Allelic loss of tumor suppressor genes in ameloblastic tumors

Nodit, Laurentia; Barnes, Leon; Childers, Esther L.B.; Finkelstein, Sydney; Swalsky, Patricia A.; Hunt, Jennifer L.

doi:10.1038/modpathol.3800147

Cited by 54 publications

(38 citation statements)

References 21 publications

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“…Others reported unusual rare sites of metastasis including vertebrae, skull, small bowel, brain, kidneys and heart [6,8,10]. The potential to metastasize has not correlated with histologic subtype or pattern [5] while the molecular signature of ameloblastoma that leads to metastasis is still unclear [12,13]. The exact events in the metastasis cascade of MetAm are elusive.…”

Section: Metastasizing Ameloblastomamentioning

confidence: 99%

“…In contrast, cytologically malignant epithelial odontogenic tumors are seen without sufficient differentiation to subclassify as AC; objective established criteria for the minimal degree required to separate odontogenic Aneuploidy is more common in AC and is considered a strong predictor of malignant potential [16]. One study reported a high frequency of allele loss in ameloblastic tumors, however, no significant difference between benign and malignant tumors was found to aid in stratification [13].…”

Section: Ameloblastic Carcinomamentioning

confidence: 99%

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Malignant Odontogenic Tumors: An Update on Selected Tumors

Richardson

Müller

2014

Head and Neck Pathol

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This is an update on selected odontogenic malignancies. The article deals with aspects of recognized odontogenic carcinomas, odontogenic sarcoma and a yet unrecognized entity, sclerosing odontogenic carcinoma. Odontogenic malignancies are exceedingly rare, complicating a thorough understanding of the biologic behavior, reproducible standardized diagnostic criteria, appropriate classification and clinical management. Without the knowledge of the tumor's biologic behavior, adequate clinical management is difficult and patient outcomes uncertain. The histopathologic features are emphasized as well as the more recent biomarker findings. These recent advances may facilitate further understanding of this group of malignancies and provide useful stratification to guide patient management.

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Section: Metastasizing Ameloblastomamentioning

confidence: 99%

Section: Ameloblastic Carcinomamentioning

confidence: 99%

Malignant Odontogenic Tumors: An Update on Selected Tumors

Richardson

Müller

2014

Head and Neck Pathol

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“…Histologically, ameloblastoma consists of epithelial strands or islands of ameloblastic epithelium [1,3]. Several studies have already demonstrated genetic and epigenetic alterations in ameloblastoma [4][5][6][7], but the precise pathogenic mechanisms have not been elucidated yet [8].…”

Section: Introductionmentioning

confidence: 99%

Loss of heterozygosity of the PTCH gene in ameloblastoma

et al. 2012

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“…Hypermethylation of CpG islands of the p16 gene was detected in the malignant parts of the tumor. Nodit et al 18 reported alleic loss of p16 genes in ameloblastic tumors, but no significant difference between ameloblastic carcinomas and benign ameloblastomas, so other genetic or epigenetic mechanism (not alleic loss) might be responsible for malignant behavior in ameloblastic carcinomas.…”

Section: ⅳ Discussionmentioning

confidence: 99%

Methylation of p16 and E-cadherin in ameloblastoma

Park

Yoon

Park

2010

J Korean Assoc Oral Maxillofac Surg

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(J Korean Assoc Oral Maxillofac Surg 2010;36:453-9) Ⅰ. Introduction Ameloblastoma is the most common benign odontogenic tumor of the jaw, but local invasive growth or recurrence after the removal can be found. Ameloblastic carcinoma is rarely occurred and may arise as a result of malignant change in a pre-existing benign ameloblastoma (carcinoma ex-ameloblastoma) or as a primary ameloblastic carcinoma not preceded by ameloblastoma (de novo carcinoma)1 .In the malignant tumors, the gene mutation, epigene alterations such as hypermethylation of CpG islands of tumor suppressor gene may lead to suppression of transcription, which induces malignant transformation 2 . Methylation is one possible step towards DNA damage, and the same evolutionary pressure will favor all processes of silencing same genes in carcinogenesis 3,4 . The DNA methylation profile of cancer cells is characterized by global hypomethylation and simultaneous hypermethylation of selected CpG island gene promoters. Recently, the epigenetic phenomenon of DNA promoter methylation has gained increasing recognition as an important mechanism for transcriptional inactivation of cancer related genes. The identification of these methylation alterations and elucidation of the mechanistic events are important, as the methylation status of cancer cells can now be manipulated in vivo with demethylating chemotherapeutics 5 . Busan, Introduction: Ameloblastic carcinoma is a rare malignant lesion, and may arise from either carcinoma ex-ameloblastoma or de novo carcinoma. Aberrant promoter hypermethylation of the tumor-associated genes leading to their inactivation is a common event in many cancer types. The p16/CDKN2/INK4A gene and p16 5 protein are involved directly in regulating the cell cycles. Cadherins are cell adhesion molecules that modulate the epithelial phenotype and regulate tumor invasion. The aim of this study was to evaluate the roles of p16 and E-cadherin methylation and loss of p16 and E-cadherin expression in the malignant transformation of an ameloblastoma. Materials and Methods: Eight cases of ameloblastoma, including 4 benign ameloblastomas without recurrence, 2 benign ameloblastomas with recurrence and 2 carcinoma ex-ameloblastomas, were examined. The promoter hypermethylation profile of the p16 and E-cadherin genes was studied using methylation-specific polymerase chain reaction (MSP) and immunohistochemical staining for p16 and E-cadherin expression. Results: 1) Aberrant CpG island methylation of the p16 gene was detected in 3 of the 4 benign ameloblastomas without recurrence and 1 of the 2 benign ameloblastomas with recurrence. 2) Aberrant CpG island methylation of the E-cadherin gene was found in 1 of the 4 benign ameloblastomas without recurrence. Methylation of p16 and E-cadherin in ameloblastoma3) A loss of p16 expression was noted in 1 of 4 benign ameloblastomas without recurrence and 1 of 2 carcinoma ex-ameloblastomas. 4) A loss of E-cadherin expression was noted in 2 of the 4 benign ameloblastomas without recurrence, 1 ...

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Allelic loss of tumor suppressor genes in ameloblastic tumors

Cited by 54 publications

References 21 publications

Malignant Odontogenic Tumors: An Update on Selected Tumors

Malignant Odontogenic Tumors: An Update on Selected Tumors

Loss of heterozygosity of the PTCH gene in ameloblastoma

Methylation of p16 and E-cadherin in ameloblastoma

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