The relationship between gastric cancer and Helicobacter pylori cytotoxin-related gene A genotypes.

Gastric cancer has been known as the third leading cause of cancer-related death in the world. It is when cancer cells form on the lining of the stomach. Early symptoms include heartburn, upper abdominal pain, nausea, and loss of appetite. Helicobacter pylori is the most common microscopic creature that has infected humans worldwide. More than half of the world's population is infected with the bacterium. It is the main cause of diseases such as stomach ulcers and stomach and intestinal disorders. H. pylori infection is related to gastric adenocarcinoma and cagA genotype is believed to be related to cancer development. cytotoxin-associated gene A (CagA) is a 120-145kDa protein encoded on the 40kb cag pathogenicity island (PAI). This study investigates the association between cagA H. pylori genotypes and gastric cancer. For this purpose, 65 stomach biopsies of the gastric cancer patients and 100 saliva samples were collected from healthy and H. pylori-infected individuals. Then genomic DNA was purified and Polymerase Chain Reaction (PCR) was performed for the studied gene using specific primers. The presence of H. pylori was investigated by PCR and a pair of specific primers for a protected region in the bacterium glmM gene. Then cagA+ and cagA- genotypes frequencies were determined in H. pylori-infected cases. Statistical analysis showed that there were significant differences between healthy and diseased ones for genotypes cagA+ and cagA-. Then the cagA+ can be a risk factor genotype for gastric cancer.

[Role of CD44(+)/ESA(+) in sorting colonic cancer stem cells].

OBJECTIVE: To isolate CD133(+)/CD44(+)/ESA(+) subsets cells from SW480 colon cancer cells, and to observe the tumor formation. METHOD: CD133(+)/CD44(+)/ESA(+) subsets cells, CD133(-)/CD44(+)/ESA(+) subsets cells and CD133(-)/CD44(-)/ESA(-) subsets cell were sorted by flow cytometry from SW480 colon cancer cells, then three subsets were separately inoculated in five NOD/SCID mice and the growth rates were calculated. RESULT: The proportion of CD133(-)/CD44(-)/ESA(-), CD133(-)/CD44(+)/ESA(+) and CD133(+)/CD44(+)/ESA(+) subsets cells in SW480 cells were (86.38±10.23)%,(1.26±0.28)% and(0.38±0.07)%. After inoculation, tumor nodules could be formed three days later in CD133(+)/CD44(+)/ESA(+) group, and they could be formed 9 days later in CD133(-)/CD44(+)/ESA(+) group, while they could be formed 15 days later in CD133(-)/CD44(-)/ESA(-) group. Eighteen days later, tumor sizes in three groups were(13.82±5.04) mm(3), (9.25±4.57) mm(3) and (4.76±3.92) mm(3) respectively, and the differences were statistically significant(P<0.05). CONCLUSION: ESA(+)-CD44(+) is one of the surface markers for colonic cancer stem cells, and CD133(+)-CD44(+)-ESA(+) cells are SW480-like cancer stem cells.