Immunoexpression of Wnt/β-catenin signaling pathway proteins in ameloblastoma and calcifying cystic odontogenic tumor

Dutra, Sabrina Nogueira; Pires, Fábio-Ramôa; Armada, Luciana; Azevedo, Rebeca Souza

doi:10.4317/jced.53100

Cited by 6 publications

(17 citation statements)

References 30 publications

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“…Interestingly, COC ghost cells express WNT1 and WNT5A ligands, as well as Beta-catenin [116,117]. In immature odontomas, ghost cells showed weak Beta-catenin immunostaining, while adjacent epithelial cells exhibited a strong pattern in the nucleus and cytoplasm.…”

Section: The Wnt Pathway and Calcifying Odontogenic Cystmentioning

confidence: 99%

Oncogenic signalling pathways in benign odontogenic cysts and tumours

et al. 2017

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The first step towards the prevention of cancer is to develop an in-depth understanding of tumourigenesis and the molecular basis of malignant transformation. What drives tumour initiation? Why do most benign tumours fail to metastasize? Oncogenic mutations, previously considered to be the hallmark drivers of cancers, are reported in benign cysts and tumours, including those that have an odontogenic origin. Despite the presence of such alterations, the vast majority of odontogenic lesions are benign and never progress to the stage of malignant transformation. As these lesions are likely to develop due to developmental defects, it is possible that they harbour quiet genomes. Now the question arises - do they result from DNA replication errors? Specific candidate genes have been sequenced in odontogenic lesions, revealing recurrent BRAF mutation in the case of ameloblastoma, KRAS mutation in adenomatoid odontogenic tumours, PTCH1 mutation in odontogenic keratocysts, and CTNNB1 (Beta-catenin) mutation in calcifying odontogenic cysts. Studies on these benign and rare entities might reveal important information about the tumorigenic process and the mechanisms that hinder/halt neoplastic progression. This is because the role of relatively common oncogenic mutations seems to be context dependent. In this review, each mutation signature of the odontogenic lesion and the affected signalling pathways are discussed in the context of tooth development and tumorigenesis. Furthermore, behavioural differences between different types of odontogenic lesions are explored and discussed based on the molecular alteration described. This review also includes the employment of molecular results for guiding therapeutic approaches towards odontogenic lesions.

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Section: The Wnt Pathway and Calcifying Odontogenic Cystmentioning

confidence: 99%

Oncogenic signalling pathways in benign odontogenic cysts and tumours

et al. 2017

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“…Genetic alterations affecting abnormal activation of the Wnt pathway have been associated with the pathogenesis of cysts odontogenic tumors in particular BOGCL [12] [18] [19] [20] [21].It has been reported that the only genetic alteration found in COC is in the beta-catenin, which reinforces the suspicion that this mutation determines an alteration of the Wnt signaling pathway and this would be at the basis of tumorigenesis in COC[22] [23]. Hence, an altered signaling in the odontogenic epithelium coordinated by beta-catenin plays a role in pathogenesis of BOGCL[23] [24][25].Beta-catenin mutations with GC formation have been found in ameloblastoma cells confirming a relationship between these two cellular types[26]. It is plausible to think that an abnormal stimulus on cellular remains of the primitive lamina of the Serres determines the development of ameloblastoid cells that have a genetic alteration of the WNT pathway with abnormal beta-catenin activity, which in turn leads to the development of a more differentiated and less aggressive tumor of the ameloblastoma.…”

mentioning

confidence: 65%

Calcifying Odontogenic Cyst of the Oral Cavity: A Clinical Case and Current Updates on the Ethiopathogenesis

Menditti¹,

D'Amato²,

Laino³

et al. 2020

OJST

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Background: The calcifying odontogenic cyst (COC) is a rare pathological entity. It falls into a group of lesions with calcifications that present benign and sometime malignant tumor variants. Case Presentation: In the present study, we report on a case of intraosseous/intrasinusal COC with impacted maxillary canine and dentinoid structures odontoma-like. The clinical, radiographical, histopathological, and molecular characteristics of this pathological entity are discussed in relation also to the problems of differential diagnosis, treatment, and prognosis. Conclusion: The true COC is a rare entity in the oral cavity and represents about less than 1% of all odontogenic lesions. Careful clinical, instrumental and histological analysis must be performed for odontogenic cysts in order to accomplish the correct surgical act and to avoid recurrence.

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“…The data pool contained 56 articles after removal of the duplicates. These were further screened to 34 after scrutinising the title and abstract and eligibility evaluation was assessed by full text reading 1–11,13–35 . The final selection included 34 articles for qualitative analysis (Figure 2).…”

Section: Resultsmentioning

confidence: 99%

“…This pathway is one of the prime regulators in the pathogenesis of odontogenic lesions, the activation of which stabilises beta catenin, facilitating its cytoplasmic accumulation and nuclear translocation. Within the nucleus it further participates in the expression of genes related to the cell cycle forming several complexes with DNA‐binding proteins such as TCF (T‐cell factor) and LEF‐1 (lymphoid enhancer factor‐1) which is involved in cell proliferation, inhibition of apoptosis, and invasion and migration of the tumour cells 4,5,7 . The inherent activation of beta catenin mediated transcription resultant from mutations in genes like adenomatous polyposis coli (APC) is suggested as a requisite in tumorigenesis in various types of benign and malignant lesions 8 .…”

Section: Introductionmentioning

confidence: 99%

Localization of beta catenin across the domain of odontogenic lesions: A systematic review

Chatterjee,

Devi,

Kamboj

et al. 2023

J Oral Pathology Medicine

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BackgroundCTNNB1 gene encodes beta catenin, a transcriptional activator of Wnt pathway involved in the pathogenesis of odontogenic lesions. Though located intramembranously, its translocation into cytoplasm and nucleus could trigger cell proliferation, inhibition of apoptosis, invasion and migration of the tumour cell.Materials and MethodsFive electronic databases including MEDLINE by PubMed, Google scholar, Scopus, Trip, Cochrane library and EMBASE until 1 January 2023 without period restriction were thoroughly searched. Those articles that identified CTNNB1 mutation and beta catenin in odontogenic lesions were included for review. Risk of bias was analysed for each study using QUADAS 2 tool and Review Manager 5.3 was used to output its result.ResultsThirty four published articles were included for data synthesis. A total of 1092 cases of odontogenic lesions were assessed for both CTNNB1 mutation and beta catenin expression. CTNNB1 mutation was observed in ameloblastoma, calcifying odontogenic cyst, calcifying cystic odontogenic tumour and all malignant odontogenic tumours. The beta catenin expression (nuclear and cytoplasmic) was maximum in odontogenic keratocyst and calcifying odontogenic cyst. The expression was variable in ameloblastomas, membranous in odontomas, calcifying cystic odontogenic tumour and nuclear in all malignant tumours.Discussion and ConclusionHigh recurrence of odontogenic keratocyst and aggressiveness of solid ameloblastoma and malignant odontogenic tumours could be associated with the nuclear translocation of beta catenin. Disparity between CTNNB1 mutation and beta catenin expression within odontogenic lesions suggests alternate routes of beta catenin activation. The review results support the unique localisation of beta catenin as a helpful diagnostic factor in the pathogenesis of odontogenic lesions.

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Immunoexpression of Wnt/β-catenin signaling pathway proteins in ameloblastoma and calcifying cystic odontogenic tumor

Cited by 6 publications

References 30 publications

Oncogenic signalling pathways in benign odontogenic cysts and tumours

Oncogenic signalling pathways in benign odontogenic cysts and tumours

Calcifying Odontogenic Cyst of the Oral Cavity: A Clinical Case and Current Updates on the Ethiopathogenesis

Localization of beta catenin across the domain of odontogenic lesions: A systematic review

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