AIM: To investigate the microsatellite instability (MSI) in cancer and pre-cancerous lesions of the stomach and its mechanisms underlying the development of gastric cancer.METHODS: Thirty-six gastric cancer samples were obtained from patients undergoing surgery. Forty-one gastric mucosa samples with dysplasia and 51 with intestinal metaplasia (IM) were obtained from patients with chronic gastritis undergoing gastro-endoscopy. Genomic DNA was extracted from the samples. Silver staining single strand conformation polymorphis-polymerize chain reaction (SSCP-PCR) was used to screen MSI markers at 5 loci (Bat-25, Bat-26, D5S346, D17S250, and D2S123)in fresh tissues and formalin-fixed, paraffin-embedded samples and their corresponding normal gastric mucosa.RESULTS: The abnormal shifting of the single-strand DNA (MSI) was identified in 21 out of 36 (58.3%) gastric cancers.Seven cases showed high-level MSI (two or more loci altered) and 14 showed low-level MSI (one locus altered).Gastric cancer with MSI had a tendency to be located in the distal stomach. MSI was also detected in 11 out of 41(26.8%) dysplasia samples and in 9 of 51 (17.6%) IM samples respectively. Three cases of dysplasia and one case of IM showed high-level MSI. Eight cases of dysplasia and 8 cases of IM displayed low-level MSI. MIS in IM was found only in moderate or severe-grade IM. No association was detected between MSI and dysplasia grade.CONCLUSION: Accumulation of MSI in dysplasia and intestinal metaplasia of gastric mucosa may be an early molecular event during gastric carcinogenesis and may contribute to the acquisition of transformed cell phenotype and the development of gastric cancer.
AIM To study the therapeutical effectiveness, dosage range and toxic adverse effects of domestic phosphorus 32 glass microsphere and evaluate its clinical significance. METHODS Ⅰ. Fifty two BALB/*!c tumor bearing male nude mice were allocated into treatment group( n =38) and control group( n =14). In the former group different doses of 32 P GMS were injected into the tumor mass, while in the latter 31 P GMS or no treatment was given. The experimental animals were sacrificed in batches, and then the tumors and their nearby tissues were examined by light and electron microscopy. Ⅱ. Through selective catheterization of hepatic artery, 32 P GMS was infused to 5 healthy domestic pigs in a dosage equivalent to the therapeutic dose for human being, and 31 P GMS was infused to another 5 healthy domestic pigs. Two pigs infused with contrast medium served as whole course blank controls. One pig from each group was surrendered to euthanasia at week 1, 4, 8 and 16 respectively. The ultrastructural histopath ological changes in liver tissues taken from different sites were evaluated semiquan titatively. Ⅲ. One hundred and twenty seven times of 32 P GMS intrahepatic artery interventional therapies were performed on 93 patients with hepatic carcinoma, including 79 cases of primary hepatic carcinoma and 14 cases of secondary hepatic carcinoma. 32 P GMS ( n =30), and group B, 32 P GMS and half dose of trans hepatic artery embolization (TAE) ( n =49) , and 18 patients with HCC by TAE only as control group C. Fourteen patients with secondary hepatic carcinoma were treated in the same way as group B or C. RESULTS Ⅰ. Comparing with the control group, the treatment group of tumor bearing nude mice attained the tumor inhibition rates of 59 7%-93 7% ( F =579 62, P <0 01) at 14*!d . At an absorbed dose of 7320Gy, the tumor cells were completely destroyed. When the absorbed doses ranged from 1830Gy to 3660Gy, most of the tumor cells showed the evidences of injury or necrosis, but there appeared some well differentiated tumor cells
LIU Lu, JIANG Zao, TENG Gao Jun, SONG Ji Zhi, ZHANG Dong Sheng, GUO Qing Ming, FANG Wen, HE Shi Cheng and GUO Jin He
