WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7150

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  • Article
    Citation - WoS: 139
    Granulocytic Sarcoma: a Systematic Review
    (e-Century Publishing Corporation, 2013) Yılmaz, Asu Fergün; Saydam, Güray; Şahin, Fahri; Baran, Yusuf
    Granulocytic sarcoma also called myeloid sarcoma is an extramedullary tumor of immature granulocytic cells. It is a rare entity, and mostly accompanied by acute myeloid leukemia. It is observed during the course of myeloproliferative disorders especially in chronic myeloid leukemia and myelodysplastic syndromes. In some rare circumstances, it is detected before clinical signs of leukemia or other diseases. When the bone marrow biopsy reveals no other hematologic malignancies, the granulocytic sarcoma is described as nonleukemic, primary or isolated. It is observed at any part of the body but the most common locations are soft tissues, bone, peritoneum and lymph nodes. Presenting signs or symptoms are mainly due to mass effect of the tumor and dysfunction of the organ, or the tissue that is affected. The diagnosis is performed by biopsy of the tumor. The tumor consists of immature granulocytic cells, which could be documented by H&E, immunohistochemistry, and flow cytometric methods. Fluorescence in-situ hybridization and molecular analysis are also performed. The optimal time and type of treatment is not clear. Surgery could be an option especially for tumors, which cause organ dysfunction and/or obstruction. Systemic treatment should be considered in all patients because without systemic treatment, relapses and progression to acute myeloid leukemia is the ultimate fate of the disease in many cases. Cytarabine-containing remission-induction chemotherapies have been the most applied therapeutic strategies, but it is not clear whether the consolidation therapies are required or not, and what kind of regimens are appropriate. The role of hematopoietic stem cell transplantation (HSC) as a consolidation regimen is not clear, but, after the relapse of the disease with or without bone marrow involvement, HSC transplantation should be considered in suitable patients after the reinduction performed by AML chemotherapies. There is only limited data about the role of radiotherapy in these patients. It could be used in patients with relapsed disease, organ dysfunction which should be quickly relieved and inadequate response to chemotherapy. The effect of radiotherapy on overall survival is not known. New prospective studies and clinical trials are needed to generate guidelines for the treatment of primary granulocytic sarcomas.
  • Article
    Citation - WoS: 15
    Changes in Molecular Biology of Chronic Myeloid Leukemia in Tyrosine Kinase Inhibitor Era
    (e-Century Publishing Corporation, 2013) Cömert, Melda; Baran, Yusuf; Saydam, Güray
    Chronic myeloid leukemia (CML) is a clonal myeloproliferative disease characterized by a reciprocal translocation between long arms of chromosomes 9 and 22 t(9; 22) that generates the BCR-ABL fusion gene. If left untreated, newly diagnosed chronic phase CML patients finally progress to accelerated and blastic phase. After the introduction of tyrosine kinase inhibitors (TKIs), treatment strategies of CML changed dramatically. However, the development of resistance to TKIs started to create problems over time. In this review, the current information about CML biology before and after imatinib mesylate treatment is summarized.
  • Conference Object
  • Conference Object
    Therapeutic Potential of Targeting Sphingolipid Signaling Pathways in Various Types of Cancers
    (Pergamon-elsevier Science Ltd, 2010) Baran, Y.; Bassoy, E. Y.; Cakir, Z.; Camgoz, A.; Gencer, E. B.; Kartal, M.; Gucluler, G.
  • Article
    Citation - WoS: 1
    Investigation of Potential Anticarcinogenic Effects of Corilagin in Lung Cancer Cells
    (Marmara Üniversitesi, 2019) Rencüzoğulları, Çağla; Çinçin, Zeynep Birsu; İplik, Elif Sinem; Baran, Yusuf; Çakmakoğlu, Bedia
    Objective: Lung cancer (LC) is the most extensive reason of cancer associated deaths in men and women in the world. LC categorizes into two main groups due to their molecular clinicopathological features and therapeutic responses. Non-small cell lung cancer (NSCLC) is the main subgroup that consists of nearly 85% of all lung cancer types. Corilagin, a biologically active ellagitannin, could be extracted from Phyllanthus species which are known as Chinese medicinal plant. It has been recently shown that Corilagin could exert anti-inflammatuar and antioxidative effects in different experimental cancer models. However, the molecular effects of Corilagin in NSCLC remain unclear. Methods: In this study, the antiproliferative and apoptotic effects of Corilagin were identified by WST-1 cell proliferation test, caspase-3 and mitochondrial membrane potential (MMP). Results: We found that Corilagin significiantly suppressed the proliferation of NSCLC cells. Furthermore, we also showed that Corilagin could contribute apoptosis by inducing activity of caspase-3 molecule and loss of MMP. Conclusion: Taken together, our study first showed that Corilagin could be a new treatment method for NSCLC after verifying its effects with in vivo and clinical studies.
  • Article
    Citation - WoS: 7
    Citation - Scopus: 8
    Mir-17 in Imatinib Resistance and Response To Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia Cells
    (Zerbinis Medical Publications, 2013) Fıratlıgil, Burcu; Biray Avcı, Çığır; Baran, Yusuf
    In this study we examined the expression levels of miR-17 which possesses oncogenic activities through downregulation of CDKN1A, p21 and E2F1 tumor suppressor genes, in imatinib sensitive and resistant chronic myeloid leukemia (CML) cells. On the other hand, we also determined the expression levels of miR-17 in response to tyrosine kinase inhibitors imatinib, nilotinib and dasatinib used for the treatment of CML. Methods: The expression profiles of miR-17 were analysed by Stem-Loop reverse transcription (RT) polymerase chain reaction (PCR). Results: The results revealed significant increase in the expression levels of miR-17 in imatinib sensitive and resistant cells compared to peripheral blood mononuclear cells (PBMCs). On the other hand, significant decrease was observed in miR-17 levels in response to imatinib, nilotinib and dasatinib. Conclusion: These results may imply that miR-17 can be used for diagnosis and treatment of CML.
  • Article
    Citation - WoS: 5
    Citation - Scopus: 7
    The Roles of Antiapoptotic Sphingosine Kinase-1 and Glucosylceramide Genes in Drug Induced Cell Death of Mcf-7 Breast Cancer Cells
    (Zerbinis Medical Publications, 2011) Güçlüler, Gözde; Pişkin, Özden; Baran, Yusuf
    Purpose: Sphingolipids are important signaling molecules mediating cell survival, proliferation, cell cycle regulation and apoptosis. Ceramide is the most vital sphingolipid which induces growth arrest, senescence, and apoptosis. In this study, we aimed to determine the roles of sphingosine kinase- 1 (SK-1) and glucosylceramide synthase (GCS) genes in paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel induced apoptosis in human MCF-7 breast cancer cells. Methods: IC50 values (drug concentration inhibiting cell growth by 50%) of the anticancer agents were calculated using XTT cell proliferation assay. Changes in mitochondrial membrane potential (MMP) were determined using JC-1 assay kit. Changes in the mRNA levels of SK-1 and GCS genes were measured by using RT-PCR technique. Results: The results demonstrated significant decrease in cellular proliferation and increase in loss of MMP in a dose-dependent manner. Paclitaxel, doxorubicin, tamoxifen, cyclophosphamide and docetaxel application downregulated SK-1 expression while paclitaxel, tamoxifen, cyclophosphamide and docetaxel but not doxorubicin downregulated GCS comparing to untreated control cells. Conclusion: These results show for the first time that these agents induce apoptosis in MCF-7 cells by downregulating the antiapoptotic SK-1 and GCS genes that may result in accumulation of apoptotic ceramides. © 2011 Zerbinis Medical Publications.