Abstract 2728: Clonal nature of benign and malignant salivary gland neoplasms

Abstract The pathogenesis of salivary gland neoplasms (SGN) has not been established. There is a real debate on clonality issues and all the definitive evidence is on the side of polyclonal tumor origin. Evidence that many tumor types may be polyclonal in origin has been published. Despite all this...

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Published inCancer research (Chicago, Ill.) Vol. 71; no. 8_Supplement; p. 2728
Main Authors Gomes, Carolina Cavalieri, Pereira, Claudia Maria, Brito, Joao Artur R, Amaral, Fabricio Rezende, Barbosa, Alvimar Afonso, de Marco, Luiz, Gomez, Ricardo Santiago
Format Journal Article
LanguageEnglish
Published 15.04.2011
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Abstract Abstract The pathogenesis of salivary gland neoplasms (SGN) has not been established. There is a real debate on clonality issues and all the definitive evidence is on the side of polyclonal tumor origin. Evidence that many tumor types may be polyclonal in origin has been published. Despite all this body of evidence, scientists have incorporated the clonal theory proposed by Knudson (1985) and only strengthen these results (and do not discuss contrary findings), because they think it is expected. There are few clonality studies on benign salivary neoplasms and almost no data on malignant neoplasms. The HUMARA assay was used in the present study to investigate the clonality of 27 samples of SGN (17 benign and ten malignant). Briefly, samples were digested with HhaI and HpaII methylation-sensitive enzymes and a PCR carried out. Eighteen out of 27 cases revealed monotypy, while three were non-informative and six showed heterotypy, indicating a true polyclonality. In summary, our results show evidence that a subset of SGN might be clonal in origin, while some samples are polyclonal. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2728. doi:10.1158/1538-7445.AM2011-2728
AbstractList Abstract The pathogenesis of salivary gland neoplasms (SGN) has not been established. There is a real debate on clonality issues and all the definitive evidence is on the side of polyclonal tumor origin. Evidence that many tumor types may be polyclonal in origin has been published. Despite all this body of evidence, scientists have incorporated the clonal theory proposed by Knudson (1985) and only strengthen these results (and do not discuss contrary findings), because they think it is expected. There are few clonality studies on benign salivary neoplasms and almost no data on malignant neoplasms. The HUMARA assay was used in the present study to investigate the clonality of 27 samples of SGN (17 benign and ten malignant). Briefly, samples were digested with HhaI and HpaII methylation-sensitive enzymes and a PCR carried out. Eighteen out of 27 cases revealed monotypy, while three were non-informative and six showed heterotypy, indicating a true polyclonality. In summary, our results show evidence that a subset of SGN might be clonal in origin, while some samples are polyclonal. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2728. doi:10.1158/1538-7445.AM2011-2728
Author Gomez, Ricardo Santiago
Brito, Joao Artur R
Amaral, Fabricio Rezende
Pereira, Claudia Maria
Barbosa, Alvimar Afonso
de Marco, Luiz
Gomes, Carolina Cavalieri
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