K-ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction

Lord, Reginald V. N., O'Grady, Roslynn, Sheehan, Catherine, Field, Andrew F. and Ward, Robyn L. (2000) K-ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction. Journal of Gastroenterology and Hepatology (Australia), 15 7: 730-736. doi:10.1046/j.1440-1746.2000.02163.x


Author Lord, Reginald V. N.
O'Grady, Roslynn
Sheehan, Catherine
Field, Andrew F.
Ward, Robyn L.
Title K-ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction
Formatted title
K-ras codon 12 mutations in Barrett’s oesophagus and adenocarcinomas of the oesophagus and oesophagogastric junction
Journal name Journal of Gastroenterology and Hepatology (Australia)   Check publisher's open access policy
ISSN 0815-9319
1440-1746
Publication date 2000-07
Sub-type Article (original research)
DOI 10.1046/j.1440-1746.2000.02163.x
Open Access Status
Volume 15
Issue 7
Start page 730
End page 736
Total pages 7
Place of publication Richmond, VIC, Australia
Publisher Wiley-Blackwell Publishing Asia
Language eng
Formatted abstract
Background: Activation of the ras oncogene is commonly found in gastrointestinal tract cancers, but the role of ras in the development and progression of Barrett’s oesophagus and associated cancers is uncertain.
Methods: The frequency of K-ras codon 12 point mutations was assessed in 52 paraffin-embedded tissues from 44 patients with oesophageal pathology. The specimens were classified pathologically as follows: adenocarcinoma of the oesophagus or oesophagogastric junction (n = 23), Barrett’s high-grade dysplasia (n = 5), low-grade dysplasia (n = 14), intestinal metaplasia (n = 4), normal oesophagus (n = 5) or normal stomach (n = 1). DNA was extracted from three consecutive sections of each paraffin block and mutations at bases 1 and 2 of K-ras codon 12 were identified using a novel restriction endonuclease-mediated selective polymerase chain reaction method.
Results: Mutations were found in 7 of 23 (30.4%) adenocarcinomas and in 2 of 5 (40%) high-grade dysplasia specimens. No mutations were found in specimens of low-grade dysplasia, intestinal metaplasia without dysplasia, or normal oesophagus and stomach. There were no significant associations between the presence of mutations and clinicopathologic features in the patients with cancer. One patient who progressed from low-grade to high-grade dysplasia was found to have developed mutant K-ras in the course of this transformation.
Conclusion: These results suggest that K-ras codon 12 mutations may occur frequently in patients with Barrett’s oesophagus with high-grade dysplasia or adenocarcinoma of the oesophagus or oesophagogastric junction. K-ras mutation may be a late event in the Barrett’s metaplasia–dysplasia– adenocarcinoma sequence
Keyword Adenocarcinoma
Barrett's oesophagus
Dysplasia
High-grade dysplasia
K- ras
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Office of the Vice-Chancellor
 
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Created: Wed, 11 Feb 2015, 12:32:14 EST by Ms Kate Rowe on behalf of Office of Deputy Vice-Chancellor (Research)