Evidence map›Paper›PMID 24203761›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2014

Identification of putative target genes for amplification within 11q13.2 and 3q27.1 in esophageal squamous cell carcinoma.

Z-Z Shi, Y-Y Jiang, J-J Hao, Y Zhang, T-T Zhang, L Shang, S-G Liu, F Shi, M-R Wang

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Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

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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

20 citing papers in PubMed, 70 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Z-Z ShiFaculty of Medicine, Kunming University of Science and Technology, Kunming, China.
Y-Y Jiang
J-J Hao
Y Zhang
T-T Zhang
L Shang
S-G Liu
F Shi
M-R Wang
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenomic aberration is a common feature of human cancers and also is one of the basic mechanisms that lead to overexpression of oncogenes and underexpression of tumor suppressor genes. Our study aims to identify frequent genomic changes and candidate copy number driving genes in esophageal squamous cell carcinoma (ESCC).

methodsWe used array comparative genomic hybridization to identify recurrent genomic alterations and screened the candidate targets of selected amplification regions by quantitative and semi-quantitative RT-PCR.

resultsThirty-four gains and 16 losses occurred in more than 50 % of ESCCs. High-level amplifications at 7p11.2, 8p12, 8q24.21, 11q13.2-q13.3, 12p11.21, 12q12 and homozygous deletions at 2q22.1, 8p23.1-p21.2, 9p21.3 and 14q11.2 were also identified. 11q13.2 was a frequent amplification region, in which five genes including CHKA, GAL, KIAA1394, LRP5 and PTPRCAP were overexpressed in tumor tissues than paracancerous normal tissues. The expression of ALG3 at 3q27.1 was higher in ESCCs, especially in patients with lymph node metastasis.

conclusionsTarget gene identification of amplifications or homozygous deletions will help to reveal the mechanism of tumor formation and explore new therapy method.

Indexed as

Gene AmplificationAdultAgedAged, 80 and overCarcinoma, Squamous CellChromosome AberrationsChromosomes, Human, Pair 11Chromosomes, Human, Pair 3Comparative Genomic HybridizationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleGene DosageGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, Fluorescence

Identifiers

PMID24203761
OpenAlexW1982478212

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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.