共 143 条
Helicobacter pylori: gastric cancer and beyond
被引:852
作者:

Polk, D. Brent
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机构:
Columbia Univ, Dept Pediat, New York, NY 10027 USA Vanderbilt Univ, Dept Med, Nashville, TN 37232 USA

Peek, Richard M., Jr.
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h-index: 0
机构:
Vanderbilt Univ, Dept Med, Nashville, TN 37232 USA
Vanderbilt Univ, Dept Canc Biol, Nashville, TN 37232 USA Vanderbilt Univ, Dept Med, Nashville, TN 37232 USA
机构:
[1] Vanderbilt Univ, Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Dept Canc Biol, Nashville, TN 37232 USA
[3] Columbia Univ, Dept Pediat, New York, NY 10027 USA
关键词:
EPIDERMAL-GROWTH-FACTOR;
ULCER-PROMOTING GENE;
EGF RECEPTOR TRANSACTIVATION;
CAG PATHOGENICITY ISLAND;
COMPLETE GENOME SEQUENCE;
NECROSIS-FACTOR-ALPHA;
BLOOD-GROUP ANTIGENS;
BETA-CATENIN SIGNAL;
NF-KAPPA-B;
EPITHELIAL-CELLS;
D O I:
10.1038/nrc2857
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Helicobacter pylori is the dominant species of the human gastric microbiome, and colonization causes a persistent inflammatory response. H. pylori-induced gastritis is the strongest singular risk factor for cancers of the stomach; however, only a small proportion of infected individuals develop malignancy. Carcinogenic risk is modified by strain-specific bacterial components, host responses and/or specific host-microbe interactions. Delineation of bacterial and host mediators that augment gastric cancer risk has profound ramifications for both physicians and biomedical researchers as such findings will not only focus the prevention approaches that target H. pylori-infected human populations at increased risk for stomach cancer but will also provide mechanistic insights into inflammatory carcinomas that develop beyond the gastric niche.
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页码:403 / 414
页数:12
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