Evidence map›Paper›PMID 28203651›Full record

ArticleJournal of digestive diseases and hepatology2016

Association between Hepatitis C Virus Infection, p53 Phenotypes, and Gene Variants of Adenomatous Polyposis Coli in Hepatocellular Carcinomas.

Leona N Council, Chandrakumar Shanmugam, Esther A Suswam, Venkat R Katkoori, Martine J Heslin, Alex Hanna, Nirag C Jhala, Sooryanarayana Varambally, Upender Manne

Open access · greenAbstract read
In one paragraph

Article in Journal of digestive diseases and hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 79% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 1 institution in 1 country.

Leona N CouncilDepartment of Pathology, University of Alabama at Birmingham, USA.
Chandrakumar ShanmugamDepartment of Pathology, University of Alabama at Birmingham, USA; Department of Surgery, University of Alabama at Birmingham, USA.
Esther A SuswamDepartment of Pathology, University of Alabama at Birmingham, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, USA.
Venkat R KatkooriDepartment of Pathology, University of Alabama at Birmingham, USA.
Martine J HeslinComprehensive Cancer Center, University of Alabama at Birmingham, USA.
Alex HannaDepartment of Pathology, University of Alabama at Birmingham, USA.
Nirag C JhalaDepartment of Pathology, University of Alabama at Birmingham, USA.
Sooryanarayana VaramballyDepartment of Pathology, University of Alabama at Birmingham, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, USA.
Upender ManneDepartment of Pathology, University of Alabama at Birmingham, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, USA.
University of Alabama at Birmingham · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
TRAINING AND CAREER DEVELOPMENTU54CA118948 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI UPENDER MANNE · 2005 to 2026
$26.6M
UAB CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCE (CCTS) UL1: BPCAUL1RR025777 · NCRR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIMBERLY, ROBERT P. · 2008 to 2011
$22.3M
Prognostic Molecular Markers of Colorectal CancerR01CA098932 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MANNE, UPENDER · 2003 to 2009
$1.5M
NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA098932NCI NIH HHS U54 CA118948NCRR NIH HHS UL1 RR025777
6 · The paper itself

Abstract

objectiveTo investigate the clinical value of p53 codon 72 single nucleotide polymorphisms (SNPs) and variants of adenomatous polyposis coli (APC) in hepatocellular carcinomas (HCCs).

methodsDNA and RNA from 51 HCCs and their matching, uninvolved liver tissues were analyzed for p53 mutations, and the methylation and expression of APC variants were determined. Proliferation of each HCC was assessed by Ki67 immunohistochemistry. The results were correlated with the demographic and clinicopathologic features and patient survival.

resultsOf 51 HCCs, 12% exhibited missense p53 mutations. SNP analysis of p53 codon 72 demonstrated the highest prevalence of the Arg/Arg (56%) phenotype, followed by Arg/Pro (33%) and Pro/Pro (11%). Four of five cases with the Pro/Pro phenotype were African Americans (AAs). All five cases with the Pro/Pro phenotype had hepatitis C virus (HCV) infections, a high Ki67 index, and lower median survival (15.5 months) compared to those with Arg/Arg or Arg/Pro phenotypes (32 months). The overall frequency of APC methylation was 31%, which was found predominantly in Caucasians. There was lower mRNA expression of APC variants-2 and -3 in both HCCs and corresponding adjacent, uninvolved liver tissues as compared to APC variant-1. The expression of APC variant-3, but not variants-1 and -2, was lower in HCCs relative to uninvolved tissues. Expression of all APC variants was lower in HCCs with APC methylation relative to HCCs without APC methylation, and low expression of APC variant-2 was associated with the Pro/Pro phenotype.

conclusionsThese findings suggest that, for AA patients with HCCs, the p53 Pro/Pro phenotype and low expression of APC variant-2 are associated with aggressive tumor behavior, HCV infection, and poor clinical outcome.

Indexed as

APCHCVHepatocellular carcinomap53 codon 72 polymorphismSurvival

Identifiers

PMID28203651
PMCPMC5305186
OpenAlexW2589219768

What OpenQuestion holds

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Registered trials

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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.