PMID- 15827559
OWN - NLM
STAT- MEDLINE
DCOM- 20050609
LR  - 20240404
IS  - 0007-0920 (Print)
IS  - 1532-1827 (Electronic)
IS  - 0007-0920 (Linking)
VI  - 92
IP  - 9
DP  - 2005 May 9
TI  - Fluorescence in situ hybridisation analysis of chromosomal aberrations in gastric 
      tissue: the potential involvement of Helicobacter pylori.
PG  - 1759-66
AB  - In this series of experiments, a novel protocol was developed whereby gastric 
      cells were collected using endoscopic cytology brush techniques, and prepared, 
      such that interphase fluorescence in situ hybridization (FISH) could be 
      performed. In total, 80 distinct histological samples from 37 patients were 
      studied using four chromosome probes (over 32,000 cells analysed). Studies have 
      previously identified abnormalities of these four chromosomes in upper GI 
      tumours. Using premalignant tissues, we aimed to determine how early in Correa's 
      pathway to gastric cancer these chromosome abnormalities occurred. Aneuploidy of 
      chromosomes 4, 8, 20 and 17(p53) was detected in histologically normal gastric 
      mucosa, as well as in gastritis, intestinal metaplasia, dysplasia and cancer 
      samples. The levels of aneuploidy increased as disease severity increased. 
      Amplification of chromosome 4 and chromosome 20, and deletion of chromosome 
      17(p53) were the more common findings. Hence, a role for these abnormalities may 
      exist in the initiation of, and the progression to, gastric cancer. Helicobacter 
      pylori infection was determined in premalignant tissue using histological 
      analysis and PCR technology. Detection rates were comparable. PCR was used to 
      subtype H. pylori for CagA status. The amplification of chromosome 4 in gastric 
      tissue was significantly more prevalent in H. pylori-positive patients (n=7) 
      compared to H. pylori-negative patients (n=11), possibly reflecting a role for 
      chromosome 4 amplification in H. pylori-induced gastric cancer. The more virulent 
      CagA strain of H. pylori was associated with increased disease pathology and 
      chromosomal abnormalities, although numbers were small (CagA+ n=3, CagA- n=4). 
      Finally, in vitro work demonstrated that the aneuploidy induced in a human cell 
      line after exposure to the reactive oxygen species (ROS) hydrogen peroxide was 
      similar to that already shown in the gastric cancer pathway, and may further 
      strengthen the hypothesis that H. pylori causes gastric cancer progression via an 
      ROS-mediated mechanism.
FAU - Williams, L
AU  - Williams L
AD  - Neath Port Talbot Hospital, Baglan, UK. lwill@doctors.org.uk
FAU - Jenkins, G J S
AU  - Jenkins GJ
FAU - Doak, S H
AU  - Doak SH
FAU - Fowler, P
AU  - Fowler P
FAU - Parry, E M
AU  - Parry EM
FAU - Brown, T H
AU  - Brown TH
FAU - Griffiths, A P
AU  - Griffiths AP
FAU - Williams, J G
AU  - Williams JG
FAU - Parry, J M
AU  - Parry JM
LA  - eng
PT  - Journal Article
PL  - England
TA  - Br J Cancer
JT  - British journal of cancer
JID - 0370635
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
SB  - IM
MH  - Aged
MH  - *Aneuploidy
MH  - Cell Line
MH  - Chromosome Aberrations
MH  - Chromosomes, Human, Pair 17
MH  - Chromosomes, Human, Pair 4
MH  - Female
MH  - Gastric Mucosa/metabolism/microbiology
MH  - Gastritis/genetics
MH  - Helicobacter Infections/complications/*genetics
MH  - *Helicobacter pylori/metabolism
MH  - Humans
MH  - Hydrogen Peroxide/pharmacology
MH  - In Situ Hybridization
MH  - Male
MH  - Metaplasia/genetics
MH  - Precancerous Conditions/genetics/metabolism/microbiology
MH  - Reactive Oxygen Species
MH  - Stomach Neoplasms/*genetics/metabolism/microbiology
PMC - PMC2362026
EDAT- 2005/04/14 09:00
MHDA- 2005/06/10 09:00
PMCR- 2006/05/09
CRDT- 2005/04/14 09:00
PHST- 2005/04/14 09:00 [pubmed]
PHST- 2005/06/10 09:00 [medline]
PHST- 2005/04/14 09:00 [entrez]
PHST- 2006/05/09 00:00 [pmc-release]
AID - 6602533 [pii]
AID - 10.1038/sj.bjc.6602533 [doi]
PST - ppublish
SO  - Br J Cancer. 2005 May 9;92(9):1759-66. doi: 10.1038/sj.bjc.6602533.