Browsing by Author "Cecener, Gülşah"
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Item Association between the anticancer efficacy of cabazitaxel and toll-like receptor 4 mediating signaling pathways in metastatic castration-resistant prostate cancer cells(SAGE Publications, 2021-07) Güney, Gamze Eskiler; Özkan, Asuman Deveci; Eryılmaz, Işıl Ezgi; Egeli, Ünal; Cecener, Gülşah; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı; https://orcid.org/0000-0002-3316-316X; GWV-3548-2022; 57189380840; 55665145000; 6508156530Background: We evaluated the effect of cabazitaxel (CAB) as a third-line taxane on Toll-like receptor 4 (TLR4)-mediated signaling pathways, especially NF-κB activity, in metastatic castration-resistant prostate cancer (mCRPC) cells. Methods: CAB cytotoxicity was determined by WST-1 assay. To assess the relationship between CAB efficacy and TLR4 signaling pathways, RT-PCR, western blot and immunofluorescence analysis were performed. Additionally, CAB-mediated apoptotic cell death was assessed by Annexin V and RT-PCR analysis. Results: Our results demonstrated that CAB exerted considerably cytotoxic and apoptotic effects on PC-3 mCRPC cells (p < 0.05). CAB treatment altered TLR4 expression level in a dose-dependent manner. Furthermore, 1 nM CAB treatment significantly induced NF-κB activity through p65 nuclear localization and increased the expression level of caspase-3, Bax and p53. Interestingly, total apoptotic cell death and IRF3 protein levels were increased at 5 nM concentration of CAB despite a decrease in the levels of both NF-κB and pro-apoptotic genes. Conclusions: Therefore, NF-κB activity may be a potential target for the efficacy of CAB in mCRPC cells.Item Chromosomal fragile sites and relationship between genetic predisposition to small cell lung cancer(Wiley, 2002) Tuncay, Berrin; Cecener, Gülşah; Engeli, U.; Gözü, Oktay; Karadağ, M.; Özyardımcı, N.; Edward, Ege; Uludağ Üniversitesi/Tıp Fakültesi/Moleküler Biyoloji ve Genetik Anabilim Dalı.; 0000-0002-1619-6680; 0000-0002-3820-424X; ABI-6078-2020; AAP-9988-2020; 23103142200; 6602965754; 6508156530; 6701760348; 6505942273; 6701341320; 8833423400Fragile sites are non-staining gaps and breaks on mammalian chromosomes. Several investigators have pointed out that these sites may act as factors that predispose to specific chromosomal rearrangements that are present in some cancer cases. The expression of common fragile sites induced by aphidicolin (Ape) was evaluated on prometaphase chromosomes obtained from the peripheral blood lymphocytes of 15 patients with lung cancer, 20 of their clinically healthy family members, and 20 age-matched normal controls. As a result of cytogenetic evaluation carried out by the High Resolution Banding (HRB) technique, 1q21, 2q33, 3p14, 7q32, 13q13, 16q23, 17q21, and 22q12 are defined as fragile sites in patients and relatives. The rate of total fragile sites and 2q33, 3p14, and 16q23 are statistically significant in both patients and relatives when compared with the control group. Therefore, our results showed that common fragile sites might be unstable factors in the human genome and they can be used as suitable markers for genetic predisposition to lung cancer.Item Investigation of the genotoxic effect in bone marrow of swiss albino mice exposed long-term to pyrimethamine(Wiley Liss, 2002) Tunca, Berrin; Egeli, U.; Aydemir, Nilüfer Cinkılıç; Cecener, Gülşah; Bilaloğlu, Rahmi; Uludağ Üniversitesi/Tıp Fakültesi/Moleküler Biyoloji ve Genetik Anabilim Dalı.; Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Biyoloji Bölümü; 0000-0002-3595-6286; 0000-0002-3820-424X; 0000-0002-1619-6680; AAH-5296-2021; AAP-9988-2020; ABI-6078-2020; 6602965754; 6701760348; 26533892300; 6508156530; 6505804122In the present study, we investigated the genotoxic effect of pyrimethamine, which is a drug used in the therapy of toxoplasmosis and malaria, in bone marrow cells of Swiss albino mice exposed to three doses (1, 4, 8 mg/kg) of this agent for eight months orally in vivo. We used a chromosome analysis and micronucleus test for evaluation of genotoxic effect. While a statistically significant change was not determined in numerical chromosome abnormalities, structural chromosome aberrations and micronuclei were increased in a dose-dependent manner by cytogenetic and statistical evaluations.Item Long noncoding RNA MALAT1 may be a prognostic biomarker in IDH1/2 wild-type primary glioblastomas(Assoc Basic Medical Sci Federation Bosnia & Herzegovina Sarajevo, 2020) Tezcan, Gülçin; Argadal, Ömer Gökay; Mutlu, Melis; Aksoy, Seçil; Kocaeli, Hasan; Tunca, Berrin; Civan, Muhammet Nafi; Egeli, Ünal; Cecener, Gülşah; Bekar, Ahmet; Taşkapılıoğlu, M. Özgür; Tekin, Çağla; Tezcan, Gülçin; Tolunay, Şahine; BursaUludağ Üniversitesi/Tıp Fakültesi/Nöroşirürji Anabilim Dalı.; 0000-0002-3760-9755; 0000-0002-1619-6680; 0000-0001-7904-883X; 0000-0002-3820-424X; 0000-0001-5472-9065; FPB-0403-2022; CCA-2925-2022; FDK-3229-2022; CMP-5265-2022; CGB-7869-2022; GDC-6329-2022; AAH-3843-2020; AAI-1612-2021; 57214765002; 57212065763; 57193933334; 6603500567; 6602965754; 57214763395; 55665145000; 6508156530; 6603677218; 25936798300; 57214764024; 25650627600Primary glioblastoma (GB) is the most aggressive type of brain tumors. While mutations in isocitrate dehydrogenase (IDH) genes are frequent in secondary GBs and correlate with a better prognosis, most primary GBs are IDH wild-type. Recent studies have shown that the long noncoding RNA metastasis associated lung adenocarcinoma transcript-1 (MALAT1) is associated with aggressive tumor phenotypes in different cancers. Our aim was to clarify the prognostic significance of MALAT1 in IDH1/2 wild-type primary GB tumors. We analyzed IDH1/2 mutation status in 75 patients with primary GB by DNA sequencing. The expression of MALAT1 was detected in the 75 primary GB tissues and 5 normal brain tissues using reverse transcription quantitative PCR (RT-qPCR). The associations between MALAT1 expression, IDH1/2 mutation status, and clinicopathological variables of patients were determined. IDH1 (R132H) mutation was observed in 5/75 primary GBs. IDH2 (R172H) mutation was not detected in any of our cases. MALAT1 expression was significantly upregulated in primary GB vs. normal brain tissues (p = 0.025). Increased MALAT1 expression in IDH1/2 wild-type primary GBs correlated with patient age and tumor localization (p = 0.032 and p = 0.025, respectively). A multivariate analysis showed that high MALAT1 expression was an unfavorable prognostic factor for overall survival (p = 0.034) in IDH1/2 wild-type primary GBs. High MALAT1 expression may have a prognostic role in primary GBs independent of IDH mutations.Item Olea europaea leaf extract and bevacizumab synergistically exhibit beneficial efficacy upon human glioblastoma cancer stem cells through reducing angiogenesis and invasion in vitro(Elsevier, 2017-04-10) Tezcan, Gülçin; Taşkapılıoğlu, Mevlut Özgür; Tunca, Berrin; Bekar, Ahmet; Demirci, Hilal; Kocaeli, Hasan; Aksoy, Seçil Ak; Egeli, Ünal; Cecener, Gülşah; Tolunay, Şahsine; Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Nöroşirürji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Patoloji Anabilim Dalı.; 0000-0001-5472-9065; 0000-0002-1619-6680; 0000-0002-3820-424X; 0000-0002-5956-8755; 0000-0001-7904-883X; AAI-1612-2021; AAH-1420-2021; ABB-8161-2020; AAH-3843-2020; AAW-5254-2020; ABI-6078-2020; AAP-9988-2020; 25650627600; 25936798300; 6602965754; 6603677218; 57193932262; 6603500567; 57193933334; 55665145000; 6508156530; 6602604390Patients with glioblastoma multiforme (GBM) that are cancer stem-cell-positive (GSC [+]) essentially cannot benefit from anti-angiogenic or anti-invasive therapy. In the present study, the potential anti-angiogenic and anti-invasive effects of Olea europaea (olive) leaf extract (OLE) were tested using GSC (+) tumours. OLE (2 mg/mL) caused a significant reduction in tumour weight, vascularisation, invasiveness and migration (p = 0.0001, p < 0.001, p = 0.004; respectively) that was associated with reducing the expression of VEGFA, MMP-2 and MMP-9. This effect was synergistically increased in combination with bevacizumab. Therefore, our current findings may contribute to research on drugs that inhibit the invasiveness of GBM.Item Pediatrik vakalarda philadelphia benzeri akut lenfoblastik lösemi(Bursa Uludağ Üniversitesi, 2020-12-11) Erdem, Ecem Efendi; Cecener, Gülşah; Tezcan, Havva; Evim, Melike Sezgin; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Çocuk Sağlığı ve Hastalıkları Anabilim Dalı/Çocuk Hematoloji ve Onkolojisi Bilim Dalı.; 0000-0001-9003-8755; 0000-0002-3820-424X; 0000-0002-0910-4258; 0000-0002-4792-269XLösemi, hematopoietik hücrelerin malign transformasyonu sonucu gelişen, heterojen neoplastik hastalıklar grubudur. Philadelphia (Ph) benzeri akut lenfoblastik lösemi (ALL), yüksek risk sınıflamasında yer alan ve kötü prognoz gösteren B- hücreli akut lenfoblastik löseminin (B-ALL) alt grubudur. Gen ekspresyon profili olarak Ph pozitif ALL’ye benzemektedir, ancak bu alt tipte BCR ABL1 füzyonu mevcut değildir. Hastalık genetik olarak heterojendir. Ayrıca, etnik kökenleri farklı olan Ph benzeri ALL vakalarının genetik değişimleri de farklılık göstermektedir. Ph benzeri ALL vakalarının B-ALL’li hastalar arasından ayırt edilerek sınıflandırılabilmesi etkin tedavi almaları için önemlidir. Son yıllarda, Ph benzeri ALL alt grubuna ait vakaların tanımlanması için, B-ALL vakalarında genetik ve klinik bulgular değerlendirilmesinin yanı sıra, gen ifade farklılıklarının analiz edildiği panellerin tasarlanması gündemdedir.