Evidence map›Paper›PMID 24167653›Full record

ArticleGenes & cancer2013

Overexpression of HGF Promotes HBV-Induced Hepatocellular Carcinoma Progression and Is an Effective Indicator for Met-Targeting Therapy.

Qian Xie, Yanli Su, Karl Dykema, Jennifer Johnson, Julie Koeman, Valeria De Giorgi, Alan Huang, Robert Schlegel, Curt Essenburg, Liang Kang and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Genes & cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. A phase Ib/II trial of capmatinib plus spartalizumabJHEP reports : innovation in hepatology · 2024
    Article
  3. Article
  4. Fibroblasts in liver cancer: functions and therapeutic translation.The lancet. Gastroenterology & hepatology · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

19 authors at 8 institutions in 5 countries.

Qian XieLaboratory of Molecular Oncology, Van Andel Research Institute, Grand Rapids, MI, USA.
Yanli Su
Karl Dykema
Jennifer Johnson
Julie Koeman
Valeria De Giorgi
Alan Huang
Robert Schlegel
Curt Essenburg
Liang Kang
Keiichi Iwaya
Shuhji Seki
Sok Kean Khoo
Boheng Zhang
Franco Buonaguro
Francesco M Marincola
Kyle Furge
George F Vande Woude
Nariyoshi Shinomiya
Van Andel Institute · USMolecular Oncology (United States) · USNational Defense Medical College · JPNovartis (United States) · USIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITNational Institutes of Health Clinical Center · USSidra Medical and Research Center · QAZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) is a well-known cause of hepatocellular carcinoma (HCC), but the regulators effectively driving virus production and HCC progression remain unclear. By using genetically engineered mouse models, we show that overexpression of hepatocyte growth factor (HGF) accelerated HCC progression, supporting the genomic analysis that an up-regulated HGF signature is associated with poor prognosis in HBV-positive HCC patients. We show that for both liver regeneration and spontaneous HCC development there is an inclusive requirement for MET expression, and when HGF induces autocrine activation the tumor displays sensitivity to a small-molecule Met inhibitor. Our results demonstrate that HGF is a driver of HBV-induced HCC progression and may serve as an effective biomarker for Met-targeted therapy. MET inhibitors are entering clinical trials against cancer, and our data provide a molecular basis for targeting the Met pathway in hepatitis B-induced HCC.

Indexed as

hepatitis Bhepatocellular carcinomahepatocyte growth factorMETtargeted therapy

Identifiers

PMID24167653
PMCPMC3807646
OpenAlexW2159209399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.