Objective To explore the clinicopathological features of osteofibrous dysplasia (OFD). Methods All the clinicopathological information of 17 cases of OFD were reviewed,including sex,age,course and radiography or histopathology features. The expression of Cytokeratin(CK) was examined by SP. Results Age of the patients ranged from 2-15 years, and the course of the lesion ranged from 1 month to 7 years. The mean age and the mean course was 7.2 years and 2.1 years respectively. Male to female ratio was 1∶1.4. The lesions all occured in tibia, presentating with localized masses. Only one invloved with both tibia and fibula. Radiographs showed there were cystic lesions in the thickened anterior cortex of the tibia with light marginal sclerosis. Histopathology showed a zonal architecture. Abundant osteoblasts in the vicinity of the trabeculae. Only two cases were positive for CK(11.8%). 8 of 10(80%) patients recurred. Conclusion OFD is predominately involved with the tibia in children. The history is long. It has a characteristic histopathologic image and clinical progress. Its a independent entity, not the same of adamantinoma.

BACKGROUNDTo investigate the roles of E-cadherin and β-catenin genes in metastasis and prognosis of non-small cell lung cancer.

METHODSThe expression of E-cadherin and β-catenin were detected in 112 non-small cell lung cancer tissues and 30 benign pulmonary lesion tissues by immunohistochemical method (LSAB method).

RESULTSThe expression of E-cadherin and β-catenin in lung cancer tissues was significantly lower than that in adjacent non-cancerous lung tissues and benign pulmonary tissues (P < 0.01); The expression of E-cadherin and β-catenin in lung cancer tissues with lymph node and/or distant metastasis was significantly lower than that in those without lymph node and distant metastasis (P < 0.01); The 5-year survival rate in patients with low E-cadherin expression and low β-catenin expression (6.78%) was remarkably lower than that in cases with high expression (6.78% vs 35.85% and 3.78% vs 37.29%) (P < 0.01).

CONCLUSIONSUnderexpressions of E-cadherin and β-catenin are very common in non-small cell lung cancer, and it may play an important role in the progression and metastasis of lung cancer. Detection of expression of E-cadherin and β-catenin in lung cancer might be helpful to predict prognosis.

OBJECTIVETo investigate the effects of genistein, a tyrosine protein kinase inhibitor, on the fenestrae, proliferation and nitric oxide (NO) synthesis of the liver sinusoidal endothelial cells from CCl(4)-induced hepatic fibrosis rats in vitro.

METHODSBy in situ collagenase perfusion and two-step percoll gradient centrifugation, SECs were isolated and cultured from normal and CCl(4)-treated Wistar rats. The fenestrae of SECs were observed by the scanning electron microscopy, and the SECs cell proliferation was determined by the MTT assay. The concentrations of NO in the cultured medium of SECs were detected indirectly by measurement of nitrates and nitrites (the stable products of NO) using the nitrate reduction method.

RESULTSScanning electron microscopic studies revealed that the number of fenestrae in SECs from all stage of hepatic fibrotic rats was decreased markedly as compared with the SECs from normal controls; however, no obvious changes in the fenestrae of SECs were observed after treated with genistein (100 mumol/L) for 24 hours. After treated with 100 mumol/L genistein for 24 hours, the cell proliferation rates of SECs from all stages of hepatic fibrosis were decreased significantly was compared with the control group (P<0.05). The synthesis of NO by SECs from all stages of hepatic fibrosis was markedly lower than those of normal controls. Treatment with 100 mumol/L genistein for 24 hours could increase the synthesis of NO by SECs from the early stage (stage I) of fibrosis; however, this effect of genistein was not observed in SECs from stage II or III of fibrosis at this concentration.

CONCLUSIONSThe results suggest that genistein may play an important role in regulating the function of SECs.

Animals ; Carbon Tetrachloride ; Cell Division ; drug effects ; Endothelium ; drug effects ; metabolism ; Genistein ; pharmacology ; Growth Inhibitors ; pharmacology ; Liver ; pathology ; Liver Cirrhosis ; chemically induced ; metabolism ; pathology ; Male ; Nitric Oxide ; metabolism ; Rats ; Rats, Wistar

BACKGROUNDTo investigate the role of protein kinase CβII (PKC-βII) expression and apoptosis in the oncogenesis and development of non-small cell lung cancer.

METHODSThe expression of PKC-βII and apoptosis were detected in 119 human non-small cell lung cancer tissues and paracancerous lung tissues by TUNEL and LSAB, and 32 benign pulmonary disease tissues as control.

RESULTSThe expression of PKC-βII (85.39%) in lung cancer tissues was significantly higher than that in paracancerous lung tissues and benign pulmonary disease tissues (65.69% and 53.22%) ( P < 0.05), and the PKC-βII expression in paracancerous samples was also remarkably higher than that in benign pulmonary disease samples ( P < 0.05). The apoptotic index (AI) (5.27%) in lung cancer tissue was significantly lower than that in the benign lung lesion tissue (15.84%) ( P < 0.05). No significant relationship was observed between the expression of PKC-βII in lung cancer tissue and clinical physiopathological characteristics ( P > 0.05). The AI in the lung cancer tissues was closely related to the stages of the cancer, size of primary tumor and lymph node metastasis ( P < 0.05), but not to the histological classification, cell differentiation and location of the tumor, and sex and age of the patient with lung cancer ( P > 0.05). A highly significant negative correlation was observed between PKC-βII expression and AI in the lung cancer group ( P < 0.01).

CONCLUSIONSThe abnormal activation of PKC-βII and the suppression of apoptosis may play important roles in the oncogenesis and development of non-small cell lung cancer. The overproliferation of cells and suppression of apoptosis transducted by PKC-βII may be one of the important mechanisms of the oncogenesis and development of non-small cell lung cancer.

BACKGROUNDTo investigate the relationship between expression of PKC-βI, apoptosis and prognosis of non-small cell lung cancer (NSCLC).

METHODSThe expression of PKC-βI and apoptosis index (AI) were detected in 119 human NSCLC tissues and paracancerous tissues by LSAB and TUNEL, with 32 benign pulmonary disease tissues as control.

RESULTS(1)The expression of PKC-βI (82.27%) in NSCLC tissues was significantly higher than those (62.85% and 50.47%) in paracancerous tissues and benign pulmonary disease tissues (P < 0.05). The AI (5.27%) in NSCLC tissues was significantly lower than that ( 15.84%) in benign pulmonary disease tissues (P < 0.05). (2) No significant relationship was observed between the expression of PKC-βI and clinical physiopathological characteristics of NSCLC (P > 0.05). The AI was closely related to pTNM stage of the cancer, size of primary tumor and lymph node metastasis (P < 0.05), but not to the histological classification, cell differentiation, sex and age of the patients with NSCLC (P > 0.05). (3) A highly significant negative correlation was observed between PKC-βI expression and AI in NSCLC group (P < 0.01). (4) The 5-year survival rate (7.37%) in patients with high PKC-βI expression was much lower than that (37.06%) in patients with low PKC-βI expression (P < 0.01). The 5-year survi-val rate ( 39.24%) in patients with high AI was much higher than that (6.14%) in patients with low AI (P < 0.01).

CONCLUSIONSThe abnormal activation of PKC-βI and suppression of apoptosis may play important roles in the oncogenesis and prognosis of lung cancer. Detection of PKC-βI expression and AI may help to predict the prognosis of patients with NSCLC and guide the postoperative multimodality therapy.

BACKGROUNDTo investigate the role of FHIT (fragile histidine triad) gene in oncogenesis and progression of human lung cancer.

METHODSThe expression of FHIT gene was detected in 166 lung cancer samples and 37 benign pulmonary lesion tissues as control by immunohistochemistry.

RESULTSThe positive rate of FHIT expression in lung cancer tissues was 63.03%±26.41%, which was significantly lower than that in tisssues adjacent to cancer (83.74%±17.46%) (P < 0.01 ), and both positive rates in cancer tissues and tissues adjacent to cancer were significantly lower than that in benign lesion tissues (92.98%±5.56%)(P < 0.01). The expression level of FHIT gene was closely related to histological classification, cancer cell differentiation, P TNM stages and lymph node involvement in lung cancer patients (P < 0.05). The positive rate of FHIT expression in smoking lung cancer patients was remarkably lower than that in non smoking ones ( 55.14% ±27.55% vs 71.93%±22.05%, P < 0.01). The postoperative survival time in patients with high FHIT expression was significantly longer than those with low expression (P < 0.05).

CONCLUSIONSReduction of FHIT gene expression might be associated with the oncogenesis and progression of human lung cancer; Smoking may be one of the important reasons of reduction of FHIT gene expression in lung cancer patients.