Evidence map›Paper›PMID 24213574›Full record

ArticleOncogene2014

Synergistic function of Kras mutation and HBx in initiation and progression of hepatocellular carcinoma in mice.

H Ye, C Zhang, B-J Wang, X-H Tan, W-P Zhang, Y Teng, X Yang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
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  4. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
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  6. Article
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  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Moderate alcohol intake promotes pancreatic ductal adenocarcinoma development in mice expressing oncogenic Kras.American journal of physiology. Gastrointestinal and liver physiology · 2020
    Article
  18. Article
  19. Alternative Splicing in Hepatocellular Carcinoma.Cellular and molecular gastroenterology and hepatology · 2020
    Review
  20. 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 2 institutions in 1 country.

H Ye1] Model Organism Division, E-institutes of Shanghai Universities, Shanghai Jiaotong University School of Medicine, Shanghai, China [2] State Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
C Zhang1] Model Organism Division, E-institutes of Shanghai Universities, Shanghai Jiaotong University School of Medicine, Shanghai, China [2] State Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
B-J WangState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
X-H TanState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
W-P ZhangDepartment of Pathophysiology, Second Military Medical University, Shanghai, China.
Y TengState Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
X Yang1] Model Organism Division, E-institutes of Shanghai Universities, Shanghai Jiaotong University School of Medicine, Shanghai, China [2] State Key Laboratory of Proteomics, Genetic Laboratory of Development and Disease, Institute of Biotechnology, Beijing, China.
State Key Laboratory of ProteomicsSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the activation of Ras pathway is frequently observed in human hepatocellular carcinoma (HCC), the in vivo role of Ras activation in HCC initiation and progression is underdetermined. To test the consequence of Kras activation in hepatocyte, we generated a hepatocyte-specific Kras(G12D) transgenic mouse strain and observed spontaneous development of HCC in these mice. Remarkably, HBV X protein (HBx) expression significantly promotes the formation and malignant progression of Kras(G12D)-driven HCC as shown with the accelerated tumor onset, the increased tumor burden and the more poorly differentiated lesions. At the cellular level, concomitant expression of Kras(G12D) and HBx results in a robust increase in hepatocellular proliferation. We reveal that the Akt, MAPK, p53 and TGF-β pathways are deregulated in the Kras(G12D)-driven HCCs. Also, the dysregulation is more pronounced in the HCCs developed in Kras(G12D) and HBx double transgenic mice. In addition, the altered expressions of β-catenin, CD44 and E-cadherin are only observed in the Kras(G12D) and HBx double transgenic mice. These results demonstrate a crucial role of Ras activation in hepatocellular carcinogenesis and the functional synergy between Kras(G12D) and HBx in HCC initiation and progression. The novel genetic mouse models that closely recapitulate the histopathologic progression and molecular alterations of human HCC may potentially facilitate the future therapeutic studies.

Indexed as

AnimalsCarcinoma, HepatocellularCell ProliferationGene Expression Regulation, NeoplasticLiver NeoplasmsMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, TransgenicMutationProto-Oncogene Proteins p21(ras)Trans-ActivatorsViral Regulatory and Accessory Proteinshepatitis B virus X proteinHras protein, mouseProto-Oncogene Proteins p21(ras)Trans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID24213574
OpenAlexW2086815392

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.