Evidence map›Paper›PMID 17908304›Full record

ArticleBMC genomics2007

DNA copy number profiles of gastric cancer precursor lesions.

Tineke E Buffart, Beatriz Carvalho, Thomas Mons, Rui M Reis, Cátia Moutinho, Paula Silva, Nicole C T van Grieken, Michael Vieth, Manfred Stolte, Cornelis J H van de Velde and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Use of DNA flow cytometry in the diagnosis, risk stratification, and management of gastric epithelial dysplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Genetic aspects of gastric cancer instability.TheScientificWorldJournal · 2012
    Review
  10. Review
  11. Article
  12. 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

15 authors at 7 institutions in 3 countries.

Tineke E BuffartDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. t.buffart@vumc.nl
Beatriz Carvalho
Thomas Mons
Rui M Reis
Cátia Moutinho
Paula Silva
Nicole C T van Grieken
Michael Vieth
Manfred Stolte
Cornelis J H van de Velde
Evelin Schrock
Anja Matthaei
Bauke Ylstra
Fátima Carneiro
Gerrit A Meijer
Amsterdam UMC Location VUmc · NLUniversidade do Porto · PTBayreuth Medical Center · DETU Dresden · DEHospital de São João · PTLeiden University Medical Center · NLUniversity of Minho · PT

Funding

Wellcome Trust
6 · The paper itself

Abstract

backgroundChromosomal instability (CIN) is the most prevalent type of genomic instability in gastric tumours, but its role in malignant transformation of the gastric mucosa is still obscure. In the present study, we set out to study whether two morphologically distinct categories of gastric cancer precursor lesions, i.e. intestinal-type and pyloric gland adenomas, would carry different patterns of DNA copy number changes, possibly reflecting distinct genetic pathways of gastric carcinogenesis in these two adenoma types.

resultsUsing a 5K BAC array CGH platform, we showed that the most common aberrations shared by the 11 intestinal-type and 10 pyloric gland adenomas were gains of chromosomes 9 (29%), 11q (29%) and 20 (33%), and losses of chromosomes 13q (48%), 6(48%), 5(43%) and 10 (33%). The most frequent aberrations in intestinal-type gastric adenoma were gains on 11q, 9q and 8, and losses on chromosomes 5q, 6, 10 and 13, whereas in pyloric gland gastric adenomas these were gains on chromosome 20 and losses on 5q and 6. However, no significant differences were observed between the two adenoma types.

conclusionThe results suggest that gains on chromosomes 8, 9q, 11q and 20, and losses on chromosomes 5q, 6, 10 and 13, likely represent early events in gastric carcinogenesis. The phenotypical entities, intestinal-type and pyloric gland adenomas, however, do not differ significantly (P = 0.8) at the level of DNA copy number changes.

Indexed as

Chromosomes, Artificial, BacterialDNA, NeoplasmGenomic InstabilityHumansPrecancerous ConditionsStomach NeoplasmsDNA, Neoplasm

Identifiers

PMID17908304
PMCPMC2147033
OpenAlexW2009684371

What OpenQuestion holds

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LicenceCC BY
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.