PIK3CA gene mutations in Northwest Chinese esophageal squamous cell carcinoma.

AIM: To evaluate PIK3CA gene mutational status in Northwest Chinese esophageal squamous cell carcinoma (ESCC) patients, and examine the associations of PIK3CA gene mutations with clinicopathological characteristics and clinical outcome. METHODS: A total of 210 patients with ESCC who underwent curative resection were enrolled in this study. Pyrosequencing was applied to investigate mutations in exons 9 and 20 of PIK3CA gene in 210 Northwest Chinese ESCCs. The associations of PIK3CA gene mutations with clinicopathological characteristics and clinical outcome were examined. RESULTS: PIK3CA gene mutations in exon 9 were detected in 48 cases (22.9%) of a non-biased database of 210 curatively resected Northwest Chinese ESCCs. PIK3CA gene mutations were not associated with sex, tobacco use, alcohol use, tumor location, stage, or local recurrence. When compared with wild-type PIK3CA gene cases, patients with PIK3CA gene mutations in exons 9 experienced significantly better disease-free survival and overall survival rates. CONCLUSION: The results of this study suggest that PIK3CA gene mutations could act as a prognostic biomarker in Northwest Chinese ESCC patients.

The origin of blood supply for cavernous hemangioma of the liver.

OBJECTIVE: To investigate the origin of blood supply to cavernous hemangioma of the liver (CHL). METHODS: To observe the relation of cavernous hemangioma of the liver to the hepatic artery and portal vein, we performed serial selective hepatic arteriography in 22 patients. Five patients after ligation of the right hepatic arteries underwent portography and liver staining by injection of methylene blue into the portal veins and 2 patients had hepatic specimens resected, which were made into a model cast by filling the hepatic veins (yellow) and portal venous branches (blue) with methyl methacrylate after vascular lavage. RESULTS: Serial selective hepatic arteriography showed that hepatic arteries and hemangioma were displayed simultaneously, and that hemangioma was supplied by one to numerous arterial branches. In the portal phase of portography, contrast medium failed to enter the tumor and the intrahepatic branches of the portal vein were pushed aside by the tumor; in the liver parenchymal phase, however, the tumor appeared to be a low-density area. Hepatic arteriography and portography revealed that the fistula between the artery and portal vein may not be existed. The liver stained with methylene blue showed that the normal hepatic parenchyma could be stained with deep blue; in contrast, the tumor was not stained at all. The casting specimens showed that the eroded tumor left a round vacant area because of its total shedding, and no blue stained branches of the portal vein extended into the tumor. CONCLUSION: Blood supply of CHL may originate from the hepatic artery.

Relationships of uPA and VEGF expression in esophageal cancer and microvascular density with tumorous invasion and metastasis.

OBJECTIVE: To investigate uPA and VEGF expression in esophageal cancer and relations with tumorous invasion and metastasis. METHODS: Immunohistochemistry was used to detect uPA and VEGF expression in the normal epithelial tissue of esophageal mucosa and cancer tissue and detect CD34 labeled micrangium and analyze the relationships with clinical pathological features and tumor angiogenesis. RESULTS: Positive rates for uPA and VEGF protein expression were significantly greater in esophageal cancer than normal epithelial tissue (P < 0.05), the two being linked (P <0.05). In addition, uPA and VEGF protein expression of the high microvessel density (MVD) group was significantly lower than in the low MVD group (P < 0.05), with relation to clinical pathological staging, differentiation and lymph node metastasis (P < 0.05). CONCLUSION: In esophageal cancer tissue, uPA and VEGF proteins are overexpressed and promote tumor angiogenesis, indicative of a poor prognosis.

Synergism between a siRNA targeted to survivin and 5-FU in inhibiting MCF-7 cell proliferation in vitro.

OBJECTIVE: To investigate the role of small interfering RNA (siRNA) targeted to survivin in combination with 5-fluorouracil (5-FU) in inhibiting the proliferation of MCF-7 cells. METHODS: A siRNA targeted to survivin was synthesized and transfected into MCF-7 cells via lipofectin. Changes of the cell growth activity in response to combined treatment with survivin siRNA and 5-FU or 5-FU treatment alone was evaluated by MTT assay. The Q method of Jin Zhenjun was used to evaluated synergism between the synthesized siRNA and 5-FU. RESULTS: Treatment with 5 nmol/L siRNA reduced the IC50 of 5-FU from 4.42 to 1.18 microg/ml, and the inhibitory effect of combined treatment on MCF-7 cells was higher than that of 5-FU alone (F=26.74, P<0.01). Synergism effect was observed between 5-FU at lower concentrations and survivin siRNA. CONCLUSION: siRNA may enhance the effectiveness of 5-FU in inhibiting the proliferation of MCF-7 cells.

[Expression of survivin in different stages of carcinogenesis and progression of breast cancer].

BACKGROUND & OBJECTIVE: Survivin is one of the newly identified apoptosis inhibitor; it can block the cell apoptosis by inhibiting the function of the enzyme caspase-3 and caspase-7. Present studies indicate that survivin is overexpressed in malignant tumor. This current study was designed to investigate the effects of survivin in tumorigenesis and progression of breast carcinoma through observing the expression of survivin in the tissue of normal mammary, cystic hyperplasia mammary, atypical hyperplasia mammary and breast carcinoma. METHODS: The expression of survivin in the tissue of normal mammary (96 cases), cystic hyperplasia mammary (56 cases), atypical hyperplasia mammary (12 cases), and breast carcinoma (119 cases) were evaluated by SP immunohistochemistry. The relationship between survivin expression and the pathologically biological features of breast cancer was assessed. RESULTS: The positive rates of survivin were 4.2%(4/96),5.4% (3/56),42.7% (5/12), and 72.3%(86/119)in the tissue of normal mammary, cystic hyperplasia mammary, atypical hyperplasia mammary, and breast carcinoma, respectively. The positive rates in the last two groups were higher than those in the former two groups (P< 0.005). Survivin was more expressed in the infiltrative nonspecial breast carcinoma (82.0%, 73/89) than in the special and early stage infiltrative breast carcinoma (37.5%,3/8)(P< 0.05). Expression of survivin was correlated with lymph node metastasis although the difference is not significant (P >0.05). CONCLUSION: Overexpression of survivin is common in tumorigenesis and progression of breast carcinoma. Altered expression of survivin may contribute to tumorigenesis and progression of breast carcinoma by inhibiting cell apoptosis, its overexpression indicates worse prognosis.