Breast carcinoma comprises a group of diseases with specific clinical, histopathologic and molecular properties. Traditional classification use morphology to divide tumors into separate categories with differing behavior and prognosis. However, there are limitations of traditional classification systems, and new molecular methods are expected to improve classification systems. Molecular subtypes of breast carcinomas have been characterized in the last 11 years, and have been studied extensively. Much of the information accumulated in recent years, and molecular taxonomy seems to be still developing and undergoing change. The main question is whether new molecular techniques such as gene expression profiling will be accepted as gold standard in determining breast cancer subtypes, and whether molecular classification is useful in specific subtypes of breast cancer as it is in ductal carcinoma (nonspecific type). In addition, critical review of the literature reveals major problems such as poor definition, lack of reproducibility and lack of quality control in current molecular techniques and classifications. Therefore, current molecular approaches are not yet used in routine clinical practice and treatment guidance since they are immature and can even lead to incorrect assessment.
VMEs into the PA and Ao beyond the VAJ are relatively common. It seems that their mere presence does not predispose to OT VTs. There are probably intrinsic arrhythmogenic properties in tissues specific to these regions in those patients who develop OT VTs.
Background/Aims: To evaluate the protective effects of acetyl L-carnitine (ALCAR) on cisplatin-induced nephrotoxicity in rats, and to gain insights into the possible protective mechanisms of ALCAR against nephrotoxicity. Methods: Twenty-eight Wistar rats were divided into four groups. Group 1 was administered saline only, group 2 was administered ALCAR, group 3 was administered cisplatin, and group 4 was administered ALCAR prior to cisplatin. Rats were sacrificed after 72 h of cisplatin/saline infusion. Serum creatinine and glomerular filtration rate values were obtained, and kidney samples were examined by light and electron microscopy. Apoptotic cell death and caspase-3, 8 and 9 activities were studied immunohistochemically. Results: In group 4, ALCAR administration resulted in an improvement in kidney function tests. Histopathological findings confirmed the biochemical data. Whilst the fusion of the foot processes of podocytes was observed in group 3, they were intact in group 4 on electron-microscopic examination. Apoptotic cell death and caspase-3, 8 and 9 activities were also decreased in group 4 compared to group 3. Conclusions: Antioxidative, antiapoptotic and anti-inflammatory properties of ALCAR were supported by the findings that this agent improves kidney function tests and has the effects of tissue protection and inhibition of apoptosis in cisplatin-induced nephrotoxicity.
Protective mechanisms of aceytl-L-carnitine against cisplatin induced apoptosis, mainly due to activation of anti-apoptotic Bcl family members' genes, and in an Akt-related gene expression dependent manner. This is the first study to indicate that acetyl-L-carnitine can be an effective agent against cisplatin ototoxicity in auditory cells, with induction of anti-apoptotic gene expression and attenuating levels of pro-inflammatory cytokines.
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