ABSTRACT
<p><b>OBJECTIVE</b>To study the clonality of polygonal cells and surface cuboidal cells in the so-called pulmonary sclerosing hemangioma (PSH).</p><p><b>METHODS</b>17 female surgically resected PSH were found. The polygonal cells and surface cuboidal cells of the 17 PSH cases were microdissected from routine hematoxylin and eosin-stained sections. Genomic DNA was extracted, pretreated through incubation with methylation-sensitive restrictive endonuclease HhaI or HpaII, and amplified by nested polymerase chain reaction for X chromosome-linked androgen receptor (AR) and phosphoglycerate kinase (PGK) genes. The length polymorphism of AR gene was demonstrated by denaturing polyacrylamide gel electrophoresis and silver staining. The PGK gene products were treated with Bst XI and resolved on agarose gel.</p><p><b>RESULTS</b>Amongst the 17 female cases of PSH, 15 samples were successfully amplified for AR and PGK genes. The rates of polymorphism were 53% (8/15) and 27% (4/15) for AR and PGK genes respectively. Polygonal cells and surface cuboidal cells of 10 cases which were suitable for clonality study, showed the same loss of alleles (clonality ratio = 0) or unbalanced methylation pattern (clonality ratio < 0.25).</p><p><b>CONCLUSIONS</b>The polygonal cells and surface cuboidal cells in PSH demonstrate patterns of monoclonal proliferation, indicating that both represent true neoplastic cells.</p>
Subject(s)
Female , Humans , Male , Chromosomes, Human, X , Genetics , DNA, Neoplasm , Genetics , Phosphoglycerate Kinase , Genetics , Polymerase Chain Reaction , Polymorphism, Genetic , Pulmonary Sclerosing Hemangioma , Genetics , Pathology , Receptors, Androgen , Genetics , X Chromosome InactivationABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of connexin 43 and E-cadherin in lung cancer and to study the interaction between the two molecules.</p><p><b>METHODS</b>The expression and correlation of connexin 43 and E-cadherin were evaluated by immunohistochemistry (S-P method) in 85 samples of primary squamous cell carcinoma and adenocarcinoma of the lung. In addition, connexin 43 expression vector was transfected into the lung giant cell carcinoma cell line LH(7) followed by analyses of connexin 43 and E-cadherin expressions, the growth rates and cell cycle profiles of the transfected cells.</p><p><b>RESULTS</b>Comparing with the adjacent non-neoplastic lung tissue, expression of connexin 43 and E-cadherin was decreased in a correlative fashion in both squamous cell carcinomas and adenocarcinomas. Their expression reversely correlated to the degree of tumor cell differentiation, P-TNM stage, and status of lymph note metastasis. The expression of connexin 43 and E-cadherin increased significantly after transfection of connexin 43 expression vector into the LH(7) cells (P < 0.05). Both expressions were limited in the cytoplasm before or after the transfection. The proliferation rate of LH(7) cells was significantly decreased by connexin43 expression (P < 0.05), along with an increase of cell population at G(1) phase and a decrease of percentage of cells in S and G(2) phases (P < 0.05).</p><p><b>CONCLUSIONS</b>Squamous cell carcinoma and adenocarcinoma of lung have a low level of connexin 43 and E-cadherin expression, which are correlated with the clinicopathologic features of the tumors. Transfection expression of connexin 43 gene induces an E-cadherin overexpression and an inhibition of LH(7) cell proliferation indicating the significant role of onnexin 43 in the regulation of cell proliferation.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Cadherins , Metabolism , Cell Adhesion , Cell Adhesion Molecules , Metabolism , Cell Proliferation , Connexin 43 , Genetics , Metabolism , Gene Expression Regulation, Neoplastic , Lung Neoplasms , Metabolism , Pathology , Neoplasm Invasiveness , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To study the expression of caveolin-1 in primary lung cancer and its relationship with microvessel density and clinicopathologic parameters.</p><p><b>METHODS</b>Immunohistochemical study for caveolin-1 and CD34 was performed on paraffin sections of 154 cases of primary lung cancer and adjacent non-neoplastic lung parenchymal tissue, as well as 36 cases with nodal metastasis. Microvessel density was analyzed by CD34 immunostaining. Western blot assay was also employed in tumor and non-neoplastic lung tissues of the 50 cases (25 cases of pulmonary squamous cell carcinoma and 25 cases of pulmonary adenocarcinoma) with fresh specimens available.</p><p><b>RESULTS</b>Immunohistochemical study showed that non-neoplastic bronchial and alveolar epithelium was positive for caveolin-1 (membranous and cytoplasmic). The expression rate of caveolin-1 in lung cancer was 59.1%, which was significantly lower than that in normal lung tissues (P < 0.01). Western blot assay confirmed that the expression of caveolin-1 in pulmonary squamous cell carcinoma and adenocarcinoma was lower than in surrounding non-neoplastic lung tissues (P < 0.01). Caveolin-1 expression in pulmonary small cell carcinoma (7.1%) was significantly lower than that in non-small cell carcinoma (64.3%) (P < 0.01). Within the group of non-small cell carcinoma, the expression of caveolin-1 was much higher in patients with lymph node metastasis (P = 0.005). The expression was also higher in stage III and IV than in stage I and II disease (P = 0.042).</p><p><b>CONCLUSIONS</b>The expression of caveolin-1 is lower in lung cancer tissues than that in non-small cell carcinoma, it is also significantly correlated with tumor stage and lymph node metastasis. Caveolin-1 may play some role in the progression of pulmonary non-small cell carcinoma.</p>