Correlation of matrix metalloproteinase suppressor genes RECK, VEGF, and CD105 with angiogenesis and biological behavior in esophageal squamous cell carcinoma.

AIM: To explore the expression of reversion inducing cysteine-rich protein with Kazal motifs (RECK), vascular endothelial growth factor (VEGF) and endoglin (CD105) protein and its correlation with occurrence, development, invasion and metastasis in esophageal squamous cell carcinoma (ESCC). METHODS: Streptavidin-peroxidase (SP) immunohisto-chemistry was used to detect expression of RECK and VEGF in 62 cases of ESCC, 31 cases of adjacent atypical hyperplastic epithelium and 62 cases of normal esophageal epithelium. CD105 Mb was used to assess microvessel density (MVD). RESULTS: The expression of RECK was closely correlated with histological grade, infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK decreased during cancer development: normal esophageal epithelium (85.5%, 53/62), adjacent atypical hyperplastic epithelium (71.0%, 22/31), and carcinoma (59.7%, 37/62). There was a significant difference among the groups (P < 0.05). The expression of VEGF protein was closely correlated with infiltrative depth and lymphatic metastasis in ESCC (P < 0.05). The expression of VEGF protein increased during cancer development: normal esophageal epithelium (29.0%, 18/62), adjacent atypical hyperplastic epithelium (54.8%, 17/31), and carcinoma (67.7%, 42/62). There was a significant difference among the groups (P < 0.05). MVDCD105 increased in accordance with histological grade, but there was no significant difference (grade I, 36.92 +/- 10.85; grade II, 37.65 +/- 9.50; and grade III, 38.06 +/- 12.19). The MVDCD105 was closely correlated with infiltration and lymphatic metastasis in ESCC (P < 0.05). The expression of RECK was inversely correlated with the expression of VEGF and CD105. CONCLUSION: RECK, VEGF and CD105 play important roles in the infiltration, metastasis and carcinogenesis in esophageal carcinoma. Angiogenesis in ESCC may be promoted by over-expression of CD105.

High incidence of coding gene mutations in mitochondrial DNA in esophageal cancer.

The aim of the present study was to detect mutations in the coding genes of mitochondrial DNA (mtDNA) in three esophageal cancer cell lines and in tumor tissues obtained from 30 patients with esophageal cancer, to investigate the relationship between protein­ and RNA­coding gene mutations and esophageal cancer. mtDNA was extracted and the coding genes were sequenced and analyzed by comparing the sequencing results with the complete mitochondrial genome of Homo sapiens. The results revealed 39 mutations in the three esophageal cancer cell lines; the genes with the highest mutation frequencies included mitochondrially encoded cytochrome B (MT­CYTB), NADH dehydrogenase 5 (MT­ND5) and MT­ND4 gene. A total of 216 mutations were identified in the 30 esophageal cancer tissues, including 182 protein­coding mutations, of which MT­CYTB and MT­ND5 genes exhibited higher mutation frequencies. The results of the present study indicated that mutations in the coding genes of mtDNA in esophageal cancer cells may be related to the occurrence of esophageal cancer.

[Clinical study of irinotecan plus cisplatin for advanced non-small cell lung cancer].

OBJECTIVE: To evaluate the efficacy and adverse effects of irinotecan combined with cisplatin in the treatment of advanced non-small cell lung cancer (NSCLC). METHODS: Fifteen patients (10 males and 5 females) aged from 32 to 58 years (median age of 47 years) with KPS>70 and the diagnosis of advanced NSCLC by pathology or cytology were treated with cisplatin 80 mg/m(2) plus irinotecan 60 mg/m(2) by intravenous infusion on 1, 8, 15 days, and the treatment was repeated every 4 weeks. After treatment for at least 2 cycles, the therapeutic effects and adverse drug reactions were evaluated. RESULTS: Of all the cases, PR was achieved in 4 (26.7%), SD in 9 (60%), and PD in 2 (13.3%), with an overall response rate of 26.7%. The median survival time was 11 months and 1-year survival rate was 46.7% (7/15). The main toxicities were delayed diarrhea and granulocytopenia. CONCLUSION: Irinotecan plus cisplatin is an effective and tolerable treatment for advanced NSCLC with low incidence of adverse effects.