Evidence map›Paper›PMID 23583282›Full record

ArticleThe American journal of pathology2013

Detailed genome-wide SNP analysis of major salivary carcinomas localizes subtype-specific chromosome sites and oncogenes of potential clinical significance.

Li Zhang, Yoshitsugu Mitani, Carlos Caulin, Pulivarthi H Rao, Merrill S Kies, Pierre Saintigny, Nianxiang Zhang, Randal S Weber, Scott M Lippman, Adel K El-Naggar

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. The Molecular Biology of MEC Salivary Gland Tumors.Annals of otolaryngology and rhinology · 2025
    Article
  3. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
    Review
  4. Article
  5. Whole-Genome Sequencing of Common Salivary Gland Carcinomas: Subtype-Restricted and Shared Genetic Alterations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  6. Article
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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 3 institutions in 1 country.

Li ZhangDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. lzhangli@mdanderson.org
Yoshitsugu Mitani
Carlos Caulin
Pulivarthi H Rao
Merrill S Kies
Pierre Saintigny
Nianxiang Zhang
Randal S Weber
Scott M Lippman
Adel K El-Naggar
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USMoores Cancer Center

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting the p53 pathway for reversal of oral premalignancyP50CA097007 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MYERS, JEFFREY NICHOLAS · 2002 to 2012
$26.1M
Molecular and Epidemiologic Characterization of Salivary Gland CarcinomasU01DE019765 · NIDCR · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EL-NAGGAR, ADEL K. · 2009 to 2013
$6.9M
NCI NIH HHS CA-16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA097007NIDCR NIH HHS U01 DE019765NIDCR NIH HHS U01DE019765
6 · The paper itself

Abstract

The molecular genetic alterations underlying the development and diversity of salivary gland carcinomas are largely unknown. To characterize these events, comparative genomic hybridization analysis was performed, using a single-nucleotide polymorphism microarray platform, of 60 fresh-frozen specimens that represent the main salivary carcinoma types: mucoepidermoid carcinoma (MEC), adenoid cystic carcinoma (ACC), and salivary duct carcinoma (SDC). The results were correlated with the clinicopathologic features and translocation statuses to characterize the genetic alterations. The most commonly shared copy number abnormalities (CNAs) in all types were losses at chromosomes 6q23-26 and the 9p21 region. Subtype-specific CNAs included a loss at 12q11-12 in ACC and a gain at 17q11-12 in SDC. Focal copy number losses included 1p36.33-p36-22 in ACC, 9p13.2 in MEC, and 3p12.3-q11-2, 6q21-22.1, 12q14.1, and 12q15 in SDC. Tumor-specific amplicons were identified at 11q23.3 (PVRL1) in ACC, 11q13.3 (NUMA1) in MEC, and 6p21.1 (CCND3), 9p13.2 (PAX5), 12q15 (CNOT2/RAB3IP), 12q21.1 (GLIPR1L1), and 17q12 (ERBB2/CCL4) in SDC. A comparative CNA analysis of fusion-positive and fusion-negative ACCs and MECs revealed relatively lower CNAs in fusion-positive tumors than in fusion-negative tumors in both tumor types. An association between CNAs and high grade and advanced stage was observed in MECs only. These findings support the pathogenetic segregation of these entities and define novel chromosomal sites for future identification of biomarkers and therapeutic targets.

Indexed as

Polymorphism, Single NucleotideAdultAgedAged, 80 and overCarcinoma, Adenoid CysticCarcinoma, DuctalCarcinoma, MucoepidermoidChromosome MappingComparative Genomic HybridizationDNA Copy Number VariationsFemaleGenome-Wide Association StudyHumansMaleMiddle AgedNeoplasm Grading

Identifiers

PMID23583282
PMCPMC3668022
OpenAlexW2106354574

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.