Abstract
Squamous cell carcinoma of the oral cavity evolves within a field of precancerized oral epithelium containing keratinocytes at different stages of transformation. Following acquisition of additional genetic alterations, these precancerous keratinocytes may become cancerous.Persons with apparently successfully treated oral squamous cell carcinoma are at high risk of developing a new carcinoma at, or close to the site of the treated tumour. This second carcinoma may have developed either from malignant keratinocytes left behind at surgery (recurrence), or from transformed keratinocytes within the field of precancerized epithelium from which the primary carcinoma had arisen (new carcinoma).The cells of the new carcinoma may have genetic changes in common with the cells of the original carcinoma because both are descended from a proliferating monoclone within the precancerized field; but if the new cancer originates from a different clone, it may have a dissimilar genetic profile even if the original and the new carcinoma are closely contiguous.The purpose of this article is to review the pathobiology of oral squamous cell carcinoma in relation to fields of precancerised oral epithelium.
Highlights
Squamous cell carcinoma of the oral cavity constitutes about ninety percent of all oral malignancies
Most oral squamous cell carcinoma (OSCC) develop within fields of precancerized epithelium which contain keratinocytes at different stages of transformation
The existence of an epithelial field of precancerisation may explain why more than one OSCC not uncommonly may manifest synchronously or metachronously, and may have similar or dissimilar molecular profiles depending upon whether they developed from subclones descended from a single monoclone or from polyclones [14]. Genomic instability as it relates to fields of precancerization The cellular genomic integrity of keratinocytes is maintained by various mechanisms including DNA monitoring and repair, checkpoints that regulate the cell cycle and genes that ensure the accurate replication and segregation of chromosomes during mitosis. Malfunction of these mechanisms may either bring about genomic instability which is associated with an increased risk of acquiring additional genetic alterations; or it may confer upon the transformed keratinocytes growth advantage over the normal neighbouring keratinocytes that can culminate in carcinoma [20,28,29,56,57,58]
Summary
Squamous cell carcinoma of the oral cavity constitutes about ninety percent of all oral malignancies. Genomic instability as it relates to fields of precancerization The cellular genomic integrity of keratinocytes is maintained by various mechanisms including DNA monitoring and repair, checkpoints that regulate the cell cycle and genes that ensure the accurate replication and segregation of chromosomes during mitosis Malfunction of these mechanisms may either bring about genomic instability which is associated with an increased risk of acquiring additional genetic alterations; or it may confer upon the transformed keratinocytes growth advantage over the normal neighbouring keratinocytes that can culminate in carcinoma [20,28,29,56,57,58]. Mutations in oncogenes conferring cellular self-sufficiency in growth signals, or in tumour suppressor genes resulting in dysfunctional anti-oncogenic activity, or mutations in both, may induce deviations in DNA replication, leading to accumulation of DNA damage and consequent genetic instability This process is not sufficient to induce a complete set of genomic alterations of a cancerous phenotype, but can be an initiating event in carcinogenesis, establishing a state of precancerization [62,67]. Author details 1Department of Periodontology and Oral Medicine, University of Limpopo, Medunsa campus, South Africa. 2School of Anatomical Sciences, Faculty of Health Sciences, University of Witwatersrand, Johannesburg, South Africa
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