Lack of mutation in exon 10 of p53 gene in thyroid tumors

Background: p53 is a nuclear protein that exerts an important role in the negative control of cellular proliferation, as well as in masterminding signaling cascades important in DNA repair and/or apoptosis. Mutations of p53 have been reported with high frequency in many cancer types and are highly p...

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Autores principales: Lia Santarosa,Patricia, Granja,Fabiana, Cristina Morari,Elaine, Leite,Janaína Luisa, Vera Montalli da Assumpção,Ligia, Ward,Laura S
Lenguaje:English
Publicado: Sociedad Médica de Santiago 2004
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Acceso en línea:http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872004001200009
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spelling oai:scielo:S0034-988720040012000092006-03-21Lack of mutation in exon 10 of p53 gene in thyroid tumorsLia Santarosa,PatriciaGranja,FabianaCristina Morari,ElaineLeite,Janaína LuisaVera Montalli da Assumpção,LigiaWard,Laura S Genes, p53 Mutation Thyroid gland Tumor protein p53-binding protein Background: p53 is a nuclear protein that exerts an important role in the negative control of cellular proliferation, as well as in masterminding signaling cascades important in DNA repair and/or apoptosis. Mutations of p53 have been reported with high frequency in many cancer types and are highly prevalent in poorly differentiated and undifferentiated thyroid carcinomas, but they are not found in benign tumors and are infrequent in well-differentiated cancer. Most mutations are located in exons 5-8 of the gene. Recently, a germline mutation in the seldom investigated exon 10, on codon 337 of p53 was described in Brazilian children who had adrenocortical tumors. Aim: To study codon 337 of exon 10 of p53 mutation in thyroid tumors. Material and methods: Seventy four thyroid tumors were studied (5 follicular carcinomas including 3 widely invasive, 22 papillary carcinomas including 6 tall cell variants, 11 follicular adenomas, 1 medullary carcinoma and 35 benign goiters). DNA was extracted from a central part of all tumors and contralateral normal thyroid tissue samples or blood from 38 of these patients. The products of PCR for exon 10 of p53 were examined by single strand conformation polymorphism (SSCP) analysis. We sequenced 2 samples suspected of presenting aberrant migrating bands and 3 additional PCR products from tumor samples with normal SSCP patterns but all were wild type. Results: In all samples studied, a wild type sequence was found. Conclusions: Exon 10 of p53 gene does not present mutations in thyroid tumors, suggesting that this mutation is specific of adrenocortical cancers. (Rev Méd Chile 2004; 132: 1513-6)info:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.132 n.12 20042004-12-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872004001200009en10.4067/S0034-98872004001200009
institution Scielo Chile
collection Scielo Chile
language English
topic Genes, p53
Mutation
Thyroid gland
Tumor protein p53-binding protein
spellingShingle Genes, p53
Mutation
Thyroid gland
Tumor protein p53-binding protein
Lia Santarosa,Patricia
Granja,Fabiana
Cristina Morari,Elaine
Leite,Janaína Luisa
Vera Montalli da Assumpção,Ligia
Ward,Laura S
Lack of mutation in exon 10 of p53 gene in thyroid tumors
description Background: p53 is a nuclear protein that exerts an important role in the negative control of cellular proliferation, as well as in masterminding signaling cascades important in DNA repair and/or apoptosis. Mutations of p53 have been reported with high frequency in many cancer types and are highly prevalent in poorly differentiated and undifferentiated thyroid carcinomas, but they are not found in benign tumors and are infrequent in well-differentiated cancer. Most mutations are located in exons 5-8 of the gene. Recently, a germline mutation in the seldom investigated exon 10, on codon 337 of p53 was described in Brazilian children who had adrenocortical tumors. Aim: To study codon 337 of exon 10 of p53 mutation in thyroid tumors. Material and methods: Seventy four thyroid tumors were studied (5 follicular carcinomas including 3 widely invasive, 22 papillary carcinomas including 6 tall cell variants, 11 follicular adenomas, 1 medullary carcinoma and 35 benign goiters). DNA was extracted from a central part of all tumors and contralateral normal thyroid tissue samples or blood from 38 of these patients. The products of PCR for exon 10 of p53 were examined by single strand conformation polymorphism (SSCP) analysis. We sequenced 2 samples suspected of presenting aberrant migrating bands and 3 additional PCR products from tumor samples with normal SSCP patterns but all were wild type. Results: In all samples studied, a wild type sequence was found. Conclusions: Exon 10 of p53 gene does not present mutations in thyroid tumors, suggesting that this mutation is specific of adrenocortical cancers. (Rev Méd Chile 2004; 132: 1513-6)
author Lia Santarosa,Patricia
Granja,Fabiana
Cristina Morari,Elaine
Leite,Janaína Luisa
Vera Montalli da Assumpção,Ligia
Ward,Laura S
author_facet Lia Santarosa,Patricia
Granja,Fabiana
Cristina Morari,Elaine
Leite,Janaína Luisa
Vera Montalli da Assumpção,Ligia
Ward,Laura S
author_sort Lia Santarosa,Patricia
title Lack of mutation in exon 10 of p53 gene in thyroid tumors
title_short Lack of mutation in exon 10 of p53 gene in thyroid tumors
title_full Lack of mutation in exon 10 of p53 gene in thyroid tumors
title_fullStr Lack of mutation in exon 10 of p53 gene in thyroid tumors
title_full_unstemmed Lack of mutation in exon 10 of p53 gene in thyroid tumors
title_sort lack of mutation in exon 10 of p53 gene in thyroid tumors
publisher Sociedad Médica de Santiago
publishDate 2004
url http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872004001200009
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