Hepatocellular carcinoma and the underlying mechanisms.

A A Oyagbemi, O I Azeez, A B Saba

Open access · greenAbstract read

In one paragraph

Article in African health sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it

0cells of the map it votes in

2citing papers in PubMed

1.1field-weighted citation impact, top 22% 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

2 citing papers in PubMed, 16 citations in OpenAlex.

How did hepatitis B virus effect the host genome in the last decade?World journal of hepatology · 2014
Review
Treatment of human hepatocellular carcinoma by the oncolytic herpes simplex virus G47delta.Cancer cell international · 2014
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

3 authors at 1 institution in 1 country.

A A OyagbemiDepartment of Veterinary Physiology, Biochemistry and Pharmacology, University of Ibadan, Oyo State, Nigeria. ademolaoyagbemi@yahoo.com

O I Azeez

A B Saba

University of Ibadan · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of hepatocellular carcinoma is increasing worldwide as well as the associated risk factors, some of which include exposure to aflatoxin B1, Hepatitis B (HBV) virus and hepatitis C (HCV) virus. Mutation of tumour suppressor gene p53 at codon 249(ser) at exon 7 has been found to contribute significantly to replication of damaged DNA and subsequent tumour progression. The x gene of HBV (HBx) is the most common open reading frame integrated into the host genome in hepatocellular carcinoma and the integrated HBx is frequently mutated in hepatocellular carcinoma. Mutant HBx proteins still retain their ability to bind to p53 thereby attenuating DNA repair and p53-mediated apoptosis.

Indexed as

Aflatoxin B1Carcinoma, HepatocellularDNA RepairHepacivirusHepatitis BHepatitis B virusHepatitis CHumansIncidenceLiver NeoplasmsMutationRisk FactorsTrans-ActivatorsTumor Suppressor Protein p53Viral Regulatory and Accessory ProteinsAflatoxin B1hepatitis B virus X proteinTrans-ActivatorsTumor Suppressor Protein p53Viral Regulatory and Accessory Proteinsaflatoxin B1HBVHCVhepatocellular carcinomap53

Identifiers

PMID20811532

PMCPMC2895801

OpenAlexW1727456404

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.