Oral Field Cancerization: A Review
The concept of oral field cancerization (OFC) has been ever changing since its first description by Slaughter et al in 1953. The concept of OFC explains the mechanisms by which second primary tumors (OPTs) develop- OPTs are the tumor-, which develop in the oral cavity in succession to the primary ma...
Main Author: | |
---|---|
Format: | Article |
Language: | English |
Published: |
Wolters Kluwer Medknow Publications
2010-01-01
|
Series: | Journal of Indian Academy of Oral Medicine and Radiology |
Subjects: | |
Online Access: | http://www.jiaomr.in/article.asp?issn=0972-1363;year=2010;volume=22;issue=4;spage=201;epage=205;aulast=Jayam;type=0 |
id |
doaj-752835736bb24a6080d94ce9a210f0b7 |
---|---|
record_format |
Article |
spelling |
doaj-752835736bb24a6080d94ce9a210f0b72020-11-25T01:24:07ZengWolters Kluwer Medknow PublicationsJournal of Indian Academy of Oral Medicine and Radiology0972-13630975-15722010-01-01224201205Oral Field Cancerization: A ReviewRaviraj JayamThe concept of oral field cancerization (OFC) has been ever changing since its first description by Slaughter et al in 1953. The concept of OFC explains the mechanisms by which second primary tumors (OPTs) develop- OPTs are the tumor-, which develop in the oral cavity in succession to the primary malignant tumors, which might vary in duration ranging from few months to years. The "classical" mechanism, which was originally observed by Slaughter describes that in the individuals with adverse habits, large areas of the aerodigestive tissue are affected by long-term exposure to carcinogens. In this preconditioned epithelium, multifocal carcinomas can develop as a result of independent mutations, and thus would not be genetically related. Although this mechanism was accepted for a quite a long time, the controversies began with the advent of new mechanism called the "clonal theory-, which explains that a single cell, on exposure to carcinogens, is transformed and give- rise to one large extended premalignant field by clonal expansion and gradual replacement of normal mucosa. In this field of various subclones, two separate tumors can develop after accumulation of additional genetic alteration-. Both tumors have the same clonal origin, and would thus share at least one early genetic event, which occurred before the initial clonal expansion. Also, the molecular studies regarding OFC have been expanding exponentially since a few years. The need for chemoprevention and the management of OFC with its resultant effect of development of second primary tumors has been challenging till today. Hence, the article tries to explain the conflicting aspects of various mechanisms by which SPTs develop, the molecular techniques, chemoprevention and therapeutic implications for oral field cancerization.http://www.jiaomr.in/article.asp?issn=0972-1363;year=2010;volume=22;issue=4;spage=201;epage=205;aulast=Jayam;type=0Oral field cancerization. Second primary tumorsMolecular methodsSynchronous/Metachronous tumorsMetastasizing/Nonmetastasizing tumors |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Raviraj Jayam |
spellingShingle |
Raviraj Jayam Oral Field Cancerization: A Review Journal of Indian Academy of Oral Medicine and Radiology Oral field cancerization. Second primary tumors Molecular methods Synchronous/Metachronous tumors Metastasizing/Nonmetastasizing tumors |
author_facet |
Raviraj Jayam |
author_sort |
Raviraj Jayam |
title |
Oral Field Cancerization: A Review |
title_short |
Oral Field Cancerization: A Review |
title_full |
Oral Field Cancerization: A Review |
title_fullStr |
Oral Field Cancerization: A Review |
title_full_unstemmed |
Oral Field Cancerization: A Review |
title_sort |
oral field cancerization: a review |
publisher |
Wolters Kluwer Medknow Publications |
series |
Journal of Indian Academy of Oral Medicine and Radiology |
issn |
0972-1363 0975-1572 |
publishDate |
2010-01-01 |
description |
The concept of oral field cancerization (OFC) has been ever changing since its first description by Slaughter et al in 1953. The concept of OFC explains the mechanisms by which second primary tumors (OPTs) develop- OPTs are the tumor-, which develop in the oral cavity in succession to the primary malignant tumors, which might vary in duration ranging from few months to years. The "classical" mechanism, which was originally observed by Slaughter describes that in the individuals with adverse habits, large areas of the aerodigestive tissue are affected by long-term exposure to carcinogens. In this preconditioned epithelium, multifocal carcinomas can develop as a result of independent mutations, and thus would not be genetically related. Although this mechanism was accepted for a quite a long time, the controversies began with the advent of new mechanism called the "clonal theory-, which explains that a single cell, on exposure to carcinogens, is transformed and give- rise to one large extended premalignant field by clonal expansion and gradual replacement of normal mucosa. In this field of various subclones, two separate tumors can develop after accumulation of additional genetic alteration-. Both tumors have the same clonal origin, and would thus share at least one early genetic event, which occurred before the initial clonal expansion. Also, the molecular studies regarding OFC have been expanding exponentially since a few years. The need for chemoprevention and the management of OFC with its resultant effect of development of second primary tumors has been challenging till today. Hence, the article tries to explain the conflicting aspects of various mechanisms by which SPTs develop, the molecular techniques, chemoprevention and therapeutic implications for oral field cancerization. |
topic |
Oral field cancerization. Second primary tumors Molecular methods Synchronous/Metachronous tumors Metastasizing/Nonmetastasizing tumors |
url |
http://www.jiaomr.in/article.asp?issn=0972-1363;year=2010;volume=22;issue=4;spage=201;epage=205;aulast=Jayam;type=0 |
work_keys_str_mv |
AT ravirajjayam oralfieldcancerizationareview |
_version_ |
1725118702942158848 |