Adenomyoepithelioma of the breast with late pulmonary metastases - case report and review of the literature.

BACKGROUND: Adenomyoepithelioma (AME) of the breast is a rare tumour of unpredictable clinical behaviour. Most of the tumours are benign with some giving local recurrences or distant metastases. CASE PRESENTATION: We report a case of late lung metastases in a woman with a history of breast adenomyoepithelioma. Partial lobectomy was performed for lung lesions and initial diagnosis was epithelial-myoepithelial carcinoma. CONCLUSION: Careful slide's revision of both breast and pulmonary lesions showed identical microscopic appearance with lung tumour performing more malignant features. Tumour cells in both: breast and pulmonary lesions were positive for cytokeratin and EMA (epithelial cells) and also for SMA, S100 and vimentin (myoepithelial cells). Two years and 7 months follow-up showed no recurrent neoplastic disease in our patient.

Oxidative Stress and Liver Morphology in Experimental Cyclosporine A-Induced Hepatotoxicity.

Cyclosporine A is an immunosuppressive drug used after organ's transplantation. The adverse effects on such organs as kidney or liver may limit its use. Oxidative stress is proposed as one of the mechanisms of organs injury. The study was designed to elucidate CsA-induced changes in liver function, morphology, oxidative stress parameters, and mitochondria in rat's hepatocytes. Male Wistar rats were used: group A (control) receiving physiological saline, group B cyclosporine A in a dose of 15 mg/kg/day subcutaneously, and group C the CsA-vehicle (olive oil). On the 28th day rats were anesthetized. The following biochemical changes were observed in CsA-treated animals: increased levels of ALT, AST, and bilirubin in the serum, statistically significant changes in oxidative stress parameters, and lipid peroxidation products in the liver supernatants: MDA+4HAE, GSH, GSSG, caspase 3 activity, and ADP/ATP, NAD(+)/NADH, and NADP(+)/NADPH ratios. Microscopy of the liver revealed congestion, sinusoidal dilatation, and focal hepatocytes necrosis with mononuclear cell infiltration. Electron microscope revealed marked mitochondrial damage. Biochemical studies indicated that CsA treatment impairs liver function and triggers oxidative stress and redox imbalance in rats hepatocytes. Changes of oxidative stress markers parallel with mitochondrial damage suggest that these mechanisms play a crucial role in the course of CsA hepatotoxicity.