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Objective To discuss the proliferation inhibition and apoptosis induction of human pancreatic cancer cell line SW1900 by dauricine and its possible mechanism. Methods The MTT colorimetric method was used to detect the inhibitory effects of cell viability. The apoptosis rate was tested by the Annexin Ⅴ-FITC / PI fluorescent staining of flow cytometric method . The expressions of phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt) and B-cell lymphoma-2 (Bcl-2) were detected by Real-time PCR and Western blotting assay. Results MTT assay showed that dauricine significantly inhibited the proliferation of SW1900 cells and the inhibitory effect was enhanced with the increasing of dauricine concentration, F = 783. 7, P < 0. 001. The apoptosis of 3 groups cells were (4. 34 ± 1. 30) % (0 mg / L dauricine), (14. 94±1. 94) % (6 mg / L dauricine) and (22. 68±3. 61) % (12 mg / L dauricine) . The mean difference was statistically significant among the three groups (F = 58. 52, P < 0. 001) . Dauricine could significantly induce apoptosis human pancreatic cancer cells with dose-dependent manner. Real-time PCR showed that the gene expressions of PI3K, Akt and Bcl-2 were lower obviously (PI3K mRNA, F = 101, P = 0. 01; Akt mRNA, F = 1666, P < 0. 01; Bcl-2 mRNA, F = 753, P<0. 001) with dose-dependent manner. Western blotting assay also showed that the protein expression of PI3K, Akt and Bcl-2 was down-regulated with dose-dependent manner. Conclusion Dauricine has proliferation inhibition and apoptosis inducement effect on human pancreatic cancer cells line SW1900. This function may be concerned with the regulation of PI3K / Akt signal pathway and lower Bcl-2 expression.
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Purpose To study the clinicopathological, immunophynotypic features of pituicytoma and its rare ependymal variant with discussion of its diagnosis and differential diagnosis. Methods 7 cases of pituicytoma, including 6 conventional pituicytomas and 1 ependymal variant tumor, were evaluated by HE staining and immunohistochemistry, and the relevant literatures were reviewed. Results Microscopically, the tumors were composed of closely packed plump spindle cells arranged in short fascicle and storiform pattern in 6 conventional pituicytomas, and whorl and papillary architecture with obvious perivascular rosette formation in the ependymal variant tumor. Immunohistochemically, all tumor cells were diffuse positive for S-100 and TTF-1, but negative for IDH1 R132H, Olig-2, CD34, NF, Syn, CgA, and pituitary hormones. Ki-67 proliferation index was less than 2％ in all cases. GFAP and EMA were only focally positive in conventional pituicytomas, whereas GFAP was diffuse positive in ependymal variant tumor with EMA dot-like staining in more than half of tumor cells. Conclusion Pituicytoma is a rare low grade glioma derived from neurohypophysis. To study helps recognition of extending morphological spectrum of pituicytoma and its new variant, which is important for its differential diagnosis consideration and clinical therapy.
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<p><b>BACKGROUND</b>Her-2/neu gene overexpression has been found in several malignancies, and is associated with poor prognosis; while its role in the tumorigenesis and progression of prostate cancer (PCa) is still controversial. This study aimed to evaluate the prognostic value of Her-2/neu protein expression and clinicopathologic factors in antiandrogen-treated Chinese men with PCa for disease progression and PCa-specific death.</p><p><b>METHODS</b>Her-2/neu protein expression was determined using immunohistochemistry (IHC) in specimens collected from 124 prostate biopsies and transurethral resection of prostate (TURP) from seven prostate cancer patients.</p><p><b>RESULTS</b>Her-2/neu protein expression was 0, 1+, 2+, and 3+ in 40 (30.5%), 8 (6.1%), 67 (51.1%), and 16 (12.2%) cases, respectively. Her-2/neu protein expression showed significant correlation as judged by Gleason score (P = 0.049), clinical tumor-node-metastases (cTNM) stage (P = 0.018) and disease progression (P = 0.001), but did not correlate with prostate-specific antigen (PSA) (P = 0.126) or PCa-specific death (P = 0.585). PSA (P = 0.001), Gleason score (P = 0.017), cTNM (P = 0.000) and Her-2/neu protein expression (P = 0.001) had prognostic value for evaluating the progression of PCa in univariate analysis. In Kaplan-Meier plots, both Gleason score (P = 0.035) and cTNM (P = 0.013) correlated with PCa-specific death. In multivariate analysis, only cTNM was significant for both disease progression (P = 0.001) and PCa-specific death (P = 0.031).</p><p><b>CONCLUSIONS</b>Her-2/neu protein expression is significantly correlated with Gleason score, cTNM and disease progression, although it is not an independent predictor of disease progression and PCa-specific death. cTNM staging serves as an independent prognostic factor for disease progression and PCa-specific death.</p>
Subject(s)
Aged , Aged, 80 and over , Humans , Male , Middle Aged , Disease Progression , Kaplan-Meier Estimate , Prognosis , Prostatic Neoplasms , Metabolism , Mortality , Pathology , Receptor, ErbB-2 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>The progression of prostate cancer (PCa) after endocrine therapy varies widely in different PCa patients. This study aims to analyze the factors that influence the progression-free survival time of PCa patients after endocrine therapy in an attempt to improve the prognosis of the disease.</p><p><b>METHODS</b>We reviewed the clinicopathological data of 116 cases of prostate cancer treated by endocrine therapy, analyzed the clinicopathological factors that influence the progression-free survival time of PCa patients using univariate (log-rank test) and multivariate Cox proportional hazard models, and investigated the correlation among these factors by Spearman rank correlation analysis.</p><p><b>RESULTS</b>In the stepwise Cox proportional hazard model, the independent prognostic factors for PCa progression after endocrine therapy were found to be Gleason score (P < 0.01) and clinical stages (P < 0.01). The hazard of PCa progression after endocrine therapy increased 2.126 times that of the baseline for each unit of increase in Gleason score, and 6.625 times for each unit of increase in the clinical stage. The pretreatment PSA level was correlated with both clinical stages (P < 0.01) and Gleason score (P < 0.01).</p><p><b>CONCLUSION</b>Clinical stages and Gleason score were important factors that influenced the progression-free survival time after endocrine therapy in this cohort of PCa patients.</p>