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<p><b>OBJECTIVE</b>To investigate the molecular alterations related to the carcinogenesis of esophageal squamous cell carcinoma (SCC), and also to find some molecular markers for the early detection of this cancer.</p><p><b>METHODS</b>The resected tumor specimens and dysplasia tissues from 34 patients with esophageal cancer as well as their matched blood DNAs were analyzed for loss of heterozygosity (LOH) at 16 microsatellites by using PCR and fluorescence-based DNA sequencing technology. Mild and moderate dysplasia was classified as light-grade dysplasia (LGD), and severe dysplasia as high-grade dysplasia (HGD). The frequencies of LOH at 16 microsatellites were compared between tissue specimens with different histological diagnosis.</p><p><b>RESULTS</b>The total frequency of LOH for 16 microsatellites increased significantly in more severe lesions. There was significant difference in the frequency of LOH among LGD and HGD as well as SCC. A total of eight loci (D3S1597, D3S2452, D3S1285, D4S174, D5S2501, D9S125, D13S153 and D17S786) presented LOH in LGD samples. A reversion from LOH to retain of heterozygosity was observed at loci D3S2452, D4S174, D9S125 and D17S261 respectively when compared HGD with SCC samples obtained from 4 patients.</p><p><b>CONCLUSIONS</b>An accumulation of molecular alterations would be needed during the carcinogenesis of esophageal cancer. LOH analysis at some specific loci would be helpful for the early detection of esophageal cancer. The genetic heterogeneity possibly exists in the tumorigenesis of esophageal cancer.</p>
Asunto(s)
Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Carcinoma de Células Escamosas , Genética , Patología , Neoplasias Esofágicas , Genética , Patología , Pérdida de Heterocigocidad , Inestabilidad de Microsatélites , Repeticiones de Microsatélite , Genética , Lesiones Precancerosas , Genética , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To investigate the relationship between the loss of heterozygosity(LOH) at 14 microsatellites in esophageal cancer and human papillomavirus (HPV) infection.</p><p><b>METHODS</b>HPV-16,18 DNA was examined in 112 tumor specimens using fluorescence quantitative PCR. 112 tumor specimens and their matched blood DNAs were analyzed for LOH at 14 microsatellites by PCR and fluorescence-based DNA sequencing technology. The frequencies of LOH at 14 microsatellites were compared between HPV positive and negative specimens.</p><p><b>RESULTS</b>High frequency of LOH was observed among chromosome arms 3p, 9p, 13q, 17p and 17q. The frequency of LOH was significantly higher at loci D13S260 and D6S497 in HPV positive specimens, comparing with HPV negative ones.</p><p><b>CONCLUSION</b>The findings regarding loci with allele loss indicated that widespread chromosome instability might have existed in esophageal cancer. HPV positive specimens with higher frequency of LOH than negative ones at locus D13S260 and D6S497 suggesting that the target of HPV in esophageal cancer might serve as candidate genes at these two loci. In addition,this result also indicated that HPV might be a high-risk factor for esophageal cancer in Sichuan area with a high incidence of this cancer.</p>
Asunto(s)
Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Inestabilidad Cromosómica , Genética , Neoplasias Esofágicas , Genética , Virología , Técnicas In Vitro , Pérdida de Heterocigocidad , Genética , Repeticiones de Microsatélite , Genética , Infecciones por Papillomavirus , Reacción en Cadena de la PolimerasaRESUMEN
Objective To investigate the role of suramin in inhibiting the angiogenesis of lung cancer. Methods The protei n expression of VEGF and its receptor fms-like tyrosine kinase(Flt), kinase ins ert domain-containing receptor(KDR) in lung cancer cell A549 and ECV-304 was studied with immunohistochemical technique. The anti-angiogenesis effect of su ramin was evaluated with immunohistochemical technique and cell culture. Results Suramin showed no effect on the production of lung cancer cel ls and their secretion of VEGF. No possitive expression of Flt, KDR in A549 was found in the suramin interfered group and non-interfered group, but VEGF w as e xpressed in both groups. The Flt and KDR expressions in ECV-304 cells were decr eased significantly after the treatment of suramin at 0.25 ng/ml and 2.5 ng/ml r espectively. There was no effect on proliferetion of A549 and ECV-304 after sur amin in terference. Conclusion The mechanism of inhibiting-angiogenes is of suramin is pro bably due to reducing the VEGF receptor expression in vascular endothelial cells and inhibiting the binding of VEGF and its receptors.
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Objective Coronary artery bypass grafting (CABG)i n 13 patients was analyzed. Methods 9 patients were performed C ABG with cardiopulmonary bypass, 4 patients undergone off-pump coronary artery bypass(OPCAB). Among the 4 patients, 3 undergone transmyocardial laser revascula rization concomitantly. 2 patients with single-vessel disease, 3 with double-v essel disease, 7 with triple-vessel disease and 1 with left main coronary arter y disease. The average bypass per patient was 2.3. Results All patients survived, 11 patients were angina free, 2 were angina relief. C onclusion CABG is a safe operation, OPCAB may reduce blood transfusion and complication, patients recover more quickly after OPCAB compared with those with CABG.
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Objective To investigate the role of suramin in inhibiting the angiogenesis of lung cancer. Methods The protei n expression of VEGF and its receptor fms-like tyrosine kinase(Flt), kinase ins ert domain-containing receptor(KDR) in lung cancer cell A549 and ECV-304 was studied with immunohistochemical technique. The anti-angiogenesis effect of su ramin was evaluated with immunohistochemical technique and cell culture. Results Suramin showed no effect on the production of lung cancer cel ls and their secretion of VEGF. No possitive expression of Flt, KDR in A549 was found in the suramin interfered group and non-interfered group, but VEGF w as e xpressed in both groups. The Flt and KDR expressions in ECV-304 cells were decr eased significantly after the treatment of suramin at 0.25 ng/ml and 2.5 ng/ml r espectively. There was no effect on proliferetion of A549 and ECV-304 after sur amin in terference. Conclusion The mechanism of inhibiting-angiogenes is of suramin is pro bably due to reducing the VEGF receptor expression in vascular endothelial cells and inhibiting the binding of VEGF and its receptors.
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Objective Coronary artery bypass grafting (CABG)i n 13 patients was analyzed. Methods 9 patients were performed C ABG with cardiopulmonary bypass, 4 patients undergone off-pump coronary artery bypass(OPCAB). Among the 4 patients, 3 undergone transmyocardial laser revascula rization concomitantly. 2 patients with single-vessel disease, 3 with double-v essel disease, 7 with triple-vessel disease and 1 with left main coronary arter y disease. The average bypass per patient was 2.3. Results All patients survived, 11 patients were angina free, 2 were angina relief. C onclusion CABG is a safe operation, OPCAB may reduce blood transfusion and complication, patients recover more quickly after OPCAB compared with those with CABG.