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 Schneiderian type papilloma of the middle ear(2020-12-01) CİNEL, ZELİHA LEYLA; Keskin B., CİNEL Z. L.Publication Metadata only A rare variant: adenomatoid ameloblastoma with dentinoid(2020-12-01) SAÇAK, BÜLENT; CİNEL, ZELİHA LEYLA; Keskin B., Tekkesin M. S., SAÇAK B., CİNEL Z. L.Publication Metadata only Chondroid syringoma: report of eight cases and review of the literature(2016-09-01) CİNEL, ZELİHA LEYLA; Mollamemisoglu H., Kombak E., Kocaaslan F. N. D., Cinel Z. L.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.