Evidence map›Paper›PMID 9094970›Full record

ReviewThe American journal of pathology1997

Hepatitis B virus X antigen in the pathogenesis of chronic infections and the development of hepatocellular carcinoma.

M A Feitelson, L X Duan

Abstract readReview
In one paragraph

Review in The American journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 226 citations in OpenAlex.

  1. Article
  2. Review
  3. Wnt signaling in liver regeneration, disease, and cancer.Clinical and molecular hepatology · 2023
    Review
  4. PROTACs in gastrointestinal cancers.Molecular therapy oncolytics · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Targeting PIN1 as a Therapeutic Approach for Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Understanding the role of PIN1 in hepatocellular carcinoma.World journal of gastroenterology · 2016
    Review
  14. Review
  15. Article
  16. HBx interacted with Smad4 to deprive activin a growth inhibition function in hepatocyte HL7702 on CRM1 manner.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Article
  18. Evidence of Hepatitis B Virus Infection in Cancer and Noncancer Stem Cells Associated with Human Hepatocellular Carcinoma.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2016
    Article
  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

M A FeitelsonDepartment of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107-6799, USA.
L X Duan
Thomas Jefferson University · US

Funding

MECHANISMS OF HBV X MEDIATED HCCR01CA066971 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1995 to 2004
$1.6M
SENESCENCE AND APOPTOSIS IN HBV ASSOCIATED HCCR01CA048656 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1994 to 2002
$727k
PRODUCTS OF THE X AND POLYMERASE GENES OF HEPADNAVIRUSESR29CA048656 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1988 to 1992
–
NCI NIH HHS CA48656NCI NIH HHS CA66971
6 · The paper itself

Abstract

Chronic infection with hepatitis B virus is associated with a high incidence of liver diseases, including hepatocellular carcinoma. Hepatitis-B-virus-encoded X antigen (HBxAg) stimulates virus gene expression and replication, which may be important for the establishment and maintenance of the chronic carrier state. Integration of viral DNA encoding HBxAg during chronic infection results in increased X antigen expression. HBxAg overexpression may alter signal transduction pathways important for the regulation of cell growth during hepatocellular regeneration. The finding that HBxAg binds to and inactivates negative growth-regulatory molecules, such as the tumor suppressor p53, suggests additional ways that HBxAg may act in hepatocarcinogenesis. HBxAg may also stimulate the expression of positive growth regulators, such as insulin-like growth factor II and the insulin-like growth factor I receptor. The finding that HBxAg may compromise DNA repair and that it may effect the normal turnover of growth-regulatory molecules in the proteasome may also contribute to its carcinogenic properties. Hence, HBxAg may contribute to the pathogenesis of chronic infection and development of hepatocellular carcinoma in a variety of ways.

Indexed as

AnimalsCarcinoma, HepatocellularHepatitis BHepatitis B AntigensHepatitis B virusHepatitis, ChronicHumansLiver NeoplasmsTrans-ActivatorsViral Regulatory and Accessory ProteinsHepatitis B Antigenshepatitis B virus X proteinTrans-ActivatorsViral Regulatory and Accessory Proteins

Identifiers

PMID9094970
PMCPMC1858185
OpenAlexW1751026994

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.