Evidence map›Paper›PMID 19383824›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2009

Mutations in the hepatitis C virus core gene are associated with advanced liver disease and hepatocellular carcinoma.

Sarah L Fishman, Stephanie H Factor, Cinzia Balestrieri, Xiaofeng Fan, Adrian M Dibisceglie, Suresh M Desai, Gary Benson, Andrea D Branch

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 72 citations in OpenAlex.

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  6. Bioinformatics Analysis of Domain 1 of HCV-Core Protein: Iran.International journal of peptide research and therapeutics · 2020
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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

8 authors at 4 institutions in 1 country.

Sarah L FishmanDepartment of Medicine, Mount Sinai School of Medicine, New York, NY, USA.
Stephanie H Factor
Cinzia Balestrieri
Xiaofeng Fan
Adrian M Dibisceglie
Suresh M Desai
Gary Benson
Andrea D Branch
Icahn School of Medicine at Mount Sinai · USSaint Louis University · USAbbott Fund · USBoston University · US

Funding

Modulation of HCV Gene ExpressionR01DK066939 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BRANCH, ANDREA D. · 2004 to 2010
$2.0M
HCV Alternate Reading Frame Protein in HIV/HCV Co-infectR01DA016156 · NIDA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI BRANCH, ANDREA D. · 2003 to 2007
$1.9M
NIDA NIH HHS DA016156NIDA NIH HHS R01 DA016156NIDDK NIH HHS DK066939NIDDK NIH HHS R01 DK066939
6 · The paper itself

Abstract

purposeHepatitis C virus (HCV) infection can promote the development of hepatocellular carcinoma (HCC). Published data implicate the HCV core gene in oncogenesis. We tested the hypothesis that core gene sequences from HCC patients differ from those of patients without cirrhosis/HCC. EXPERIMENTAL

designFull-length HCV sequences from HCC patients and controls were obtained from the investigators and GenBank and compared with each other. A logistic regression model was developed to predict the HCC risk of individual point mutations and other sequence features. Mutations in partial sequences (bases 36-288) from HCC patients and controls were also analyzed. The first base of the AUG start codon was designated position 1.

resultsA logistic regression model developed through analysis of full-length core gene sequences identified seven polymorphisms significantly associated with increased HCC risk (36G/C, 209A, 271U/C, 309A/C, 435A/C, 481A, and 546A/C) and an interaction term (for 209A-271U/C) that had an odds ratio <1.0. Three of these polymorphisms could be analyzed in the partial sequences. Two of them, 36G/C and 209A, were again associated with increased HCC risk, but 271U/C was not. The odds ratio of 209A-271U/C was not significant.

conclusionsHCV core genes from patients with and without HCC differ at several positions. Of interest, 209A has been associated with IFN resistance and HCC in previous studies. Our findings suggest that HCV core gene sequence data might provide useful information about HCC risk. Prospective investigation is needed to establish the temporal relationship between appearance of the viral mutations and development of HCC.

Indexed as

Carcinoma, HepatocellularCase-Control StudiesHepacivirusHepatitis CHumansLiver CirrhosisLiver NeoplasmsMutationViral Core ProteinsViral Core Proteins

Identifiers

PMID19383824
PMCPMC3142862
OpenAlexW2011221934

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.