Person: CİNEL, ZELİHA LEYLA
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CİNEL
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ZELİHA LEYLA
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Publication Open Access Adenoid ‘ameloblastoma: Clinicopathological description of 4 additional BRAF-negative cases(2023-12-01) CİNEL, ZELİHA LEYLA; Khalaj F., CİNEL Z. L., Aminishakib P., Mosavat F., SOLUK TEKKEŞİN M.Objective: Adenoid ameloblastoma (AA) is an epithelial odontogenic tumor that was recognized as a separate entity in the last odontogenic classification of WHO in 2022. The etiology is unknown, and the pathogenesis remains controversial. The objective of this study is to contribute the clinicopathological features of 4 additional BRAF-negative cases to the existing literature, aiming to enhance the molecular understanding of this unique tumor in the forthcoming classification. Materials and methods: This study consists of a case series of four patients diagnosed with AA. The patients’ demographic and clinical information were collected from the universities’ medical achieves. Histopathologically, all cases were reexamined according to the latest update of the WHO odontogenic tumor classification. In addition to H&E and immunohistochemical stains, cytogenetics was also evaluated. Results: Well-defined unilocular radiolucent lesions were observed in all cases. Ameloblastoma-like components exhibited reserved nuclear polarity, suprabasal stellate reticulum-like epithelium, duct-like structure, whorls/morules, and cribriform architecture were common features. Variable immunoreactivity to CK7, CK19, CK14, p63, and p40 were determined, and proliferative activity was greater than 15%. The BRAF molecular study revealed no mutations. Conclusions: When diagnosing AA, the essential histopathological characteristics must be rigorously applied, and a significant portion of the lesion should contain these features. Additionally, despite limited molecular data, since the BRAF mutation commonly observed in ameloblastomas is not present in the majority of AA cases, we propose changing the term \"ameloblastoma\" to \"ameloblastic\" and referring to it as \"adenoid ameloblastic tumor\" in the forthcoming classification.Publication Metadata only Baş-boyun spesimenleri patolojik değerlendirme ve raporlama rehberi(buluş, 2021-03-01) CİNEL, ZELİHA LEYLA; Cinel Z. L., Gökcan M. K., Veral A., Çomunoğlu N., Soluk Tekkeşin M.Publication Open Access Severe allergic dysregulation due to a gain of function mutation in the transcription factor STAT6(2023-01-01) BARIŞ, SAFA; YÜCELTEN, AYŞE DENİZ; BOZKURTLAR, EMİNE; CİNEL, ZELİHA LEYLA; AYDINER, ELİF; ÖZEN, AHMET OĞUZHAN; BARIŞ S., Benamar M., Chen Q., Catak M. C., Martínez-Blanco M., Wang M., Fong J., Massaad M. J., Sefer A. P., Kara A., et al.Background: Inborn errors of immunity have been implicated in causing immune dysregulation, including allergic diseases. STAT6 is a key regulator of allergic responses. Objectives: This study sought to characterize a novel gain-of-function STAT6 mutation identified in a child with severe allergic manifestations. Methods: Whole-exome and targeted gene sequencing, lymphocyte characterization, and molecular and functional analyses of mutated STAT6 were performed. Results: This study reports a child with a missense mutation in the DNA binding domain of STAT6 (c.1114G>A, p.E372K) who presented with severe atopic dermatitis, eosinophilia, and elevated IgE. Naive lymphocytes from the affected patient displayed increased TH2- and suppressed TH1- and TH17-cell responses. The mutation augmented both basal and cytokine-induced STAT6 phosphorylation without affecting dephosphorylation kinetics. Treatment with the Janus kinase 1/2 inhibitor ruxolitinib reversed STAT6 hyperresponsiveness to IL-4, normalized TH1 and TH17 cells, suppressed the eosinophilia, and improved the patient\"s atopic dermatitis. Conclusions: This study identified a novel inborn error of immunity due to a STAT6 gain-of-function mutation that gave rise to severe allergic dysregulation. Janus kinase inhibitor therapy could represent an effective targeted treatment for this disorder.Publication Open Access Evaluation of LRIG1 expression in larynx pathologies(2022-03-01) CİNEL, ZELİHA LEYLA; YUMUŞAKHUYLU, ALİ CEMAL; Gündoğdu Y., Asya O., Gönen A., Muradov T., Erçetin S. Y., Cinel Z. L., Yumuşakhuylu A. C.Objective: Studies have been performed on many biomolecules to determine the prognosis of LSCC and predict the course of the disease. However, a molecular marker that can be used clinically has not yet been found. Therefore, in this study, we aimed to investigate the expression levels of LRIG 1 in laryngeal cancer. Materials and Methods: In our study, 219 cases who underwent surgery due to LSCC and 88 randomly selected patients whose pathologic result were benign and premalignant lesions in Marmara University Pendik Education and Research Hospital between 2003 and 2018 were analyzed. Patients’ data were obtained from the medical records. The tissue microarray method was used to evaluate specimens. Results: There was a statistically significant difference between the tumor differentiation, diagnosis, and the expression of LRIG1 (respectively p=0.045, p<0.001). Also, an increase in the degree of dysplasia in premalignant lesions correlates with a decrease in LRIG1 expression (p=0.015). Conclusion: Our findings suggest that LRIG1 plays a role in the early tumorigenesis of LSCC. Therefore, LRIG1 can be a target molecule for treatment approaches. However, LRIG1 was not correlated with overall survival of the LSCC.Publication Metadata only Periferal ossifiying fibromanın periodontal cerrahi yaklaşımla tedavisi: bir olgu sunumu(2022-11-06) İYİGÜN, SEZGİ; CİNEL, ZELİHA LEYLA; KÖSE, KEMAL NACİ; İyigün S., Türk C. B., Cinel Z. L., Köse K. N.Periferal ossifying fibroma (POF), genellikle maksilla anterior bölgede, sıklıkla kadınlarda ve 2-3. dekatta rastlanan iyi huylu reaktif doku büyümesidir. Etyolojisi kesin değildir, periodontal ligament veya periostun enflamatuvar hiperplazisinden kaynaklandığı düşünülmektedir. Sıklıkla diş etinde, interdental papilla alanından başlamakta, %16-20 oranlarında tekrarlama riski bulunmaktadır. Tedavi protokolü, başlangıç periodontal tedavi (BPT), gerektiğinde lezyonun cerrahi uzaklaştırılması ve periodontal dokuların yeniden yapılandırılmasını içerir. Bu sunuda, POF olgusunun tedavisi sunulmaktadır. Diş etinde 6 aydır mevcut olan büyüme şikâyeti ile kliniğimize başvuran 63 yaşındaki tip 2 diyabetli kadın hastanın ağız içi muayenesinde, 23 numaralı dişin distalinden başlayıp vestibüle ve posterior dişsiz bölgeye uzanan saplı, hiperemik, yüzeyi ülsere, 20x18 mm boyutlarında dişeti büyümesi saptandı. Öyküsünde yeni yapılan hareketli bölümlü protezini kullanmaya başladıktan sonra büyümenin olduğu belirtilmişti. Klinik ve radyografik değerlendirme sonrası kronik periodontitis ve lokalize saplı dişeti büyümesi teşhisi kondu. İki kez BPT seansı uygulandı. Bu süreçte, hastanın özellikle protezini kullanırken şikayetlerinin artması sebebiyle lezyonun BPT tamamlanmadan uzaklaştırılması kararlaştırıldı. İnsizyon, lezyon ve bir miktar sağlıklı dokuyu da içerecek şekilde planlanarak mukoperiosteal flap kaldırıldı, kitle uzaklaştırıldı ve degranülasyon gerçekleştirildi. Alveolar kemikteki lezyon invazyonlarının uzaklaştırıldığından emin olmak amacıyla lezyonun invaze olduğu düşünülen bölgeler ostektomi ve osteoplastiyle temizlendi. Açıkta kalan kemik ve kök yüzeyi, 3.0 ipek sütur kullanılarak primer kapatıldı. Dikişler 7 gün sonra alındı. Postoperatif dördüncü haftada iyileşme sorunsuzdu. Histopatolojik incelemede lezyon POF ile uyumlu bulundu. Altı aylık takibinde rekürrens izlenmedi. Bu olguda, POF’un mukoperiosteal flep ile uzaklaştırılmasını da içeren BPT’si sunulmaktadır. Bazı durumlarda cerrahi yaklaşımların BPT planlamasına dahlinin hasta konforunun sağlanması ve tedavinin başarısındaki önemi vurgulanmıştır.