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    Cancer and cancer stem cells: New molecular perspectives
    (Begell House Inc., 2019) Gurel C.; Inetas G.; Hortu I.; Tunc E.; Kuscu G.C.; Dindaroglu F.C.; Sahin O.; Buhur A.; Oktema G.
    Cancer, which causes the deaths of millions of people, is an important public health problem worldwide. Despite significant advances in the diagnosis and treatment of cancer, survival rates are still insufficient in progressive cancers. Today, one of the most important reasons for not being able to reach the desired level in the fight against progressive cancer types is cancer stem cells (CSCs). The ineffectiveness of conventional therapies on CSCs has made it necessary to investigate the molecular mechanisms and signaling pathways used in the survival, drug resistance, and metastasis of CSCs. In this context, studies investigating the biology of CSCs suggest that lipid metabolism and extracellular vesicles are critical for understanding the stemness and metastasis of these cells. These studies have demonstrated that a number of molecules play a vital role in resistant to apoptosis in CSCs, including the cellular FLICE-inhibitor protein (c-FLIP), which inhibits TRAIL-induced extrinsic apoptosis. Another important output of these studies is the demonstration of the relationship of the cancer microenvironment in terms of epithelial-mesenchymal transition, which CSCs frequently use in the metastasis process. In addition, studies investigating the differences in glycosylation observed in CSCs and investigating cancer vaccines are promisng. These findings will strengthen our aresnal in the fight against cancer. In this article, we summarize current molecular studies on CSCs, an important target in novel cancer therapies. © 2019 Begell House, Inc.
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    Fluvastatin attenuates doxorubicin-induced testicular toxicity in rats by reducing oxidative stress and regulating the blood–testis barrier via mTOR signaling pathway
    (SAGE Publications Ltd, 2019) Gurel C.; Kuscu G.C.; Buhur A.; Dagdeviren M.; Oltulu F.; Karabay Yavasoglu N.U.; Yavasoglu A.
    Doxorubicin (DOX) is an anthracycline derivative antibiotic that still frequently used in the treatment of solid tumors and hematological malignancies. The clinical use of DOX is largely restricted due to acute and chronic renal, cardiac, hematological, and testicular toxicities. Previous studies have indicated that oxidative stress, lipid peroxidation, and apoptosis in germ cells are the main factors in DOX-induced testicular toxicity, but the entire molecular mechanisms that responsible for DOX-induced testicular damage are not yet fully understood. Fluvastatin is a cholesterol-lowering agent that acts by inhibiting hydroxylmethyl glutaryl coenzyme A, the key enzyme for cholesterol biosynthesis. In addition to its cholesterol-lowering effect, fluvastatin showed an antioxidant effect by cleaning hydroxyl and superoxide radicals and this drug could have a protective effect by acting on the mammalian target of rapamycin (mTOR) signal pathway in testicular damage caused by obesity. This study aimed to investigate the possible protective and therapeutic effects of fluvastatin on the DOX-induced testicular toxicity model by histochemical, immunohistochemical, biochemical, and real-time polymerase chain reaction analyses. The present study indicates that fluvastatin may have a protective and therapeutic effect by removing reactive oxygen species and by regulating the mTOR, connexin 43, and matrix metalloproteinase 9 protein and messenger ribonucleic acid expressions, which play an important role in regulating the blood–testis barrier. On the other hand, the use of fluvastatin as a protective/prophylactic agent was found to be more effective than the use of this drug for treatment. In light of this information, fluvastatin may be a candidate agent that can be used to prevent testicular toxicity observed in men receiving DOX treatment. © The Author(s) 2019.