Molecular pathology of odontogenic tumors

Abstract

Odontogenic tumors are lesions derived from the elements of the tooth-forming apparatus and are found exclusively within the jawbones. This review represents a contemporary outline of our current understanding of the molecular and genetic alterations associated with the development and progression of odontogenic tumors, including oncogenes, tumor-suppressor genes, oncoviruses, growth factors, telomerase, cell cycle regulators, apoptosis-related factors, regulators of tooth development, hard tissue-related proteins, cell adhesion molecules, matrix-degrading proteinases, angiogenic factors, and osteolytic cytokines. It is hoped that better understanding of related molecular mechanisms will help to predict the course of odontogenic tumors and lead to the development of new therapeutic concepts for their management.

Molecular etiopathogenesis of ameloblastoma – current concepts revisited

“…[22] Rb Kumamoto et al, (2006) demonstrated increased expression of retinoblastoma (Rb) and phosphorylated Rb in AB than in tooth germs which might have a role in cell proliferation and diff erentiation of odontogenic epithelium. However, another study by Lim and Ahn et al, (2006) using DNA microarray and reverse polymerase chain reaction (more sensitive compared to IHC) revealed downregulation of Rb1 in AB in comparison with dentigerous cyst.…”

“…Further studies are needed to confi rm their role. [19] Platelet-derived growth factor (PDGF) AA isoform and its receptor PDGF-α receptor levels were more in malignant ameloblastic tumors when compared to non-metastasizing AB. PDGF ligand and receptor system might participate in malignant transformation of odontogenic epithelium.…”

A molecular insight in the prevalence of odontogenic tumor

“…Its overexpression was seen in ameloblastoma which suggest that these oncogenes play a role in the pathogenesis of OT through impairment of cell proliferation. [2] Tumor suppressor gene P53 gene also known as TP53 gene has been describes as "the guardian of the genome" is the key gene altered in tumors. It plays a role genomic destruction by persuading apoptosis or arresting the cell cycle.…”

“…Abundant oncogenes have been recognized, and their genetic material function as growth factors, growth factor receptors, serine/threonine kinases (Mos), nonreceptor tyrosine kinases (Src, Abl), transcription factors (Myc, Fos), and signal transducers (Ras) which contribute in cellular functions related to propagation and differentiation. [2] Activated ras oncogene is the acutely transforming component of Harvey sarcoma virus 15. There are three cellular homologs: K-ras, H-ras, and N-ras.…”

“…The etiology and pathology behind the OT stay unidentified, recent studies have identified various molecular alterations accountable for their growth and evolution. [2] The aim of this review is to provide a current sketch in knowing and considering of the molecular and genetic events linked with OT.…”