Evidence map›Paper›PMID 15140403›Full record

ArticleNeoplasia (New York, N.Y.)

Clustering of molecular alterations in gastroesophageal carcinomas.

Natalie Koon, Alexander Zaika, Christopher A Moskaluk, Henry F Frierson, Sakari Knuutila, Steven M Powell, Wa'el El-Rifai

Open access · goldAbstract readComparative Study
In one paragraph

Article in Neoplasia (New York, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Prognostic impact of S100A9 overexpression in non-small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Chromosome 6p amplification and cancer progression.Journal of clinical pathology · 2007
    Review
  16. Review
  17. Article
  18. Review
  19. Article
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 4 institutions in 3 countries.

Natalie KoonDigestive Health Center of Excellence, University of Virginia Health System, Charlottesville, VA 22908-0708, USA.
Alexander Zaika
Christopher A Moskaluk
Henry F Frierson
Sakari Knuutila
Steven M Powell
Wa'el El-Rifai
University of Virginia · USUniversity of Virginia Health System · USDigestive Health Research Institute · FRUniversity of Helsinki · FI

Funding

Molecular Pathobiology of Barrett's TumorigenesisR01CA106176 · NCI · VANDERBILT UNIVERSITY · PI EL-RIFAI, WAEL · 2003 to 2014
$3.3M
NCI NIH HHS 1 R01 CA106176NCI NIH HHS R01 CA106176
6 · The paper itself

Abstract

Gene expression levels are regulated at many levels. Integration of genome-wide analyses for the study of DNA and RNA provides a unique tool to detect genetic alterations in the cancer genome. In this study, we generated and integrated DNA amplification data from comparative genomic hybridization (CGH) and serial analyses of gene expression (SAGE) in order to obtain a molecular profile of gastroesophageal junction (GEJ) carcinomas. DNA amplifications mapped to specific chromosomal regions and were frequently seen at 1q, 4q, 5q, 6p, 7p, 8q, 17q, and 20q. Using SAGE, we obtained over 156,432 tags from GEJ adenocarcinomas and normal gastric mucosa. These tags were assigned to UniGene clusters. Chromosomal positions for overexpressed genes were obtained to produce a GEJ carcinoma transcriptome map. A total of 123 genes was significantly overexpressed (more than fivefold; P <.01) in one or more SAGE libraries. This gene overexpression map was integrated and compared to the chromosomal CGH ideogram. Several chromosomal arms that had frequent DNA amplifications showed frequent gene expression alterations such as chromosomes 1 (15 genes), 2 (9 genes), 6 (6 genes), 11 (6 genes), 12 (8 genes), and 17 (13 genes). Despite the relatively large DNA amplification regions, overexpressed genes frequently mapped and clustered to small chromosomal regions at early-replicating (Giemsa light) bands such as 1q21.3 (nine genes), 6p21.3 (five genes), and 17q21 (eight genes). These results provide a comprehensive tool to search for DNA amplifications and overexpressed genes in GEJ carcinoma. The observed phenomenon of the presence of large amplification areas, yet clustering of overexpressed genes to relatively small loci, may suggest a high organization of chromatin and cancer-related genes in the nucleus.

Indexed as

Gene ExpressionGenome, HumanAdenocarcinomaChromosomes, HumanEsophageal NeoplasmsGastric MucosaGene AmplificationGene Expression ProfilingGene SilencingHumansMultigene FamilyNucleic Acid HybridizationReverse Transcriptase Polymerase Chain ReactionRNA, MessengerStomach NeoplasmsRNA, Messenger

Identifiers

PMID15140403
PMCPMC1502088
OpenAlexW1997048855

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.