E Autenrieth, Stella E Authenrieth, Michael Römer, Andreas Zell and 7 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. RHO GTPase family in hepatocellular carcinoma.Experimental hematology & oncology · 2022
    Review
  10. Smad3 Phospho-Isoform Signaling in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Identification of PparProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
    Authenrieth, Stella E [corrected to Autenrieth, Stella E]
5 · Who and what money

Authors and funding

17 authors at 6 institutions in 2 countries.

Stefan OhrnbergerDepartment for Molecular Biology, Interfaculty Institute of Cell Biology, Tuebingen University, Germany.
Abhishek Thavamani
Albert Braeuning
Daniel B Lipka
Milen Kirilov
Robert Geffers
Stella E Autenrieth
Stella E Authenrieth
Michael Römer
Andreas Zell
Michael Bonin
Michael Schwarz
Günther Schütz
Peter Schirmacher
Christoph Plass
Thomas Longerich
Alfred Nordheim
University of Tübingen · DEGerman Cancer Research Center · DEHeidelberg University · DEDKFZ-ZMBH Alliance · DEHelmholtz Centre for Infection Research · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledThe ubiquitously expressed transcriptional regulator serum response factor (SRF) is controlled by both Ras/MAPK (mitogen-activated protein kinase) and Rho/actin signaling pathways, which are frequently activated in hepatocellular carcinoma (HCC). We generated SRF-VP16iHep mice, which conditionally express constitutively active SRF-VP16 in hepatocytes, thereby controlling subsets of both Ras/MAPK- and Rho/actin-stimulated target genes. All SRF-VP16iHep mice develop hyperproliferative liver nodules that progresses to lethal HCC. Some murine (m)HCCs acquire Ctnnb1 mutations equivalent to those in human (h)HCC. The resulting transcript signatures mirror those of a distinct subgroup of hHCCs, with shared activation of oncofetal genes including Igf2, correlating with CpG hypomethylation at the imprinted Igf2/H19 locus.

conclusionSRF-VP16iHep mHCC reveal convergent Ras/MAPK and Rho/actin signaling as a highly oncogenic driver mechanism for hepatocarcinogenesis. This suggests simultaneous inhibition of Ras/MAPK and Rho/actin signaling as a treatment strategy in hHCC therapy.

Indexed as

Animalsbeta CateninCell ProliferationCpG IslandsDNA MethylationGene Expression ProfilingHepatocytesHerpes Simplex Virus Protein Vmw65HumansInsulin-Like Growth Factor IILiver Neoplasms, ExperimentalLymphocytesMiceMutationSerum Response Factorbeta CateninCTNNB1 protein, mouseHerpes Simplex Virus Protein Vmw65Insulin-Like Growth Factor IISerum Response Factor

Identifiers

PMID25266280
PMCPMC4365683
OpenAlexW1984650634

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.