Search

Background: Serine threonine kinase 15 (STK15) is a kind of mitotic kinase. The overexpression of STK15 is significantly associated with carcinogenesis in many tumors, however, its expression and significance in human lung cancer are still unclear. The aim of this study is to investigate the expression of STK15 in squamous cell carcinoma and adenocarcinoma of the lung and to analyze the correlation between STK15 expression and clinicopathological factors., Methods: The pattern of STK15 protein expression was detected in 44 squamous cell carcinomas, 36 adenocarcinomas and 20 paracancerous lung tissue samples by immunohistochemistry method using anti-STK15 antibody. The relative quantity of STK15 protein expression was detected by Western blot, and STK15 mRNA expression was detected by RT-PCR in 40 fresh lung cancer samples and corresponding paracancerous lung tissues., Results: Positive expression rate of STK15 protein was 68.75% (55/80) in lung cancer tissues and 0% in paracancerous controls (P < 0.001). STK15 expression was significantly related to differentiation grade of lung cancer (P=0.011), but not to histological classification, TNM stages or lymphatic metastasis (P > 0.05). The relative expression levels of STK15 protein (P < 0.001 ) and STK15 mRNA (P < 0.001) in lung cancer tissues were both significantly higher than those of corresponding paracancerous lung tissues., Conclusions: The expression of STK15 protein and STK15 mRNA is significantly higher in lung cancer tissues than that in paracancerous lung tissues. The expression of STK15 correlates with differentiation of lung cancer.

Background: So-called pulmonary sclerosing hemangioma (PSH) is an uncommon tumor of the lung and its histogenesis and origin are uncertain to date. A general consensus appears to have been reached that PSH is a benign neoplasm, but a few PSHs are found to invade and metastasize. The expression of p53 protein and mutation of p53 gene are significant parameters which can reflect biological behavior of tumor cells. The aim of this study is to investigate the p53 protein expression and p53 gene mutation in PSH, and explore their significance., Methods: The expression of p53 protein and mutation of p53 gene were examined in polygonal cells and cuboidal cells of PSH by immunohistochemical method, laser capture microdissection (LCM), single-stranded conformation polymorphism (SSCP) and DNA sequencing., Results: The positive rate of p53 protein was 21.1% (4/19) and the mutation rate of p53 gene was 26.3% (5/19) by SSCP and 42.1% (8/19) by DNA sequencing respectively. In 4 cases of immunopositive PSH tissues, 2 were missense mutations, and 1 was both missense and frameshift mutation. Out of 15 cases of immunonegative PSH tissues, 4 were frameshift mutations and 1 was missense mutation. Of 8 PSH tissues with p53 gene mutation, 5 were identified in only polygonal cells, and 2 in only cuboidal cells and 1 in both polygonal and cuboidal cells., Conclusions: The expression of p53 protein may not be indicative of p53 gene mutation in PSH. The alteration of p53 gene and the expression of p53 protein are identified in both polygonal and cuboidal cells. The high mutation rate of p53 gene may indicate that PSH has potentially malignant biological behavior.

Background: So-called pulmonary sclerosing hemangioma (PSH) is a rare kind of pulmonary tumor. Its histological origin and nature, which have become research hot spots for many years, are still uncertain. The aim of this study is to investigate the immunophenotype of cuboidal cells and polygonal cells through observing the expression of E-cadherin, β-catenin and p120ctn in cuboidal cells and polygonal cells of PSH., Methods: Expression of E-cadherin, β-catenin and p120 ctn was detected in 25 cases of PSH samples and 8 cases of pulmonary inflammatory pseudotumor samples by immunohistochemistry., Results: Immunohistochemistry results showed that the surface cuboidal cells of PSH were strongly positive on membrane for E-cadherin, β-catenin and p120 ctn , with cytoplasmic positive expression of β-catenin. However,the polygonal cells were negative for E-cadherin, cytoplasmic positive for β-catenin and predominantly cytoplasmic positive and weakly membranous positive for p120ctn . In polygonal cells, all the three adhesion molecules showed heterogenicity staining. The cytoplasm and membrane of inner covering cells in the hemorrhagic pattern were positively stained for E-cadherin, β-catenin and p120ctn . The expression of the three adhesion molecules in hyperplastic type II alveolar cells of pulmonary inflammatory pseudotumor was similar to cuboidal cells of PSH., Conclusions: It is concluded that cuboidal cells of PSH may be the hyperplastic type II alveolar cells, whereas polygonal cells are true tumor cells lacking the E-cadherin/catenin complex which is expressed in well differentiated epithelial cells. The inner covering cells in the hemorrhagic pattern of PSH are perhaps epithelial cells as cuboidal cells rather than vascular endothelial cells.