Evidence map›Paper›PMID 20676143›Full record

ArticleOncogene2010

Characterization of ΔNp73 expression and regulation in gastric and esophageal tumors.

A E Vilgelm, S-M Hong, M K Washington, J Wei, H Chen, W El-Rifai, A Zaika

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2010. 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
1.7field-weighted citation impact, top 17% 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, 27 citations in OpenAlex.

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  11. Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Review
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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

7 authors at 2 institutions in 1 country.

A E VilgelmDepartment of Surgery, Vanderbilt University Medical Center and Vanderbilt-Ingram Cancer Center, Nashville, TN 37232, USA.
S-M Hong
M K Washington
J Wei
H Chen
W El-Rifai
A Zaika
Vanderbilt University Medical Center · USJohns Hopkins University · US

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
Regulation of the Oncogenic Stress Response in Helicobacter pylori-infected cellsR01CA138833 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALEXANDER I. ZAIKA · 2010 to 2026
$4.3M
The Role of p73 in Upper Gastrointestinal CarcinomasR01CA108956 · NCI · VANDERBILT UNIVERSITY · PI ZAIKA, ALEXANDER I. · 2005 to 2010
$1.3M
NCI NIH HHS CA108956NCI NIH HHS R01 CA108956NCI NIH HHS R01 CA138833NCRR NIH HHS UL1 RR024975NCRR NIH HHS UL1RR024975
6 · The paper itself

Abstract

p73 is a member of the p53 protein family. Although the tumor suppressor function of p53 is clearly defined, the role of p73 in tumorigenesis is still a matter of debate. A complex pattern of expression of p73 isoforms makes it difficult to unambiguously interpret the experimental results. Previously, we along with others have found that the N-terminally truncated isoform of p73, ΔNp73, has potent anti-apoptotic and oncogenic properties in vitro and in vivo. In this study, we analyzed, for the first time, the regulation of ΔNp73 in a large number of gastric, gastroesophageal junction and esophageal tumors. We found that expression of ΔNp73 mRNA and protein is increased in these neoplasms. Furthermore, the upregulation of the ΔNp73 protein is significantly associated with poor patient survival. Oncogenic properties of ΔNp73 were further confirmed by finding that ΔNp73 facilitates anchorage-independent growth of gastric epithelial cells in soft agar. As little is currently known about the regulation of ΔNp73 transcription, we investigated the alternative p73 gene promoter that mediates the ΔNp73 expression. Analyzing the ΔNp73 promoter in silico as well as by using chromatin immunoprecipitation, site-directed mutagenesis and deletion analyses, we identified the evolutionary conserved region within the ΔNp73 promoter that contains binding sites for HIC1 (hypermethylated in cancer) protein. We found that HIC1 negatively regulates ΔNp73 transcription in mucosal epithelial cells. This leads to a decrease in ΔNp73 protein levels and may normally control the oncogenic potential of the ΔNp73 isoform.

Indexed as

Base SequenceChromatin ImmunoprecipitationConserved SequenceDNA-Binding ProteinsEsophageal NeoplasmsGene ExpressionGene Expression Regulation, NeoplasticHumansMolecular Sequence DataMutagenesis, Site-DirectedNuclear ProteinsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticProtein IsoformsReverse Transcriptase Polymerase Chain ReactionRNA, Messengerdelta Np73 protein, humanDNA-Binding ProteinsNuclear ProteinsProtein IsoformsRNA, MessengerTP73 protein, humanTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID20676143
PMCPMC4152004
OpenAlexW2026264889

What OpenQuestion holds

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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.