PMID- 11535550
OWN - NLM
STAT- MEDLINE
DCOM- 20011025
LR  - 20231213
IS  - 1055-9965 (Print)
IS  - 1055-9965 (Linking)
VI  - 10
IP  - 9
DP  - 2001 Sep
TI  - Polymorphisms of two fucosyltransferase genes (Lewis and Secretor genes) 
      involving type I Lewis antigens are associated with the presence of 
      anti-Helicobacter pylori IgG antibody.
PG  - 971-7
AB  - Helicobacter pylori attach to the gastric mucosa with adhesin, which binds to 
      Lewis b (Le(b)) or H type I carbohydrate structures. The Secretor (Se) gene and 
      Lewis (Le) gene are involved in type I Le antigen synthesis. The present study 
      was performed to investigate the possibility that Se and Le gene polymorphisms 
      alter the risk of H. pylori infection. Two hundred thirty-nine participants were 
      genotyped for Se and Le and tested for the presence of anti-H. pylori IgG 
      antibodies. Using the normal gastric mucosa from 60 gastric cancer patients, we 
      assessed immunohistochemically whether type I Le antigen expression depended on 
      the Se and Le genotypes. The H. pylori infection rate was positively associated 
      with the number of Se alleles (se/se group, 45.1%; Se/se group, 64.6%; and Se/Se 
      group, 73.3%) and negatively associated with the number of Le alleles (le/le 
      group, 76.4%; Le/le group, 68.3%; and Le/Le group, 55.6%). When the subjects were 
      classified into three groups [low risk, (se/se, Le/Le) genotype; high risk, 
      (Se/Se, le/le), (Se/Se, Le/le), and (Se/se, le/le) genotypes; moderate risk, 
      other than low- or high-risk group], the odds ratio relative to the low-risk 
      group was 3.30 (95% confidence interval, 1.40-7.78) for the moderate-risk group 
      and 10.33 (95% confidence interval, 3.16-33.8) for the high-risk group. 
      Immunohistochemical analysis supported the finding that Se and Le genotypes 
      affected the expression of H. pylori adhesin ligands. We conclude that Se and Le 
      genotypes affect susceptibility to H. pylori infection.
FAU - Ikehara, Y
AU  - Ikehara Y
AD  - Division of Oncological Pathology, Aichi Cancer Center Research Institute, Nagoya 
      464-8681, Japan. yikehara@aichi.cc.pref.aichi.jp
FAU - Nishihara, S
AU  - Nishihara S
FAU - Yasutomi, H
AU  - Yasutomi H
FAU - Kitamura, T
AU  - Kitamura T
FAU - Matsuo, K
AU  - Matsuo K
FAU - Shimizu, N
AU  - Shimizu N
FAU - Inada, K
AU  - Inada K
FAU - Kodera, Y
AU  - Kodera Y
FAU - Yamamura, Y
AU  - Yamamura Y
FAU - Narimatsu, H
AU  - Narimatsu H
FAU - Hamajima, N
AU  - Hamajima N
FAU - Tatematsu, M
AU  - Tatematsu M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Epidemiol Biomarkers Prev
JT  - Cancer epidemiology, biomarkers & prevention : a publication of the American 
      Association for Cancer Research, cosponsored by the American Society of 
      Preventive Oncology
JID - 9200608
RN  - 0 (Antibodies, Bacterial)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Lewis Blood Group Antigens)
RN  - 0 (Lewis X Antigen)
RN  - 0 (Lewis Y antigen)
RN  - EC 2.4.1.- (Fucosyltransferases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Bacterial/blood
MH  - Asian People/genetics
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Fucosyltransferases/*genetics
MH  - Gastric Mucosa/microbiology
MH  - Genotype
MH  - Helicobacter Infections/complications/epidemiology/*immunology
MH  - Helicobacter pylori/*immunology
MH  - Humans
MH  - Immunoglobulin G/*blood
MH  - Immunohistochemistry
MH  - Japan/epidemiology
MH  - Lewis Blood Group Antigens
MH  - Lewis X Antigen/*blood
MH  - Male
MH  - Middle Aged
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Genetic
MH  - Polymorphism, Restriction Fragment Length
MH  - Prevalence
MH  - Risk Factors
MH  - Stomach Neoplasms/etiology/genetics
MH  - Galactoside 2-alpha-L-fucosyltransferase
EDAT- 2001/09/06 10:00
MHDA- 2001/10/26 10:01
CRDT- 2001/09/06 10:00
PHST- 2001/09/06 10:00 [pubmed]
PHST- 2001/10/26 10:01 [medline]
PHST- 2001/09/06 10:00 [entrez]
PST - ppublish
SO  - Cancer Epidemiol Biomarkers Prev. 2001 Sep;10(9):971-7.