Int J Clin Exp Patho
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Int J Clin Exp Patho · Jan 2012
ReviewRole of epigenetic alterations in the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma.
Barrett's esophagus, a pre-malignant condition that can lead to esophageal adenocarcinoma, is characterized by histological changes in the normal squamous epithelium of the esophagus. Numerous molecular changes occur during the multistage conversion of Barrett's metaplasia to dysplasia and frank adenocarcinoma. Epigenetic changes, especially changes in DNA methylation are widespread during this process. ⋯ We also show that genome wide analysis of methylation surprisingly reveals that global hypomethylation and not hypermethylation is the dominant change during Barrett's metaplasia. The transformation of Barrett's esophagus to frank adenocarcinoma is in turn characterized by much smaller wave of selective promoter hypermethylation. These studies reveal many novel, potential targets for new therapies and illustrate the utility of incorporating these epigenetic changes as biomarkers during endoscopic surveillance interval for patients with Barrett's esophagus.
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Int J Clin Exp Patho · Jan 2012
Case ReportsTumor-to-tumor metastasis: pathology and neuroimaging considerations.
The phenomenon of tumor-to-tumor metastasis has been reported in the literature for over a century. However, it remains fairly uncommon, with fewer than 100 cases being described during that time. Virtually any benign or malignant tumor can be a recipient, but meningiomas have been implicated as the most common intracranial neoplasm to harbor metastasis. ⋯ In addition, we report two cases of metastatic prostate adenocarcinoma to a meningioma; to date of which only three cases have been published. The terms "tumor-to-tumor metastasis" and "collision tumor" are addressed, as are details of the pathology. The limitations of standard radiological imaging techniques, such as standard CT and MR, which cannot reliably identify the presence of metastasis within a meningioma are compared with physiology-based neuroimaging methods, such as perfusion MR and MR spectroscopy, which may be more useful in noninvasively differentiating tumor histology.
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Int J Clin Exp Patho · Jan 2012
The cell death of C6 astrocytoma cells induced by oridonin and its mechanism.
Many studies have shown that oridonin, a compound purified from Rabdosia rubescens, was able to suppress proliferation and induce apoptosis in many cell types. In this study, In order to investigate the proliferation suppression and apoptosis-inducing effect of oridonin on Rat C6 astrocytoma cells, we treated C6 cells with different concentrations of oridonin for various time intervals. Oridonin concentration-time viability curve were used to test the effect of oridonin on the C6 cells. ⋯ Hochest 33258 staining and flow cytometry revealed that oridonin induced apoptosis and arrested the entry into G2/M phase of C6 cells. According to the results of Western blot, oridonin down-regulated Bcl-2, up-regulated Bax protein, and activated caspase-3 in the oridonin-treated C6 cells. All together, our results suggested that oridonin can cause the suppression of proliferation in C6 astrocytoma cells and the cell death induced by oridonin might be associated with mitochondria- mediated apoptosis by activating caspase-3.
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Int J Clin Exp Patho · Jan 2012
Idiopathic pulmonary fibrosis: immunohistochemical analysis provides fresh insights into lung tissue remodelling with implications for novel prognostic markers.
This study explored the cellular and biological interrelationships involved in Idiopathic Pulmonary Fibrosis (IPF) lung tissue remodelling using immunohistochemical analysis. ⋯ The pathogenesis of IPF is complex and involves multiple factors, possibly including EMT. Histological analysis suggests TGF-β-stimulated myofib rob lasts initiate a contractile response within established fibroblastic foci while proliferating ATII cells attempt to instigate alveolar epithelium repair. Marker expression (N-cadherin and Ki-67) correlation with histological disease activity (as reflected by fibroblastic foci extent) may emerge as future prognostic indicators for IPF.
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Int J Clin Exp Patho · Jan 2012
Down-regulation of GAP-43 by inhibition of caspases-3 in a rat model of neuropathic pain.
Neuropathic pain remains a prevalent and persistent clinical problem due to incomplete understanding of its pathogenesis. ⋯ Caspase-3 mediated neuron apoptosis is probably responsible for the neuropathic pain in CCI rats. Inhibition of caspase-3 may serve as a treatment of neuropathic pain.