Browsing by Author "Özcan S.S."

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    Adropin and MOTS-c as new peptides: Do levels change in neurodegenerative diseases and ischemic stroke?
    (John Wiley and Sons Inc, 2023) Saçmacı H.; Çakır M.; Özcan S.S.
    Background: Neurological diseases such as Alzheimer's disease and Parkinson's disease (AD, PD), acute ischemic stroke (AIS), and multiple sclerosis (MS) are thought to be deeply affected by changes in the pathophysiological processes of neurons. As new peptides, it was aimed to evaluate the level of adropin and MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) and its possible relationship with NSE (neuron-specific enolase) and NF-L (neurofilament light chain) in terms of neuronal interaction. Methods: This study was conducted with 32 patients from each subgroup and group-appropriate controls. Disease identifiers and hemogram/biochemical parameters specific to the groups of participants were obtained. Additionally, plasma adropin, MOTS-c, NSE, and NF-L levels were evaluated by the ELISA method. Results: Plasma adropin levels were decreased in the AD group and decreased in MOTS-c, AIS, and AD groups compared to the control (p < 0.05). Similar values were found in the MS group compared to its control (p > 0.05). In correlation analysis of these markers with laboratory parameters, while platelet and cholesterol levels were negatively correlated with adropin levels; platelet, lymphocyte, and triglyceride levels were positively correlated with MOTS-c (p < 0.05). Conclusion: This study provides new information about adropin may be potentially important markers in AD and MOTS-C in AIS and AD. Future studies are needed to examine the relationship between changes in metabolic profiles and these peptides. © 2022 Wiley Periodicals LLC.
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    Transcriptomic analysis of plasma exosomes provides molecular information of response to cabazitaxel treatment in men with metastatic castration-resistant prostate cancer
    (John Wiley and Sons Inc, 2023) Vardaki I.; Özcan S.S.; Fonseca P.; Lin S.-H.; Logothetis C.J.; Yachnin J.; Ullen A.; Panaretakis T.
    Background: Prostate cancer is the second most common cancer type and the second most common cancer-related cause of death in men. Cabazitaxel, a next-generation taxane, shows favorable toxicity profile and is effective in docetaxel-resistant tumors. Despite initial responses, in most cases, prostate cancer patients acquire resistance to cabazitaxel. There is a need to identify molecular markers that can monitor and predict treatment response. Methods: We performed transcriptional exosome profiling (Human Transcriptome Array-HTA 2.0) from the plasma of 19 patients with castration-resistant prostate cancer at baseline and in patients after one cycle of cabazitaxel (C1). The patients were stratified in two groups (responders and nonresponders) according to their clinical response to cabazitaxel. Gene set enrichment analysis and ingenuity pathway analysis platforms were used for gene and pathway analysis. Results: We detected molecular differences in the exosomes from two groups of patients (nonresponders vs. responders) at baseline in pathways related to prostate cancer, oncogenic signaling, cytoskeleton, and immune system. In nonresponders, we found enrichment of cytoskeleton related gene (Stathmin-1 and ITSN1) that have been associated with resistance to cabazitaxel. Monitoring of exosomal transcripts after the first cycle of treatment revealed changes in pathways associated with response to treatment. Conclusions: Sequential transcriptional profiling of plasma-derived exosomes reveals differential expression of genes that may reflect resistance to cabazitaxel treatment and therapy response. © 2023 Wiley Periodicals LLC.