K-ras mutations in gastric stump carcinomas and in carcinomas from the non-operated stomach.
OBJECTIVE
Partial gastrectomy is a well-established pre-malignant condition. It is postulated that in the gastric stump an accelerated neoplastic process takes place, similar to that of (intestinal type) adenocarcinoma from the non-operated stomach. K-ras codon 12 mutation is one of the most frequent oncogenic alterations in human solid neoplasms. It is rare in conventional gastric carcinoma and has not been studied in gastric stump carcinoma. The aim of this study was to compare the prevalence of K-ras codon 12 point mutations in gastric stump carcinomas with those in conventional carcinomas from the non-operated stomach.


METHODS
Twenty-four gastric stump carcinomas were compared with 26 conventional gastric carcinomas. Stage, histology, and demographics were comparable in both groups. Mutations in codon 12 of the K-ras gene were examined with a polymerase chain reaction (PCR)-based method and subsequent dot blot hybridization with mutation-specific probes. The results of Helicobacter pylori infection, Epstein-Barr virus infection and p53 immunohistochemistry were partially known from a previous study.


RESULTS
In one of the gastric stump carcinomas as well as in one of the conventional gastric carcinomas a K-ras codon 12 point mutation was found. p53 immunohistochemistry results were comparable in both groups. Interestingly, Helicobacter pylori infection rate and Epstein-Barr virus in situ hybridization for EBER1, as previously studied, appeared were significantly different in the two groups.


CONCLUSIONS
K-ras codon 12 point mutations are rare in both gastric stump carcinomas and conventional gastric carcinomas. This supports the postulated hypothesis that the pathways of carcinogenesis in both gastric stump carcinoma and conventional gastric carcinoma share common features. However, these groups differ in infection rate of Helicobacter pylori and of Epstein-Barr virus, which suggests that some neoplastic stimuli differ as well.
van Rees
B P
BP
Department of Pathology, Academic Medical Center, University of Amsterdam, The Netherlands. b.p.vanrees@amc.uva.nl
Musler
A
A
Caspers
E
E
Drillenburg
P
P
Craanen
M E
ME
Polkowski
W
W
Chibowski
D
D
Offerhaus
G J
GJ
D000368:Aged; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000473:pathology; D005260:Female; D018530:Gastric Stump / Q000473:pathology*; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D016481:Helicobacter Infections / Q000235:genetics / Q000473:pathology; D016480:Helicobacter pylori / Q000235:genetics; D006801:Humans; D008297:Male; D017354:Point Mutation / Q000235:genetics*; D016133:Polymerase Chain Reaction; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics*; D012367:RNA, Viral / Q000235:genetics; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics
C099537:Epstein-Barr virus encoded RNA 1; D012367:RNA, Viral; D016159:Tumor Suppressor Protein p53; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras)