Evidence map›Paper›PMID 14724583›Full record

ArticleOncogene2004

Mutations of BRAF and KRAS2 in the development of Barrett's adenocarcinoma.

Florian Sommerer, Michael Vieth, Annett Markwarth, Knut Röhrich, Susanne Vomschloss, Andrea May, Christian Ell, Manfred Stolte, Ulrich R Hengge, Christian Wittekind and 1 more

Abstract read
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In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Targeting the human EGFR family in esophagogastric cancer.Nature reviews. Clinical oncology · 2011
    Review
  14. Biology of Barrett's esophagus and esophageal adenocarcinoma.Gastrointestinal endoscopy clinics of North America · 2011
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Selective Raf inhibition in cancer therapy.Expert opinion on therapeutic targets · 2007
    Review
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

11 authors at 6 institutions in 1 country.

Florian SommererInstitute of Pathology, University of Leipzig, Liebigstrasse 26, Leipzig 04103, Germany.
Michael Vieth
Annett Markwarth
Knut Röhrich
Susanne Vomschloss
Andrea May
Christian Ell
Manfred Stolte
Ulrich R Hengge
Christian Wittekind
Andrea Tannapfel
Leipzig University · DEBayreuth Medical Center · DEHeinrich Heine University Düsseldorf · DEHelios Dr. Horst Schmidt Kliniken Wiesbaden · DEKliniken Schmieder · DEOtto-von-Guericke University Magdeburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the Raf/MEK/ERK (MAPK) signal transduction cascade by RAS mutations has been found in a variety of human cancers. Mutations of BRAF provide an alternative route for activation of this signalling pathway. To determine the role of mutations in BRAF and KRAS2 in the neoplastic progression of Barrett's adenocarcinoma, we analysed both genes for common mutations. After microdissection, DNA of 19 Barrett's adenocarcinomas, 56 Barrett's intraepithelial neoplasias (n=29 low-grade intraepithelial neoplasia (LGIN) and n=27 high-grade intraepithelial neoplasia (HGIN)), 30 Barrett's mucosa without neoplasia and normal squamous, as well as gastric epithelium, were analysed for BRAF and KRAS2 mutation. Activating BRAF mutations were identified in 2/19 Barrett's adenocarcinomas (11%) and in 1/27 HGIN (4%). KRAS2 mutations were found in four out of 19 (21%) Barrett's adenocarcinomas examined and in three cases of HGIN (11%). In LGIN as well as in normal gastric or oesophageal mucosa, neither BRAF nor KRAS2 mutations were detected. All lesions with KRAS2 mutations had an intact BRAF gene. The status of mismatch-repair proteins was neither related to BRAF nor KRAS2 mutations. These data indicate that RAS or BRAF mutations are detected in about 32% of all Barrett's adenocarcinomas. We conclude that the disruption of the Raf/MEK/ERK (MAPK) kinase pathway is a frequent but also early event in the development of Barrett's adenocarcinoma.

Indexed as

AdenocarcinomaBarrett EsophagusBase SequenceDNA Mutational AnalysisGenes, rasHumansImmunohistochemistryMitogen-Activated Protein KinasesMutationProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)ras ProteinsBRAF protein, humanKRAS protein, humanMitogen-Activated Protein KinasesProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID14724583
OpenAlexW1989743013

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.