Gene polymorphisms in odontogenic keratocysts and ameloblastomas: A systematic review

Objectives The aim of this systematic review was to critically analyze available data on gene polymorphisms in odontogenic keratocysts (OKC) and ameloblastomas, including their possible relationship with clinical and histological features of these lesions. Materials and Methods A comprehensive searc...

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Bibliographic Details
Published in:Oral diseases 2022-09, Vol.28 (6), p.1421-1430
Main Authors: Andric, Miroslav, Jacimovic, Jelena, Jakovljevic, Aleksandar, Nikolic, Nadja, Milasin, Jelena
Format: Article
Language:English
Subjects:
ameloblastoma
association study
Brain tumors
Clinical trials
Codons
Gene polymorphism
Glioma
keratocystic odontogenic tumor
Lesions
Matrix metalloproteinase
Metalloproteinase
odontogenic keratocyst
p53 Protein
Quality control
Risk factors
single nucleotide polymorphism
Survivin
Systematic review
Tumor necrosis factor
Tumor necrosis factor-TNF
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Summary:Objectives The aim of this systematic review was to critically analyze available data on gene polymorphisms in odontogenic keratocysts (OKC) and ameloblastomas, including their possible relationship with clinical and histological features of these lesions. Materials and Methods A comprehensive search of Web of Science Scopus, PubMed, Cochrane Central Register of Controlled Trials and EMBASE was conducted using relevant key terms and supplemented by a gray literature search. Quality assessment of included studies was performed using criteria from the Strengthening the Reporting of Genetic Association (STREGA) statement. Results Ten studies were included in the final review. Survivin ‐31G/C, interleukin IL‐1α ‐889 C/T, p53 codon 72 G/C, tumor necrosis factor TNF‐α (−308G>A) and its receptor TNF‐R1 (36A>G), glioma‐associated oncogene homolog 1 rs2228224 and matrix metalloproteinase 2 rs243865 gene polymorphisms were reported to be associated with OKC. For ameloblastomas, p53 codon 72 G/C, X‐ray repair cross‐complementing protein 1—codons 194 and 399 and matrix metalloproteinase 9 rs3918242 gene polymorphisms were identified as risk factors. It was not possible to establish a relationship between specific polymorphisms and clinical and histological features of investigated lesions. Conclusions Several gene polymorphisms might be considered as a risk factor for the development of these lesions. Future studies should investigate whether these polymorphisms might be used to identify patients with increased risk of recurrence or aggressive disease.
ISSN:1354-523X
1601-0825
DOI:10.1111/odi.13865