Five cases of ectopic liver, two of retro-peritoneal cavity and three of gallbladder, and a case of accessory lobe of the liver, are reported. One of these cases with ectopic liver was accompanied by multiple cysts of the liver and kidney, and biliary microhamartoma, which was observed laparoscopically on the surface of the main liver and histologically proven in the ectopic liver.

Summary Previous study has demonstrated that squamous cell carcinoma antigen (SCCA) 1 attenuates apoptosis induced by TNFα, NK cell or anticancer drug. In this study, we have examined the effect of SCCA2, which is highly homologous to SCCA1, but has different target specificity, against radiation-induced apoptosis, together with that of SCCA1. We demonstrated that cell death induced by radiation treatment was remarkably suppressed not only in SCCA1 cDNA-transfected cells, but also in SCCA2 cDNA-transfected cells. In these transfectants, caspase 3 activity and the expression of activated caspase 9 after radiation treatment were suppressed. Furthermore, the expression level of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) was suppressed compared to that of the control cells. The expression level of upstream stimulator of p38 MAPK, phosphorylated MKK3/MKK6, was also suppressed in the radiation-treated cells. Thus, both SCCA1 and SCCA2 may contribute to survival of the squamous cells from radiation-induced apoptosis by regulating p38 MAPK pathway.

Abstract. there is strong evidence that the angiopoietin family is involved in the regulation of tumour progression. recently, it has been reported that angiopoietin-like 4 (Angptl4) expression in cancer cells promotes the metastatic process by increasing vascular permeability. the present study was conducted to examine Angptl4 expression and its association with clinicopathological factors and prognosis in human colorectal cancers. We examined 144 cases of surgically-resected human colorectal adenocarcinomas by immunohistochemistry, rt-pcr and Western blot analysis. Also, overall survival was investigated. Among 144 cases of adenocarcinoma, 95 cases (66.0%) showed positive staining in the cytoplasm of the carcinoma cells for Angptl4. Histologically, well, moderately, poorly differentiated adenocarcinoma or mucinous carcinoma showed 55.2, 79.3, 61.5 or 44.4% expression of Angptl4, respectively. the expression of Angptl4 was correlated with the depth of tumour invasion (p<0.0005), Vienna classification (category 3-5) (p<0.00005), venous invasion (p<0.0005) and Duke's classification (p<0.005). However, Angptl4 expression was not correlated with overall survival. However, all patients (100%) with distant metastasis showed immunopositivity for Angptl4. the mrnA and the protein expression of Angptl4 were shown in four resected samples and cultured cell lines by rt-pcr or Western blot analysis. These findings suggest that Angptl4 is one of the factors involved in the progression of human colorectal cancer, especially venous invasion and distant metastasis. Introductioncolorectal cancer is one of the most common cancer types in the world today (1). the occurrence and progression of cancer are considered to be a series of genetic events affecting the structure and/or expression of a number of oncogenes, tumour suppressors, and growth factors (2,3). the deep invasive carcinomas, such as colorectal cancer, have higher rates of lymph duct and venous invasions, and lymph node metastasis (3). However, the mechanisms of invasion and metastasis of colorectal cancer are not fully understood.there is strong evidence that the angiopoietin family is involved in the regulation of tumour progression, cellular growth, and differentiation (4-6). Angiopoietin-like 4 (Angptl4) is a member of the family of angiopoietins and is also known as hepatic fibrinogen/angiopoietin-related protein (HeArp) (7), peroxisome proliferator-activated receptor-γ (ppArγ) angiopoietin-related gene (pgAr) (8), or fasting-induced adipose factor (FIAF) (9). Angptl4 is a circulating plasma protein and is expressed in the liver, adipose tissue, placenta, as well as in ischemic tissue (8,9). similar to angiopoietins and other angiopoietin-like proteins, Angptl4 contains an amino-terminal coiled-coil domain and a carboxyl-terminal fibrinogen-like domain (10). Angptl4 induces a strong proangiogenic response, independently of vascular endothelial growth factor (11), and is known to undergo hypoxia-induced gene expression in endothelial cells. this protein is up-regu...

ANGPTL4 may play an important role in metastasis through lymphovascular invasion, and may potentially affect prognosis.

No abstract

Abstract. Cortactin is a ubiquitously expressed actin filament (F-actin)-binding protein that stabilizes F-actin networks and promotes actin polymerization by activating the actinrelated protein 2/3 (Arp2/3) complex. Overexpression of cortactin in cancer cells stimulate cell migration, invasion, and experimental metastasis; however, the underlying mechanism in cortactin involvement in tumor progression is not fully understood. Recently, a direct interaction between zonula occludens-1 (ZO-1) and cortactin in epithelial cells was reported. The present study aimed to further clarify the significance of the interaction between cortactin and ZO-1 in cancer progression. Cortactin expression and localization in colorectal human cancer tissues were evaluated by immunohistochemistry and immunofluorescence. Co-immunoprecipitation and immunofluorescence analysis revealed cortactin and ZO-1 interaction and localization in cancer cells. In our study, the localization of cortactin is a crucial marker for lymph node metastasis in colorectal cancer. We show how the localization of cortactin effects cancer development. A molecular interaction between cortactin and ZO-1 in migrating or polarized cancer cells was revealed. This is the first report to show the interaction of cortactin and ZO-1 in colorectal cancer progression. We conclude that localization of cortactin in cancer cells and interaction between ZO-1 and cortactin are crucial for cancer progression.

Rationale: Bronchopulmonary dysplasia (BPD) is a chronic lung disease that adversely affects long-term pulmonary function as well as neurodevelopmental outcomes of preterm infants. Elastolytic proteases have been implicated in the pathogenesis of BPD. Cathepsin S (cat S) is a cysteine protease with potent elastolytic activity. Increased levels and activity of cat S have been detected in a baboon model of BPD. Objectives: To investigate whether deficiency of cat S alters the course of hyperoxia-induced neonatal lung injury in mice. Methods: Newborn wild-type and cat S-deficient mice were exposed to 80% oxygen for 14 days. Histologic and morphometric analysis were performed and bronchoalveolar lavage protein and cells were analyzed. Lung elastin was assessed by real-time polymerase chain reaction, in situ hybridization, desmosine analysis, and Hart's stain. Distribution of myofibroblasts was analyzed by immunofluorescence. Hydroxyproline content of lung tissues was measured. Measurements and Main Results: Hyperoxia-exposed cat S-deficient mice were protected from growth restriction and had improved alveolarization, decreased septal wall thickness, lower number of macrophages, and lower protein concentration in bronchoalveolar lavage fluid. a-Smooth muscle actin-expressing myofibroblasts accounted for at least some of the increased interstitial cellularity in hyperoxia-exposed mouse lungs and were significantly less in cat S-deficient lungs. Lung hydroxyproline content was increased in hyperoxia-exposed wild-type, but not in cat S-deficient lungs. Desmosine content was significantly reduced in both genotypes with hyperoxia. Conclusions: Cathepsin S deficiency improves alveolarization, and attenuates macrophage influx and fibroproliferative changes in hyperoxia-induced neonatal mouse lung injury.Keywords: cathepsin; bronchopulmonary dysplasia; hyperoxia; myofibroblast Advanced perinatal care over the past decade has resulted in improved survival of very-low-birth-weight (VLBW) (birth weight , 1,500 g) infants (1). However, surviving VLBW infants have increased risk of major morbidities, particularly bronchopulmonary dysplasia (BPD). BPD has a negative impact on not only short-term and long-term pulmonary function but also on overall growth and neurodevelopment of VLBW infants (2-4). The major pathologic findings associated with BPD in surfactant-treated lungs are inflammation, disrupted alveolar development, and variable amounts of fibrosis (5). Exposure of the immature lung to hyperoxia, prolonged mechanical ventilation, and antenatal or postnatal infections are primary risk factors for BPD (6, 7). However, the molecular mechanisms that link these factors to disruption of alveolarization are not completely understood and there are currently no evidence-based strategies to prevent or treat BPD.Several studies have shown that alveolar elastin expressed by myofibroblasts is a critical component of alveolar development (8, 9). The impaired alveolar development in BPD is also accompanied by changes in deposition of elas...

Pulmonary tumour thrombotic microangiopathy (PTTM) is characterised by wide spread tumour emboli along with fibrocellular intimal proliferation and thrombus formation in small pulmonary arteries and arterioles. PTTM is a rare but fatal complication of carcinoma, but the pathogenesis remains to be clarified. An autopsy case of PTTM caused by gastric adenocarcinoma is described, in which tumour cells in the PTTM lesion had positive immunoreactivity for platelet-derived growth factor (PDGF) and PDGF receptor (PDGFR), and proliferating fibromuscular intimal cells also showed expression of PDGFR. In addition, the overexpression of PGDF was detected in the alveolar macrophages. These findings suggest that PDGF derived from alveolar macrophages and from tumour cells may act together in promoting fibrocellular intimal proliferation. To the best of the authors' knowledge, the possible involvement of activated alveolar macrophages in PTTM has not been previously reported.