Evidence map›Paper›PMID 19670330›Full record

ArticleInternational journal of cancer2009

Chromosomal abnormalities and novel disease-related regions in progression from Barrett's esophagus to esophageal adenocarcinoma.

Tadayuki Akagi, Tetsuo Ito, Motohiro Kato, Zhe Jin, Yulan Cheng, Takatsugu Kan, Go Yamamoto, Alexandru Olaru, Norihiko Kawamata, Jessica Boult and 5 more

Abstract read
In one paragraph

Article in International journal of cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  10. Molecular epigenomic subtypes of Barrett neoplasia.Nature reviews. Gastroenterology & hepatology · 2020
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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

15 authors at 4 institutions in 2 countries.

Tadayuki AkagiDivision of Hematology and Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA, USA. tadayuki@staff.kanazawa-u.ac.jp
Tetsuo Ito
Motohiro Kato
Zhe Jin
Yulan Cheng
Takatsugu Kan
Go Yamamoto
Alexandru Olaru
Norihiko Kawamata
Jessica Boult
Harmik J Soukiasian
Carl W Miller
Seishi Ogawa
Stephen J Meltzer
H Phillip Koeffler
Cedars-Sinai Medical Center · USJohns Hopkins Medicine · USJohns Hopkins University · USThe University of Tokyo · JP

Funding

INTEGRATED DEVELOPMENT OF NOVEL MOLECULAR MARKERSU01CA084986 · NCI · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 1999 to 2014
$33.8M
Comprehensive Biomarker Development in early EsophagogasU01CA085069 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI MELTZER, STEPHEN J · 1999 to 2009
$4.8M
Genomics: Esophageal Metaplasia-Associated MalignancyR01CA001808 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI MELTZER, STEPHEN J · 2002 to 2006
$1.9M
The temporal epigenomic program of Barrett's neoplastic progressionR01DK087454 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI MELTZER, STEPHEN J · 2009 to 2013
$1.8M
Validation studies of circulating methylation biomarkersR21CA106763 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI MELTZER, STEPHEN J · 2005 to 2005
$129k
NCI NIH HHS CA01808NCI NIH HHS CA106763NCI NIH HHS CA 84986NCI NIH HHS CA85069NCI NIH HHS R01 CA001808NCI NIH HHS R21 CA106763NCI NIH HHS U01 CA084986NCI NIH HHS U01 CA085069NIDDK NIH HHS R01 DK087454
6 · The paper itself

Abstract

Barrett's esophagus (BE) is a metaplastic condition caused by chronic gastroesophageal reflux which represents an early step in the development of esophageal adenocarcinoma (EAC). Single-nucleotide polymorphism microarray (SNP-chip) analysis is a novel, precise, high-throughput approach to examine genomic alterations in neoplasia. Using 250K SNP-chips, we examined the neoplastic progression of BE to EAC, studying 11 matched sample sets: 6 sets of normal esophagus (NE), BE and EAC, 4 of NE and BE and 1 of NE and EAC. Six (60%) of 10 total BE samples and 4 (57%) of 7 total EAC samples exhibited 1 or more genomic abnormalities comprising deletions, duplications, amplifications and copy-number-neutral loss of heterozygosity (CNN-LOH). Several shared abnormalities were identified, including chromosome 9p CNN-LOH [2 BE samples (20%)], deletion of CDKN2A [4 BE samples (40%)] and amplification of 17q12-21.2 involving the ERBB2, RARA and TOP2A genes [3.1 Mb, 2 EAC (29%)]. Interestingly, 1 BE sample contained a homozygous deletion spanning 9p22.3-p22.2 (1.2 Mb): this region harbors only 1 known gene, basonuclin 2 (BNC2). Real-time PCR analysis confirmed the deletion of this gene and decreased the expression of BNC2 mRNA in the BE sample. Furthermore, transfection and stable expression of BNC2 caused growth arrest of OE33 EAC cells, suggesting that BNC2 functions as a tumor suppressor gene in the esophagus and that deletion of this gene occurs during the development of EAC. Thus, this SNP-chip analysis has identified several early cytogenetic events and novel candidate cancer-related genes that are potentially involved in the evolution of BE to EAC.

Indexed as

Chromosome AberrationsOligonucleotide Array Sequence AnalysisAdenocarcinomaAgedAged, 80 and overBarrett EsophagusBiomarkers, TumorBlotting, WesternDisease ProgressionDNA-Binding ProteinsEsophageal NeoplasmsEsophagusFemaleGene DosageGene Expression ProfilingGenome, HumanBiomarkers, TumorBNC2 protein, humanDNA-Binding ProteinsRNA, Messenger

Identifiers

PMID19670330
PMCPMC2766567
OpenAlexW1965001189

What OpenQuestion holds

Textmetadata
LicenceTDM
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.