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Osteopontin (OPN) has close relationship with metastasis in hepatocellular carcinoma but its downstream signal pathways have not been well defined in hepatocellular carcinoma. The object of this study is to identify the associated signal pathways in human HCC tissues. The expressions of OPN, intergrin aV, CD44v6, P-FAK, FAK, P-Src, Src, P-ERK and P-AKT were assayed using TMA analysis. The relationship of OPN with P-ERK, P-Src and P-AKT were explored and the role in HCC metastasis was analysed. The expression levels of OPN, intergrin aV, CD44v6, P-FAK, P-Src, Src, P-ERK and P-AKT in HCC tissue were significantly higher than that in normal tissue (P value is less than 0.05). No significant difference was found between the expression levels of FAK in HCC tissue and normal tissue (P value is more than 0.05). OPN expression was significantly associated with Integrin av (P value is less than 0.01), CD44V6 (P value is less than 0.01) and P-ERK (P value is less than 0.05) but not with P-Src, P-FAK and P-AKT (P value is more than 0.05). The expressions of P-FAK (P value is less than 0.05), P-Src (P value is less than 0.01) and P-AKT (P value is less than 0.05) were significantly associated with Integrin av and the P-FAK expression was also significantly associated with CD44V6 (P value is less than 0.01). OPN promotes HCC metastasis though Integrin av/CD44V6/MAPK pathway in human HCC.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Carcinoma, Hepatocellular , Metabolism , Pathology , Cell Line, Tumor , Focal Adhesion Kinase 1 , Metabolism , Integrin alphaVbeta3 , Metabolism , Liver Neoplasms , Metabolism , Pathology , Osteopontin , Metabolism , Proto-Oncogene Proteins c-akt , Metabolism , Signal TransductionABSTRACT
Objective To study the relationship between protein expressions of p16, FGFR-4 and c-erbB-2 and biological behaviors of pituitary adenomas. Methods Immunohistochemical techniques were used to detect the expression levels ofpl6, FGFR-4 and c-erbB-2 in the 95 cases with pituitary adenomas and 30 cases among them were followed up for 5 years. Results The positive expression rates of p16, FGFR-4 and c-erbB-2 were respectively 54.7%, 98.9% and 82.4%. Significant differences in the p16 expression existed among the endocrine function groups (with function, 33 cases; without function, 19 cases), Hardy's classification groups (grade 0, 4 cases; grade 1, 13 cases; grade 2, 32 cases; grade 3, 3 cases), invasiveness groups (invasive, 3 cases; noninvasive, 23 cases) and follow-up groups (recurred, 1 case; not recurred, 15 cases). The positive expression of FGFR-4 was obviously correlated with the size of pituitary adenomas (grade 0: "+～++", 5 cases and "+++", 2 cases; grade 1: "+～++", 4 cases and "+++", 10 cases; grade 2: "+～++", 12 cases and "+++", 48 cases; grade 3: "+～++", 4 cases and "+++", 9 cases). The expression of FGFR-4 was not related to invasiveness. The expressions of FGFR-4 and p16 were respectively positively and negatively correlated with that of c-erbB-2. Conclusions The decreased expression of p16 was responsible for the proliferation, invasiveness and recurrence of pituitary adenomas, while the increased expression of FGFR-4 plays an important role in the proliferation of pituitary adenomas. FGFR-4, c-erbB-2 and p16 may regulate cell growth cycle of tumor cells through synergic effects in the process of oncogenesis.
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<p><b>OBJECTIVE</b>To investigate the clinical pathological characteristics and prognosis of gastrointestinal stromal tumors (GISTs).</p><p><b>METHODS</b>One hundred and seven cases, admitted to our hospital from Apr. 1996 to Oct. 2005, were detected by Envision immunohistochemical method and diagnosed as GISTs. Their pathological features, immunohistochemical phenotypes, clinical manifestations and imaging findings were analyzed.</p><p><b>RESULTS</b>Of the 107 GISTs, 107 cases were positive for vimentin (107/107, 100%), 107 cases were positive for CD117 (107/107, 100%), 89 cases were positive for CD34 (89/107, 83.2%), 14 cases were positive for SMA (14/107, 13.1%), 10 cases were positive for desmin (10/107, 9.3%), 22 cases were positive for S-100 (22/87, 20.6%) and 15 cases were positive for NSE (15/107, 14.0%). Among all the GISTs, 73 cases occurred in stomach (68.2%), 28 in small intestine (26.2%), 1 in colon (0.9%) and 5 occurred in other position including mesentery, omentum, and retroperitoneum (4.7%). Fifteen cases were diagnosed as very low grade (14.0%), 25 cases as low grade (23.4%), 33 cases as low malignancy (30.8%) and 34 cases as high malignancy (31.8%). The follow-up was obtained successfully in 89 cases (83.2%). Fourteen cases (13.1%) were confirmed to have recurrences or metastases by review and medical records.</p><p><b>CONCLUSIONS</b>The diagnosis of GIST depends on pathological observation and immunohistochemical study. CD117 is a sensitive marker for the diagnosis of GIST. Surgical resection is the choice for treating GIST. Extended resection, even combined resection of involved organs, is required for malignant GIST.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Gastrointestinal Stromal Tumors , Diagnosis , Pathology , General Surgery , ImmunohistochemistryABSTRACT
Objective To detect genetic alterations in pleomorphic xanthoastrocytoma (PXA), and to investigate the mechanism of development of this neoplasm. Methods Three patients with PXA were studied. Comparative genomic hybridization (CGH) was performed to study chromosomal imbalances in PXA. Using immunohistochemical analysis, the expression of EGFR was detected in PXA. Results Using CGH analysis, genetic imbalance was detected on at least one chromosome for each case. One patient revealed multiple genetic alterations, including gains of 2p14-pter, 4p15-pter, 7p21-qter, 11q24-qter, 12 and 15q14-qter,as well as losses of 8p11.2-pter, 9p11-p23, 10p12-pter, and 13q14-qter. This patient experienced tumor recurrence and died one year later. Gain on Chromosome 7 and loss on Chromosome 8p were demonstrated in 2 of the 3 patients. Immunohistochemically, no EGFR positive reaction was found in all cases. Conclusion Detection of genetic alterations is very important in understanding the pathogenesis of PXA.
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Objective To detect the genome-wide genetic alterations in central neurocytoma,and to study the pathogensis of central neurocytoma. Methods Comparative genomic hybridization(CGH) analysis was performed in 10 central neurocytomas. Results Chromosomal imbalances were demonstrated in 6 cases.Overrepresentation of genetic material was detected in 4 cases on Chromosome 2p and 10q,and 3 cases on Chromosome 18q. Conclusion(Genetic abnormalities) on Chromosome 2p,10q and 18q may be associated with the pathogenesis of central neurocytoma.
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Objective To investigate the pathologic appearances,immunohistochemical features,and genetic changes of malignant triton tumor(MTT). Methods One case of MTT was studied pathologically and immunohistochemically,and the related literatures were reviewed. Results A huge mass,demonstrated in the thorax by X ray and CT scan was seen in the posterior mediastinum in the surgery.Histologically,the tumor was composed of spindle cells with significant atypia.Some of the tumor cells had dense eosinophilic cytoplasm.Immunohistochemical staining revealed positive for myoglobin,desmin and S-100 in most of the tumor cells.The pathological diagnosis was MTT of the posterior mediastinum. Conclusion Cases of MTT in the mediastinum are very rare,with less specific clinical and imaging manifestations.The diagnosis is mainly made on the basis of pathological examination and immunohistochemical staining.
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Objective To investigate the pathological features and differential diagnosis of mixed epithelial and stromal tumor of the kidney(MESTK). Methods Three patients with MESTK were studied by light microscopy and immunohistochemistry,and related literatures were reviewed. Results In the three patients,two were females and one was male,with the mean age of 20 years old.Examined grossly,the tumors were well circumscribed and typically composed of multiple cysts and solid areas.Microscopically,the tumors were composed of epithelial and spindle cells,both of the which were well differentiated with no atypia and mitosis of the nuclei.The immunohistochemical staining showed positive for the cytokeratin in the epithelial cells,and Vimentin,SMA,actin,PgR or ER and WT-1 in the spindle cells.No tumor recurrence and metastasis was found in all the three patients by 25 to 29 months of follow up. ConclusionMESTK is an uncommon mixed renal neoplasm with a favorable prognosis.
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Objective To investigate the clinicopathologic features,diagnosis,differential diagnosis and treatment of sclerosing angiomatoid nodular transformation(SANT). Methods The clinical data,pathologic characteristics,immunophenotype and postoperative follow-up of SANT were analysed. Results There were no specific findings in the clinical manifestations of the 4 cases of SANT.Grossly,the cut surface of the masses was gray-white and vague nodularity was observed.Microscopically,it was characterized by the multinodular angiomatoid appearance in a fibrosclerotic stroma.The nodules were composed of slit-like,sinusoid-like vascular spaces and were interspersed with a population of spindly or ovoid cells.It was revealed by immunohistochemistry that the expression of CD34 in some vessels' endothelial cells was positive,and CD8 was negative.While in another vessels' endothelial cells,CD8 was positive and CD34 was negative.The expression of SMA,Actin,Vimentin,Collage IV and CD68 was positive in all of the 4 cases,while that of CD21,Desmin and NSE was negative.No relapse or metastasis was found during the follow-up.Conclusion SANT is a rarely encountered benign lesion of the spleen,which should be distinguished from the malignant tumor of the spleen.The diagnosis counts on the pathologic and immunohistochemical findings.It could be cured by splenectomy with a favourable prognosis.
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Objective To investigate the value of thyroid transcription factor-1(TTF-1) in the diagnosis and biological behavior assessment of hepatocellular carcinoma (HCC). Methods Thirty liver specimens obtained from benign lesions were analysed, among which 25 were hepatic cirrhosis and inflammatory diseases, and the other 5 were adenomas. And there were 176 specimens of liver tumors, among which 142 were HCC (well differentiated, n=12; moderately differentiated, n=57; poorly differentiated, n=73), 17 were intrahepatic cholangiocellular carcinoma (ICC) and the other 17 were liver metastatic carcinoma (MC). The expression of TTF-1 was examined immunohistochemically in the above tissues, and the difference in expression of TTF-1 among different tissues was examined by Fisher's exact test, Kruskal-Wallis test and Spearman rank correlation analysis. Results TTF-1 was significantly expressed in the cytoplasms of all the hepatocytes besides tumors and liver benign lesions. The expression rate of TTF-1 in HCC was 78.9% (112/142), however, TTF-1 was negatively expressed in ICC and MC(P
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Objective To investigate the regulatory effects of tuberculin on growth and apoptosis of liver cancer and lung cancer cell lines. Methods HePG2(liver cancer) and A549(lung cancer) cell lines were treated with TB supernatant(TB-SN) with different concentrations. Cell viability was detected by using LIVE/DEAD Viability/Cytotoxicity cell kits including specific fluorescence primer,and cell apoptosis was detected by Vybrant apoptosis assay. Results After treatment with 5% TB-SN for 5 d,cell apoptosis was significantly increased in HePG2 and A549 cell lines.Cell growth of HePG2 and A549 cell lines was inhibited after treatment with TB-SN. Conclusion Tuberculin can induce cell apoptosis and inhibit cell growth of liver cancer and lung cancer cell lines.
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<p><b>OBJECTIVE</b>To study the genetic alterations of ganglioglioma through the entire genome, and to investigate the pathogenesis of this neoplasm.</p><p><b>METHODS</b>Comparative genomic hybridization was used to provide an overview of genetic abnormalities in gangliogliomas.</p><p><b>RESULTS</b>Five cases of gangliogliomas, including 3 males and 2 females, were studied genetically. Loss of genetic materials on the short arm of chromosome 9(9p) was a common genetic alteration found in 3 of 5 cases. Overrepresentation of chromosome 7 was another recurrent chromosomal imbalance, which was further confirmed by fluorescence in situ hybridization. Immunohistochemical analysis was performed on epidermal growth factor receptor (EGFR), which was located on 7p11-p13. All five cases revealed no abnormal expression of EGFR. On the other hand, genetic imbalances were also involved in multiple chromosomes including 2q33-q34, 8q12-q22, 14q21-qter, 15q26-qter and Y.</p><p><b>CONCLUSION</b>Loss of genetic materials on chromosome 9p and gain on chromosome 7 may be associated with the pathogenesis of this neoplasm.</p>
Subject(s)
Adolescent , Adult , Female , Humans , Male , Brain Neoplasms , Genetics , Metabolism , Chromosome Aberrations , Chromosome Deletion , Chromosomes, Human, Pair 7 , Chromosomes, Human, Pair 9 , Follow-Up Studies , Ganglioglioma , Genetics , Metabolism , In Situ Hybridization, Fluorescence , Nucleic Acid Hybridization , ErbB Receptors , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate global genetic alterations in medulloblastoma, and to localize critical chromosomal loci with allelic imbalances associated with the development of medulloblastoma.</p><p><b>METHODS</b>A high-resolution genome-wide allelotype analysis, including 384 microsatellite markers, was performed in 12 medulloblastomas.</p><p><b>RESULTS</b>An average of 238 (62.3%) allelic imbalances were detected on all 39 autosomal arms. Non-random allelic gains or losses were detected on chromosomes 7q (58.3%), 8p (66.7%), 16q (58.3%), 17p (58.3%) and 17q (66.7%). In addition, chromosomal arms with frequencies of allelic imbalances higher than the mean percentage were identified on 3p (33.3%), 3q (33.3%), 4q (41.7%), 7p (33.3%), 8q (41.7%), 10q (41.7%), 13q (33.3%), 14q (33.3%) and 20q (33.3%). No relationship was found between the frequency of allelic imbalances and the clinical outcome of the patients.</p><p><b>CONCLUSIONS</b>A global view of the genetic alterations in medulloblastoma was provided. The allelic imbalances involving chromosomes 7q, 8p, 16q, 17p and 17q may play an important role in the pathogenesis of medulloblastoma.</p>