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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Eukaryotic Gene Expression
Импакт фактор: 1.841 5-летний Импакт фактор: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Печать: 1045-4403
ISSN Онлайн: 2162-6502

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Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v21.i3.20
pages 237-254

Alterations in Cell Proliferation Related Gene Expressions in Gastric Cancer

Kyungtae Kim
Research Institute, National Cancer Center, Republic of Korea
Kyung-Hee Chun
Research Institute, National Cancer Center, Republic of Korea
Pann-Ghill Suh
Biosignal Network Laboratory, Ulsan National Institute of Science and Technology, Republic of Korea
In-Hoo Kim
National Cancer Center

Краткое описание

Gastric cancer remains the fourth most prevalent cancer and the second leading cause of cancer-related death in the world. The predominant form of gastric cancer is adenocarcinoma, which originates from glandular epithelium of the gastric mucosa. The major risk factors for gastric cancer include diet, individual genetic variation, and, most importantly, infection with Helicobacter pylori (H. pylori). Certain strains of H. pylori assisted by some of its virulence factors seem to play a critical role in gastric cancer development. Several of these H. pylori virulence factors, which influence cellular proliferation signaling, have been identified. In addition, changes in the expression of several cell proliferation regulating genes accompany or cause the progression of gastric cancer. These changes include modifications of cell cycle regulators, oncogene activation, tumor suppressor inactivation, and miRNA profile alterations. Many of these changes result from H. pylori infection, although their impact on the cellular proliferation system underlying gastric cancer development has not yet been fully elucidated. We review certain features of gastric cancer, the role of H. pylori infection in its etiology and pathogenesis, and gene expression changes during gastric carcinogenesis.