Metin Eser

Dr. Metin Eser


Research Focus & Metrics

Academic Career Length

10Years (2017-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2021 in Seizure: European Journal of Epilepsy
Verified
Journal Article
Closed access
BBBuse Rahime Hasırcı Bayır
Buse Rahime Hasırcı Bayır
KTKemal Tutkavul
Kemal Tutkavul
MEMetin Eser
Metin Eser
BBBetül Baykan
Betül Baykan

13 December 2022 in Clinical Neurology and Neurosurgery
Verified
Journal Article
Closed access
TUTuğçe Aksu Uzunhan
Tuğçe Aksu Uzunhan
BEBiray Ertürk
Biray Ertürk
KAKürşad Aydın
Kürşad Aydın
AAAkif Ayaz
Akif Ayaz
UAUmut Altunoğlu
Umut Altunoğlu
HKHülya Kayserili
Hülya Kayserili

26 December 2024 in Molecular Genetics and Genomics
Verified
Journal Article
Closed access
PDF file
MEMetin Eser
Metin Eser
GHGulam Hekimoglu
Gulam Hekimoglu
BKBusra Kutlubay
Busra Kutlubay
SŞsafiye güneş şentürk
safiye güneş şentürk
ATAyberk Turkyilmaz
Ayberk Turkyilmaz

25 October 2017 in The Turkish Journal of Pediatrics
Verified
Journal Article
Open access
MEMetin Eser
Metin Eser
AAAkif Ayaz
Akif Ayaz
GYGözde Yeşil
Gözde Yeşil
Rubinstein-Taybi syndrome (RSTS) is a developmental disorder characterized by a wide spectrum of multiple congenital anomalies and cognitive impairment. RSTS is primarily due to mutations in CREBBP (approximately 55% of cases) or EP300 (approximately 8% of cases) genes. A 2 month-old boy had atypical facial findings such as low anterior hairline, triangular face, hirsutism on forehead, down-slanting palpebral fissures, beaked nose, broad nasal bridge, triangular mouth and pointed chin and skeletal finding including broad great thumbs and halluces, and accessory nipple. With this paper, we reported a novel frameshift mutation which is led to premature stop codon in CREBBP gene. As a result, c.2057dupC, reported in this paper enlarges the molecular spectrum of disease-causing CREBBP gene.

7 February 2024 in Clinical Endocrinology
Verified
Journal Article
Closed access
FDFatma Dursun
Fatma Dursun
ITihsan turan
ihsan turan
EBEda Çelebi Bitkin
Eda Çelebi Bitkin
EBElvan Bayramoğlu
Elvan Bayramoğlu
ACAtilla Cayir
Atilla Cayir
GKGülay Karagüzel
Gülay Karagüzel

1 May 2018 in Balkan Medical Journal
Verified
Journal Article
Closed access
MEMetin Eser
Metin Eser
AAAkif Ayaz
Akif Ayaz
Background: Ovotesticular disorder is characterized by the presence of testicular and ovarian tissues in the same individual. Single gene mutations in SRY, SOX9, DMRT1 and DAX1 can lead to ovotesticular disorder of sexual development. Case Report: Herein, we report a 3-month-old phenotypically female baby in whom differentiated tissues of both Mullerian and Wolffian ducts were detected on pathological analysis of laparoscopic biopsy material. Chromosomal analysis observed 46, XY, der(9)t(3;9) (p25;p24) with deletion of 9p24.3p23 including the DMRT gene cluster and duplication of 3p26.3p24.3 on array comparative genomic hybridisation. Conclusion: In support of previous literature, we found that haploinsufficiency of the DMRT gene cluster leads to ovotesticular disorder of sexual development. In addition, we emphasize that array comparative genomic hybridisation is an important technique in the molecular diagnosis of ovotesticular disorder of sexual.