Evidence map›Paper›PMID 19201080›Full record

ReviewCancer letters2009

Putative roles of hepatitis B x antigen in the pathogenesis of chronic liver disease.

Mark A Feitelson, Helena M G P V Reis, N Lale Tufan, Bill Sun, Jingbo Pan, Zhaorui Lian

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. [Effect of transforming growth factor-β1 on HBV replication and antigen synthesis in HepG2.2.15 cells with steatosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Molecular mechanisms of hepatic apoptosis.Cell death & disease · 2014
    Review
  19. Article
  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

6 authors at 4 institutions in 2 countries.

Mark A FeitelsonDepartment of Biology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA. feitelso@temple.edu
Helena M G P V Reis
N Lale Tufan
Bill Sun
Jingbo Pan
Zhaorui Lian
Temple University · USPamukkale University · TRTemple College · USThomas Jefferson University · US

Funding

Early antibody markers of HCCR01CA111427 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 2005 to 2009
$1.4M
Beta-Catenin Signaling in HBxAg Mediated HCC.R01CA104025 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 2006 to 2010
$1.3M
NCI NIH HHS R01 CA104025NCI NIH HHS R01 CA111427
6 · The paper itself

Abstract

Under most circumstances, hepatitis B virus (HBV) is noncytopathic. However, hepatocellular regeneration that accompanies each bout of hepatitis appears to be associated with increased integration of HBV DNA fragments expressing the virus encoded hepatitis B x antigen (HBxAg). Intrahepatic HBxAg staining correlates with the intensity and progression of chronic liver disease (CLD), and additional work has shown that HBxAg blocks immune mediated killing by Fas and by tumor necrosis factor alpha (TNFalpha). This is not only associated with the blockage of caspase activities by HBxAg, but also by the constitutive stimulation of hepatoprotective pathways, such as nuclear factor kappa B (NF-kappaB), phosphoinositol 3-kinase (PI3K), and beta-catenin (beta-catenin). HBxAg also appears to promote fibrogenesis, by stimulating the production of fibronectin. HBxAg also stimulates the production and activity of transforming growth factor beta1 (TGFbeta1) by several mechanisms, thereby promoting the profibrogenic and tumorigenic properties of this important cytokine. In addition, HBxAg appears to remodel the extracellular matrix (ECM) by altering the expression of several matrix metalloproteinases (MMPs), which may promote tumor metastasis. Hence, HBxAg appears to promote chronic infection by preventing immune mediated apoptosis of infected hepatocytes, by promoting the establishment and persistence of fibrosis and cirrhosis preceding the development of HCC, and by promoting the remodeling of EMC during tumor progression.

Indexed as

Apoptosisbeta CateninExtracellular Matrix ProteinsHepatitis B, ChronicHumansPhosphatidylinositol 3-KinasesTrans-ActivatorsTransforming Growth Factor beta1Viral Regulatory and Accessory Proteinsbeta CateninExtracellular Matrix Proteinshepatitis B virus X proteinPhosphatidylinositol 3-KinasesTrans-ActivatorsTransforming Growth Factor beta1Viral Regulatory and Accessory Proteins

Identifiers

PMID19201080
PMCPMC2789742
OpenAlexW1981775449

What OpenQuestion holds

Textmetadata
LicenceTDM
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.