Combined Metabolomic and Quantitative RT-PCR Analyses Revealed the Synthetic Differences of 2-Acetyl-1-pyrroline in Aromatic and Non-Aromatic Vegetable Soybeans.

Aroma is an important economic trait of vegetable soybeans, which greatly influences their market value. The 2-acetyl-1-pyrroline (2AP) is considered as an important substance affecting the aroma of plants. Although the 2AP synthesis pathway has been resolved, the differences of the 2AP synthesis in the aromatic and non-aromatic vegetable soybeans are unknown. In this study, a broad targeted metabolome analysis including measurement of metabolites levels and gene expression levels was performed to reveal pathways of aroma formation in the two developmental stages of vegetable soybean grains [35 (S5) and 40 (S6) days after anthesis] of the 'Zhexian No. 8' (ZX8, non-aromatic) and ZK1754 (aromatic). The results showed that the differentially accumulated metabolites (DAMs) of the two varieties can be classified into nine main categories including flavonoids, lipids, amino acids and derivatives, saccharides and alcohols, organic acids, nucleotides and derivatives, phenolic acids, alkaloids and vitamin, which mainly contributed to their phenotypic differences. Furthermore, in combination with the 2AP synthesis pathway, the differences of amino acids and derivatives were mainly involved in the 2AP synthesis. Furthermore, 2AP precursors' analysis revealed that the accumulation of 2AP mainly occurred from 1-pyrroline-5-carboxylate (P5C), not 4-aminobutyraldehyde (GABald). The quantitative RT-PCR showed that the associated synthetic genes were 1-pyrroline-5-carboxylate dehydrogenase (P5CDH), ∆1-pyrroline-5-carboxylate synthetase (P5CS), proline dehydrogenase (PRODH) and pyrroline-5-carboxylate reductase (P5CR), which further verified the synthetic pathway of 2AP. Furthermore, the betaine aldehyde dehydrogenase 2 (GmBADH2) mutant was not only vital for the occurrence of 2AP, but also for the synthesis of 4-aminobutyric acid (GABA) in vegetable soybean. Therefore, the differences of 2AP accumulation in aromatic and non-aromatic vegetable soybeans have been revealed, and it also provides an important theoretical basis for aromatic vegetable soybean breeding.

Whole-cell biotransformation for large scale production of carcinine in Escherichia coli.

Carcinine is a natural imidazole-containing peptide derivative. It is widely used in the cosmetics industry as anti-aging supplement with antioxidant, anti-glycation and glycation reversal functions, and it also has a notable pharmacological effect as anti-tumor drug and in protection against retinopathy. However, a technological method for synthesis and production of carcinine has not been established. In this study, a whole-cell transformation system converting ß-alanine and histamine to carcinine by the enzymes Ebony and phosphopantetheine transferase (Sfp) has been developed. The results revealed that the catalytic efficiency of the strain containing the fusion protein of Ebony and Sfp (Sfp-glycine-serine-glycine-Ebony, SGE) in Escherichia coli W3110 (WSGE strain) is significantly higher (7.45 mM) than the combinatorial strain of pET28a-ebony and pACYCDuet-sfp in E. coli BL21(DE3) (BSE strain) (2.17 mM). Under the optimal reaction conditions (25 â„ƒ, pH 7.0, 12.5 g/L wet cells, 20 mM ß-alanine and 40 mM histamine), the carcinine can be quickly synthesized within 24 h up to a concentration of 22.63 mM. To achieve a continuous and efficient conversion of the precursors, a batch-feeding catalysis was designed. With this system, ß-alanine (40 mM) and histamine (40 mM) could be completely transformed to carcinine (40.34 mM) in 36 h with a productivity of 0.204 g/L h reaching a titer of 7.34 g/L. Hence, the batch-feeding whole-cell biocatalysis is a promising technology for the high yield production of carcinine which can promote the industrial production of carcinine.

Primary breast diffuse large B-cell lymphoma in a patient with systemic lupus erythematosus: A case report and review of the literature.

RATIONALE: Pilot studies have reported that patients with systemic lupus erythematosus (SLE) appear more likely to develop into neoplasia, especially lymphatic hyperplasia diseases. To our knowledge, this is the first case report of the concomitant onset of SLE and primary breast diffuse large B-cell lymphoma (PB-DLBCL). PATIENT CONCERNS: We reported an unusual case of the occurrence of primary breast diffuse large B-cell lymphoma in a 25-year-old female patient who had been diagnosed with SLE and treated with immunosuppressive drugs for about 4 years. She presented a 7-week history of a painless mass above the left breast and no history suggestive of any nipple discharge, fever, and weight loss. DIAGNOSIS: Ultrasonography of the breast showed that there was 1 mass in the left breast. After breast mass surgical resection, histopathological examinations were performed and revealed that it was primary breast diffuse large B-cell lymphoma. INTERVENTIONS: Treatment strategy with vincristine and dexamethasone was used to improve symptoms. However, the patient's renal function deteriorated and the blood potassium rose continuously and she and their family members refused the follow-up treatments. OUTCOMES: The patient died 8 months after she was discharged from the hospital. LESSONS: PB-DLBCL is a rare occurrence in SLE patients. Therefore, a careful examination is very important in SLE cohort, as activity of the disease and malignancy may mimic each other. Meanwhile, when symptoms cannot be explained or insensitive to treatment, the occurrence of malignant tumors must be highly considered.

PDE4 and Epac1 Synergistically Promote Rectal Carcinoma via the cAMP Pathway.

OBJECTIVE: To assess the expression levels of exchange protein 1 directly activated by cAMP (Epac1) and phosphodiesterase 4 (PDE4) in rectal carcinoma, and their associations with clinicopathological indexes. In addition, the associations of PDE4 and Epac1 with A-kinase anchor protein 95, connexin 43, cyclin D1, and cyclin E1 were evaluated. METHODS: The PV-9000 two-step immunohistochemistry method was used to determine protein expression in 44 rectal carcinoma tissue samples and 16 paracarcinoma tissue specimens. RESULTS: The positive rate of PDE4 protein expression in rectal carcinoma tissues was higher than that of paracarcinoma tissues (59.09% vs. 12.5%, P < 0.05). Similar findings were obtained for Epac1 (55% vs. 6.25%, P < 0.05). No significant associations of PDE4 and Epac1 with degree of differentiation, histological type, and lymph node metastasis were found in rectal carcinoma (P > 0.05). Correlations between PDE4 and Epac1, PDE4 and Cx43, PDE4 and cyclin E1, and Epac1 and Cx43 were observed (all P < 0.05). There was no correlation between the other protein pairs examined (P > 0.05). CONCLUSION: PDE4 and Epac1 expression levels are increased in rectal carcinoma tissues, suggesting that the two proteins may be involved in the development of this malignancy. Meanwhile, correlations between PDE4 and Epac1, PDE4 and Cx43, PDE4 and cyclin E1, and Epac1 and Cx43 suggested synergistic effects of these proteins in promoting rectal carcinoma.

[Nucleocytoplasmic translocation of ING5 protein in breast cancer and its correlation with poor clinicopathological characteristics of breast cancer].

Objective To investigate the nucleocytoplasmic translocation of inhibitor of growth family member 5 (ING5) gene in human breast cancer and the negative correlation between the nuclear high expression of ING5 protein and the clinicopathological characteristics of breast cancer. Methods We collected 260 cases of clinical primary breast cancer, 55 cases of metastatic cancer in lymph node, 61 cases of breast fibroadenoma, 110 cases of adenomatosis, and 91 cases of para-cancerous tissues. With the tissue microarrays, we detected ING5 expression in the nucleus and cytoplasm through immunohistochemistry, and statistically analyzed the correlations of nuclear and cytoplasmic ING5 expression with the clinicopathological characteristics of breast cancer. Results The expression of nuclear ING5 in the para-cancerous tissues was obviously higher than that in the fibroadenoma, adenomatosis and primary breast cancer; it was higher in the adenomatosis than in the primary breast cancer, and higher in the primary breast cancer than in the metastatic cancer in lymph node. The cytoplasmic ING5 expression in the para-carcinoma tissue was higher than that in the fibroadenoma, adenomatosis and primary breast cancer. These data suggested the nucleocytoplasmic translocation of ING5 protein in breast cancer. Moreover, nuclear ING5 high expression was negatively correlated with distant metastasis and positively with P53 expression, while cytoplasmic ING5 high expression was positively correlated with tumor size and estrogen receptor expression. The cytoplasm ING5 expression of triple-negative breast cancer was lower than that in the non-triple-negative breast cancer. Conclusion Nucleocytoplasmic translocation of ING5 protein occurs in breast cancer, and the high expression of nuclear ING5 is inversely related to some poor clinicopathological behaviors of breast cancer.

Rare RET Variant p.D707E in a Chinese Pedigree with Hereditary Medullary Thyroid Carcinoma.

BACKGROUND: Hereditary medullary thyroid carcinoma (HMTC) is thought to be associated with germline mutations of the RET proto-oncogene. METHODS: We detected RET proto-oncogene germline mutations from a pedigree with HMTC in the east of China and investigated the characteristics of these mutations in this pedigree and their correlation with HMTC by direct sequencing of all 21 exons in the RET gene of all 46 subjects. RESULTS AND CONCLUSION: (1) Thirteen types of RET gene variants were detected in this pedigree. Of these, p.F285S in exon 4, c.854_855CA in exon 4, and p.D707E in exon 11 are reported for the first time in our study. (2) Both linkage disequilibrium analysis and logistic regression analysis showed a significant correlation between the p.D707E variant and HMTC (LOD = 3.69, OR = 4.413, p = 0.000167), indicating that this variant is a risk factor for medullary thyroid carcinoma (MTC). (3) The single-nucleotide polymorphisms (SNP) G691S in exon 11 (rs1799939), S904S in exon 15 (rs1800863), and rs2075912 and rs2565200 in the 3'-untranslated region of the RET proto-oncogene are in complete linkage disequilibrium (D' = 1, r2 = 1); no correlation of these SNP and MTC was observed in this pedigree. (4) No hot-spot mutation of the RET proto-oncogene was detected in this pedigree. We drew the conclusion that the heterozygous nonsynonymous variant p.D707E in the RET proto-oncogene is rare, but it is a risk factor for hereditary MTC.

Protective Role of Grape Seed Proanthocyanidins Against Ccl4 Induced Acute Liver Injury in Mice.

BACKGROUND: We investigated the effect of grape seed proanthocyanidins (GSPs) on carbon tetrachloride (CCl4)-induced acute liver injury. MATERIAL/METHODS: Sixty SPF KM mice were randomly divided into 6 groups: the control group, CCl4-model group, bifendate group (DDB group), and low-, moderate-, and high-dose GSP groups. The following parameters were measured: serum levels of alanine aminotransferase (ALT); aspartate aminotransferase (AST); tumor necrosis factor (TNF)-α; interleukin-6 (IL-6); high-mobility group box (HMGB)-1; body weight; liver, spleen, and thymus indexes; superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity; HMGB1 mRNA; malondialdehyde (MDA) content; hepatocyte proliferation; and changes in liver histology. RESULTS: Compared to the CCl4-model group, decreases in liver index and increases in thymus index significantly increased SOD and GSH-Px activities and reduced MDA content, and higher hepatocyte proliferative activity was found in all GSP dose groups and the DDB group (all P<0.001). Compared with the CCl4-model group, serum TNF-α and IL-6 levels and HMGB 1 mRNA and protein expressions decreased significantly in the high GSP dose group (all P<0.05). CONCLUSIONS: Our results provide strong evidence that administration of GSPs might confer significant protection against CCl4-induced acute liver injury in mice.

Synergistic effects of AKAP95, Cyclin D1, Cyclin E1, and Cx43 in the development of rectal cancer.

OBJECTIVE: To explore the expression of A-kinase anchor protein 95 (AKAP95), Cyclin D1, Cyclin E1, and Connexin43 (Cx43) in rectal cancer tissues and assess the associations between each of the proteins and pathological parameters, as well as their inter-relationships. METHODS: AKAP95, Cyclin D1, Cyclin E1, and Cx43 protein expression rates were evaluated by immunohistochemistry in 50 rectal cancer specimens and 16 pericarcinoma tissues. RESULTS: The positive rates of AKAP95, Cyclin E1, and Cyclin D1 proteins were 54.00 vs. 18.75%, 62.00 vs. 6.25%, and 72.00 vs. 31.25% in rectal cancer specimens and pericarcinoma tissues, respectively, representing statistically significant differences (P < 0.05). The positive rate of Cx43 protein expression in rectal cancer tissues was 44.00% and 62.50% in pericarcinoma tissues, and the difference between them was not significant (P > 0.05). No significant associations were found between protein expression of AKAP95, Cyclin E1, Cyclin D1, and Cx43, and the degree of differentiation, histological type, and lymph node metastasis of rectal cancer (P > 0.05). However, significant correlations were obtained between the expression rates of AKAP95 and Cyclin E1, Cyclin E1 and Cyclin D1, Cyclin E1 and Cx43 protein, and Cyclin D1 and Cx43, respectively (P < 0.05). CONCLUSION: AKAP95, Cyclin E1, and Cyclin D1 protein expression rates were significantly higher in rectal cancer tissues compared with pericarcinoma samples, suggesting an association between these proteins and the development and progression of rectal cancer. In addition, the significant correlations between the proteins (AKAP95 and Cyclin E1, Cyclin E1 and Cyclin D1, Cyclin E1 and Cx43 protein, and Cyclin D1 and Cx43) indicate the possible synergistic effects of these factors in the development and progression of rectal cancer.

Elevated expression of nuclear protein kinase CK2α as a poor prognosis indicator in lymph node cancerous metastases of human thyroid cancers.

AIM: To investigate the expression of protein kinase CK2α (CK2α) in human thyroid disease and its relationship with thyroid cancer metastasis. MATERIALS AND METHODS: Using immunohistochemistry we measured the expression of CK2α in 76 benign and malignant human thyroid cancer tissues, including 10 pairs of papillary carcinoma tissues with or without lymph node cancerous metastasis and similarly 10 pairs of lymph nodes. RESULTS: The expression of CK2α was found to be higher in thyroid carcinoma cases (papillary carcinoma, follicular carcinoma, anaplastic carcinoma and medullary carcinoma) than in ones such as chronic lymphocytic thyroiditis, nodular goiter and adenoma. These findings were also confirmed by RT-PCR and Western blotting. More strikingly, elevated expression of CK2α in thyroid papillary carcinoma tissues was not only significantly associated with lymph node cancerous metastasis and clinical stage of thyroid cancers; but also correlated with epithelial-mesenchymal transition (EMT) and high tenascin C (TNC) expression. In addition, EMT and high TNC expression in thyroid carcinoma tissues was significantly associated with lymph node cancerous metastasis. CONCLUSIONS: Elevated expression of nuclear CK2α is a poor prognosis indicator in lymph node cancerous metastasis of human thyroid cancers.

Nonuniform shrinkage and stretching of polymerized nanostructures fabricated by two-photon photopolymerization.

We propose a method to measure the nonuniform shrinkage and stretching of polymerized nanostructures by marking them with periodical points. The method was tested, and the results showed that suspended lines themselves shrank after fabrication, but they were also stretched due to the shrinkage of their support anchors, a phenomenon that has not been investigated much before. The extension strain was measured from the change in the separation points, which reached 75% for a 2 µm-long line with a width of 40 nm.

Uniform suspended nanorods fabricated by bidirectional scanning via two-photon photopolymerization.

Suspended nanorods fabricated by two-photon photopolymerization gradually thickened in the scanning direction when the scanning speed was faster than 60 µm s(-1). For a 2 µm long suspended nanorod, the lateral widths of the thin and the thick ends were about 50 and 150 nm. A bidirectional scanning technique was proposed to effectively eliminate the size difference, resulting in uniform suspended nanorods of 100 nm in width and 2 µm in length.

Gene expression and clonality analysis of the androgen receptor and phosphoglycerate kinase genes in polygonal cells and cuboidal cells in so-called pulmonary sclerosing hemangioma.

The histogenesis of polygonal cells and cuboidal cells in so-called pulmonary sclerosing hemangioma remains unclear. To understand their histogenesis, polygonal and cuboidal cells were obtained from pulmonary sclerosing hemangioma tissue using a laser capture microdissection technique. Genomic DNA and total RNA were extracted and mRNA levels of cytokeratin, epithelial membrane antigen, vimentin, surfactant protein B, thyroid transcription factor-1, synaptophysin, and chromogranin-A were analyzed by RT-PCR. DNA was digested with the methylation-sensitive enzymes HhaI or HpaII, followed by nested PCR of the androgen receptor and phosphoglycerate kinase genes. Samples with polymorphisms were identified and a clonality analysis was performed. The cytokeratin, epithelial membrane antigen, and surfactant protein B genes were clearly expressed in cuboidal cells, while the vimentin and synaptophysin genes were clearly expressed and the epithelial membrane antigen gene was weakly expressed in polygonal cells. Thyroid transcription factor-1 was expressed in both cell types, while neither cell type expressed chromogranin-A. Clonality analysis showed the same loss of allele in both cell types (clonality ratio=0) or an unbalanced methylation pattern (clonality ratio<0.25). Polygonal and cuboidal cells in pulmonary sclerosing hemangioma exhibited a uniform pattern of monoclonality, indicating that both cell types are highly likely to originate from a common precursor. The differences in their morphological phenotype might result from their different mature status.

Expression of E-cadherin, beta-catenin and p120ctn in the pulmonary sclerosing hemangioma.

BACKGROUND: The major two types of cells in pulmonary sclerosing hemangiomas (PSH) may be not equally maturity, but this viewpoint needs more evidences. AIM: To determine E-cadherin, beta-catenin and p120(ctn) expression phenotype in cuboidal and polygonal cells, which are the two major cell types in pulmonary sclerosing hemangiomas. METHODS: Specimens were obtained from 25 patients with PSH and 8 patients with pulmonary inflammatory pseudotumors. The expression levels of E-cadherin, beta-catenin and p120(ctn) were detected using a streptavidin peroxidase (SP) immunohistochemical method. RESULTS: E-cadherin, beta-catenin and p120(ctn) were expressed strongly on the cuboidal cell membranes, while beta-catenin was also expressed the cuboid cytoplams in 25 PSH patients. However, in the polygonal cell membranes, the expression levels of these molecules were decreased, and mainly cytoplamic. Specifically, E-cadherin, beta-catenin and p120(ctn) were expressed in both the cytoplasm and on the cell membranes in the intracavitary lining cells of the hemorrhagic regions. The expression phenotype in proliferating type II pneumocytes in the eight pulmonary inflammatory pseudotumors was similar to that in the cuboidal cells in PSH patients. CONCLUSION: The cuboidal cells, resembling inflammatory proliferative type II pneumocytes, display several characteristics of epithelial cells, including normal expression of E-cadherin and catenin. Comparatively, polygonal cells are not as mature as cuboidal cells and lack of expression of E-cadherin and catenin.

Polymerized nanotips via two-photon photopolymerization.

We present new methods to produce polymerized nanotips via two-photon photopolymerization. By gradually changing the laser power, we fabricate a single polymerized tip with the size of 120nm. When two rectangle anchors with protuberances are close enough, lines with the slimmest part of about 20-30nm and tips with the widths of about 35nm are produced between anchors, which are the best resolution obtained with the resin SCR-500 to our knowledge. As the tips are adhered to larger polymerized structures, they can survive post processing in spite of their small sizes.

[Expression of connexin 43 in lung cancer and its correlation with E-cadherin].

OBJECTIVE: To investigate the expression of connexin 43 and E-cadherin in lung cancer and to study the interaction between the two molecules. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Expression of serine threonine kinase 15 is associated with poor differentiation in lung squamous cell carcinoma and adenocarcinoma.

Serine threonine kinase 15 (STK15, also named BTAK, Aurora-A, aurora-2, or AIKI) is a type of mitotic kinase. The overexpression of STK15 is significantly associated with carcinogenesis in many tumors. The purpose of the present study was to investigate the expression of STK15 in lung squamous cell carcinoma and adenocarcinoma and analyze the correlation between STK15 expression and clinicopathological factors. The expression patterns of STK15 were examined by immunohistochemistry in 80 lung squamous cell carcinomas and adenocarcinomas and 20 normal lung tissues. The protein and mRNA expression of STK15 were evaluated by western blot and reverse transcription-polymerase chain reaction (RT-PCR) in 40 lung cancer samples and corresponding normal lung tissues. Immunohistochemically, the positivity of STK15 expression was 68.75% (55/80). The STK15 expression was significantly higher in poorly differentiated lung cancers than in well-differentiated or moderately differentiated lung cancers (P = 0.011). Western blot and RT-PCR showed that the protein and mRNA expression of STK15 were correlated (P = 0.044) and significantly higher in tumors than in corresponding normal lung tissues (P < 0.05). These results indicate that the overexpression of STK15 contributes to the carcinogenesis and de-differentiation of lung cancers.

[Study of androgen receptor and phosphoglycerate kinase gene polymorphism in major cellular components of the so-called pulmonary sclerosing hemangioma].

OBJECTIVE: To study the clonality of polygonal cells and surface cuboidal cells in the so-called pulmonary sclerosing hemangioma (PSH). METHODS: 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. RESULTS: 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). CONCLUSIONS: The polygonal cells and surface cuboidal cells in PSH demonstrate patterns of monoclonal proliferation, indicating that both represent true neoplastic cells.

[Significance of caveolin-1 expression in primary lung cancer].

OBJECTIVE: To study the expression of caveolin-1 in primary lung cancer and its relationship with microvessel density and clinicopathologic parameters. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

[Expression of E-cadherin, ß-catenin and p120ctn in so-called pulmonary sclerosing hemangioma].

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, ß-catenin and p120ctn in cuboidal cells and polygonal cells of PSH. METHODS: Expression of E-cadherin, ß-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, ß-catenin and p120 ctn , with cytoplasmic positive expression of ß-catenin. However,the polygonal cells were negative for E-cadherin, cytoplasmic positive for ß-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, ß-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.

[Significance of p53 protein expression and p53 gene mutation in so-called pulmonary sclerosing hemangioma].

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.