8 results on '"Ozgenc I"'
Search Results
2. Geochemical constraints on petrogenesis of Late Cretaceous alkaline magmatism in east-central Anatolia (Hasancelebi–Basören, Malatya), Turkey
- Author
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Ozgenc, I. and Ilbeyli, N.
- Published
- 2009
- Full Text
- View/download PDF
3. Carbonatite-hosted fluorite and britholite mineralization at Sofular area, Malatya, Turkey
- Author
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Ozgenc, I
- Abstract
The Sofular carbonatite complex is located approximately 670 km of capital Ankara, within the easternmost part of Anatolide-Tauride platform and consists of Upper Cretaceous to Lower Paleocene carbonatite ring dikes and a number of alkali syenitic intrusions which were emplaced into autochtonous carbonates of Tauride. Carbonatite represents the last stage of alkali intrusions and: was responsible for the fenitization of syenites and deposition of small quantities of fluorite (30,000 tons of 52% CaF2) and britholite (1000 tons of:57.73% RE2O3; 2.68% ThO2 and 2.49% Y2O3). Mineralization occurs as veins in calcite carbonatite and alkali syenitic fenite. Fluid inclusions in fluorite indicate high temperature-high salinity (460 degrees C and 40 wt% NaCl equiv.) ore fluid exolved from carbonatite magma which was generated by postcollisional lithospheric attenuation.
- Published
- 1999
4. Geochemical constraints on petrogenesis of Late Cretaceous alkaline magmatism in east-central Anatolia (Hasancelebi–Basören, Malatya), Turkey
- Author
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Ozgenc, I., primary and Ilbeyli, N., additional
- Published
- 2008
- Full Text
- View/download PDF
5. Prostate Cancer Awareness in the Middle East: A Cross-Sectional International Study.
- Author
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Sayan M, Eren AA, Tuac Y, Langoe A, Alali B, Aynaci O, Mohammadipour S, Vahedi F, Daneshmand B, Abbas W, Hawsawi Y, Nader T, Joseph J, Wahby R, Ozgenc I, Mula-Hussain L, Moningi S, Orio PF, Atalar B, and Eren MF
- Subjects
- Humans, Male, Cross-Sectional Studies, Middle East epidemiology, Middle Aged, Adult, Surveys and Questionnaires, Aged, Early Detection of Cancer psychology, Prostatic Neoplasms epidemiology, Prostatic Neoplasms diagnosis, Prostatic Neoplasms psychology, Health Knowledge, Attitudes, Practice
- Abstract
Purpose: Prostate cancer has emerged as a significant public health challenge in the Middle East, characterized by rising incidence rates and a concerning mortality-to-incidence ratio. Yet, despite these alarming trends, data regarding prostate cancer awareness in the region remain limited. To address this critical knowledge gap, this study investigates prostate cancer awareness within the Middle East., Materials and Methods: A cross-sectional survey was performed among 5,913 men age 40 years and older across 14 Middle Eastern countries between January 1, 2022, and July 31, 2023. Excluding those with a history of prostate cancer, a validated questionnaire assessed prostate cancer awareness. Data were analyzed using frequencies and percentages for categorical variables, medians and ranges for continuous variables, and Pearson chi-square analysis for relationships between education levels and awareness of prostate cancer., Results: The survey achieved a 74.9% response rate, with 4,431 male participants. Regarding prostate cancer awareness, 83.8% of participants had heard of the disease. However, only 31.0% correctly identified it as the most common malignancy in men, and 21.8% believed it affects both sex. Awareness of screening was limited, with just 19.1% recognizing the prostate-specific antigen test's role. Additionally, participants had a pessimistic view, with a mean perception that 75% of patients with prostate cancer die from the disease, rather than from other causes. Higher education levels were associated with significantly increased awareness of prostate cancer ( P < .001)., Conclusion: This study reveals that while general awareness of the disease exists, crucial knowledge deficits regarding risk factors, screening, and prognosis are evident. Addressing these knowledge gaps through culturally tailored education may improve early detection rates, treatment outcomes, and ultimately reduce the burden of prostate cancer in the Middle East.
- Published
- 2024
- Full Text
- View/download PDF
6. Activation of Tumor-Cell STING Primes NK-Cell Therapy.
- Author
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Knelson EH, Ivanova EV, Tarannum M, Campisi M, Lizotte PH, Booker MA, Ozgenc I, Noureddine M, Meisenheimer B, Chen M, Piel B, Spicer N, Obua B, Messier CM, Shannon E, Mahadevan NR, Tani T, Schol PJ, Lee-Hassett AM, Zlota A, Vo HV, Ha M, Bertram AA, Han S, Thai TC, Gustafson CE, Venugopal K, Haggerty TJ, Albertson TP, Hartley AV, Eser PO, Li ZH, Cañadas I, Vivero M, De Rienzo A, Richards WG, Abu-Yousif AO, Appleman VA, Gregory RC, Parent A, Lineberry N, Smith EL, Jänne PA, Miret JJ, Tolstorukov MY, Romee R, Paweletz CP, Bueno R, and Barbie DA
- Subjects
- Cell Line, Tumor, Cell- and Tissue-Based Therapy, Humans, Receptors, Chimeric Antigen, Immunotherapy, Adoptive, Killer Cells, Natural, Membrane Proteins agonists, Mesothelioma, Malignant
- Abstract
Activation of the stimulator of interferon genes (STING) pathway promotes antitumor immunity but STING agonists have yet to achieve clinical success. Increased understanding of the mechanism of action of STING agonists in human tumors is key to developing therapeutic combinations that activate effective innate antitumor immunity. Here, we report that malignant pleural mesothelioma cells robustly express STING and are responsive to STING agonist treatment ex vivo. Using dynamic single-cell RNA sequencing of explants treated with a STING agonist, we observed CXCR3 chemokine activation primarily in tumor cells and cancer-associated fibroblasts, as well as T-cell cytotoxicity. In contrast, primary natural killer (NK) cells resisted STING agonist-induced cytotoxicity. STING agonists enhanced migration and killing of NK cells and mesothelin-targeted chimeric antigen receptor (CAR)-NK cells, improving therapeutic activity in patient-derived organotypic tumor spheroids. These studies reveal the fundamental importance of using human tumor samples to assess innate and cellular immune therapies. By functionally profiling mesothelioma tumor explants with elevated STING expression in tumor cells, we uncovered distinct consequences of STING agonist treatment in humans that support testing combining STING agonists with NK and CAR-NK cell therapies., (©2022 American Association for Cancer Research.)
- Published
- 2022
- Full Text
- View/download PDF
7. Integrating CD4 + T cell help for therapeutic cancer vaccination in a preclinical head and neck cancer model.
- Author
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Shibata H, Xu N, Saito S, Zhou L, Ozgenc I, Webb J, Fu C, Zolkind P, Egloff AM, and Uppaluri R
- Subjects
- Animals, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Histocompatibility Antigens Class II, Mice, Vaccination, Cancer Vaccines, Head and Neck Neoplasms therapy
- Abstract
Head and neck squamous cell carcinomas (HNSCC) are well suited for cancer vaccination strategies. In addition to tumor-associated antigens (TAAs) and endogenous retrovirus (ERV) encoded proteins, HNSCCs have a relatively high tumor mutational burden encoding potential neoepitopes. Peptide vaccine candidates are prioritized by predicted high-affinity to major histocompatibility complex (MHC) class I with MHC-II affinity largely not being considered. Herein, we extend previous studies to evaluate therapeutic vaccination in the mouse oral cancer (MOC) 22 model. Two distinct MOC22 derived SLPs were tested - a TSA-oriented mutant intercellular adhesion molecule 1 (mICAM1) and p15E, an ERV encoded antigen. In silico prediction revealed mICAM1 SLP bore strong MHC-I and MHC-II epitopes sharing a mutant residue with vaccination significantly increasing both antigen-specific IFN-γ producing CD4
+ and CD8+ T cells. By contrast, p15E SLP had a predicted high-affinity MHC-I epitope but lacked an MHC-II epitope and vaccination induced antigen-specific CD8+ but not CD4+ T cell responses. Therapeutic mICAM1 vaccination attenuated tumor growth effectively with mICAM1-specific T cells displaying durable IFN-γ production compared with p15E SLP. Furthermore, mICAM1 SLPs carrying weakened MHC-II binding epitopes were unable to control tumor growth. These data underscore the potential value of therapeutic targeting of HNSCC epitopes and highlight the importance of studying distinct antigen classes in this setting. Moreover, they raise the possibility that, at least in part, CD4+ T cell help is critical for cancer vaccination in this preclinical HNSCC model and suggest in silico prediction approaches prioritize overlapping MHC-I and MHC-II epitopes to generate potent cancer vaccines., Competing Interests: RU serves on a Merck scientific advisory board. The MOC models developed by RU have been filed with the Washington University Office of Technology Management and are currently licensed for distribution by Kerafast., (© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.)- Published
- 2021
- Full Text
- View/download PDF
8. Yap1 Mediates Trametinib Resistance in Head and Neck Squamous Cell Carcinomas.
- Author
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Mudianto T, Campbell KM, Webb J, Zolkind P, Skidmore ZL, Riley R, Barnell EK, Ozgenc I, Giri T, Dunn GP, Adkins DR, Griffith M, Egloff AM, Griffith OL, and Uppaluri R
- Subjects
- Animals, Biopsy, Cell Line, Tumor, Female, Gene Expression Regulation, Neoplastic, Gene Knockout Techniques, Head and Neck Neoplasms genetics, Head and Neck Neoplasms pathology, Hippo Signaling Pathway genetics, Humans, MAP Kinase Signaling System genetics, Mice, Pyridones therapeutic use, Pyrimidinones therapeutic use, RNA-Seq, Squamous Cell Carcinoma of Head and Neck genetics, Squamous Cell Carcinoma of Head and Neck pathology, Exome Sequencing, Xenograft Model Antitumor Assays, YAP-Signaling Proteins genetics, Drug Resistance, Neoplasm genetics, Head and Neck Neoplasms drug therapy, Pyridones pharmacology, Pyrimidinones pharmacology, Squamous Cell Carcinoma of Head and Neck drug therapy, YAP-Signaling Proteins metabolism
- Abstract
Purpose: In a head and neck squamous cell carcinoma (HNSCC) "window of opportunity" clinical trial, we reported that trametinib reduced MEK-Erk1/2 activation and resulted in tumor responses in a subset of patients. Here, we investigated resistance to trametinib and molecular correlates in HNSCC cell lines and patient samples., Experimental Design: HNSCC cell lines were treated with trametinib to generate resistant lines. Candidate bypass pathways were assessed using immunoblotting, CRISPR knockout, and survival assays. Effectiveness of combined trametinib and verteporfin targeting was evaluated. Patient-derived xenografts (PDXs) from responder patients were treated with trametinib and resistant tumors were analyzed. Window trial clinical samples were subjected to whole-exome and RNA sequencing., Results: HNSCC cell lines developed resistance (CAL27-TR and HSC3-TR) after prolonged trametinib exposure. Downstream effectors of the Hippo pathway were activated in CAL27-TR and HSC3-TR, and combined trametinib and verteporfin treatment resulted in synergistic treatment response. We defined the Hippo pathway effector Yap1 as an induced survival pathway promoting resistance to trametinib in HSC3-TR. Yap1 was necessary for HSC3-TR trametinib resistance, and constitutively active Yap1 was sufficient to confer resistance in parental HSC3. Analysis of trametinib neoadjuvant trial patient tumors indicated canonical MEK-Erk1/2 pathway activating mutations were infrequent, and Yap1 activity increased following trametinib treatment. Trametinib treatment of a PDX from a responder patient resulted in evolution of resistance with increased Yap1 expression and activity., Conclusions: These studies identify a Yap1-dependent resistance to trametinib therapy in HNSCCs. Combined Yap1 and MEK targeting may represent a strategy to enhance HNSCC response., (©2021 American Association for Cancer Research.)
- Published
- 2021
- Full Text
- View/download PDF
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