| Popis: |
The Gram-negative (−) bacterium Helicobacter pylori colonizes in the mucus gel layer above the gastric epithelium and has been considered to be a major etiologic factor in several gastric health complications including peptic ulcers, gastric MALT, gastritis, and gastric cancer in approximately 50% of the world’s population. Besides inducing colon carcinogenesis, the bacterium shows to be associated with different extragastric disorders. Eradication of H. pylori is reported to reduce 33–47% of gastric cancer; however, treatment of H. pylori against colon cancer is less effective in older people. Several targets of H. pylori to induce colorectal carcinogenesis have been hypothesized, and an association of gastric H. pylori with colorectal adenomatous polyps (CAPs) has been experimentally revealed. CAPs are precancerous lesions of epithelial cells and lead to colorectal cancer (CRC) from the adenomatous stage. Pathway analysis decrypts the cascade mechanism of CAPs via inducing matrix metalloproteinase (MMP), prostaglandin-endoperoxide synthase, and mucin with other molecular targets. Several therapeutic approaches have been established to eradicate H. pylori before inoculation and during histologic progression in early stages. This book chapter explains the impact and molecular mechanism of H. pylori in colon carcinogenesis and methods of therapeutic approaches. |
