Evidence map›Paper›PMID 22072328›Full record

ArticleGenes, chromosomes & cancer2012

Genome-wide expression and copy number analysis identifies driver genes in gingivobuccal cancers.

Srikant Ambatipudi, Moritz Gerstung, Manishkumar Pandey, Tanuja Samant, Asawari Patil, Shubhada Kane, Rajiv S Desai, Alejandro A Schäffer, Niko Beerenwinkel, Manoj B Mahimkar

Open access · bronzeAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. The prognostic value and molecular mechanisms ofTranslational cancer research · 2026
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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

10 authors at 7 institutions in 3 countries.

Srikant AmbatipudiCancer Research Institute (CRI), Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre (TMC), Navi Mumbai, India.
Moritz Gerstung
Manishkumar Pandey
Tanuja Samant
Asawari Patil
Shubhada Kane
Rajiv S Desai
Alejandro A Schäffer
Niko Beerenwinkel
Manoj B Mahimkar
Tata Memorial Hospital · INCancer Research Institute · USAdvanced Centre for Treatment, Research and Education in Cancer · INETH Zurich · CHNational Institutes of Health · USRagas Dental College & Hospital · INSIB Swiss Institute of Bioinformatics · CH

Funding

Case Studies In GeneticsZIALM000097 · NLM · NATIONAL LIBRARY OF MEDICINE · PI SCHAFFER, ALEJANDRO A · 2009 to 2019
$4.6M
Intramural NIH HHS ZIA LM000097
6 · The paper itself

Abstract

The molecular mechanisms contributing to the development and progression of gingivobuccal complex (GBC) cancers-a sub-site of oral cancer, comprising the buccal mucosa, the gingivobuccal sulcus, the lower gingival region, and the retromolar trigone-remain poorly understood. Identifying the GBC cancer-related gene expression signature and the driver genes residing on the altered chromosomal regions is critical for understanding the molecular basis of its pathogenesis. Genome-wide expression profiling of 27 GBC cancers with known chromosomal alterations was performed to reveal differentially expressed genes. Putative driver genes were identified by integrating copy number and gene expression data. A total of 315 genes were found differentially expressed (P ≤ 0.05, logFC > 2.0) of which 11 genes were validated by real-time quantitative reverse transcriptase-PCR (qRT-PCR) in tumors (n = 57) and normal GBC tissues (n = 18). Overexpression of LY6K, in chromosome band 8q24.3, was validated by immunohistochemical (IHC) analysis. We found that 78.5% (2,417/3,079) of the genes located in regions of recurrent chromosomal alterations show copy number dependent expression indicating that copy number alteration has a direct effect on global gene expression. The integrative analysis revealed BIRC3 in 11q22.2 as a candidate driver gene associated with poor clinical outcome. Our study identified previously unreported differentially expressed genes in a homogeneous subtype of oral cancer and the candidate driver genes that may contribute to the development and progression of the disease. © 2011 Wiley Periodicals, Inc.

Indexed as

AdultAntigens, LyBiomarkers, TumorCarcinoma, Squamous CellCase-Control StudiesChromosome DuplicationChromosomes, Human, Pair 8FemaleGene DosageGene ExpressionGenome-Wide Association StudyGingival NeoplasmsGPI-Linked ProteinsHumansKaplan-Meier EstimateMaleAntigens, LyBiomarkers, TumorGPI-Linked ProteinsLY6K protein, human

Identifiers

PMID22072328
PMCPMC3233671
OpenAlexW2056170952

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.