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Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas

Sarcomas were induced in Fl mice between C57BL/6N and C3H/He strains by subcutaneous injection of methylcholanthrene. The c‐myc oncogene was found to be amplified in 16 cases among 43 sarcomas of C57BL/6N × C3H/He mice and 1 case among 5 sarcomas of the reciprocal cross. The origin of the amplified...

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Detalles Bibliográficos
Autores principales: Niwa, Ohtsura, Kominami, Ryo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918713/
https://www.ncbi.nlm.nih.gov/pubmed/1483933
http://dx.doi.org/10.1111/j.1349-7006.1992.tb02744.x
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author Niwa, Ohtsura
Kominami, Ryo
author_facet Niwa, Ohtsura
Kominami, Ryo
author_sort Niwa, Ohtsura
collection PubMed
description Sarcomas were induced in Fl mice between C57BL/6N and C3H/He strains by subcutaneous injection of methylcholanthrene. The c‐myc oncogene was found to be amplified in 16 cases among 43 sarcomas of C57BL/6N × C3H/He mice and 1 case among 5 sarcomas of the reciprocal cross. The origin of the amplified allele was determined by the polymerase chain reaction single strand conformation polymorphism analysis. Among the 17 sarcomas, only one had both of the alleles amplified. The rest of the tumors carried the amplified c‐myc allele coming either from C57BL/6N (9 cases) or from C3H/He (8 cases). These results indicate that the c‐myc allele is amplified randomly in methylcholanthrene‐induced mouse sarcomas irrespective of its origin, such as paternal or maternal allele and C57BL/6N or C3H/He allele. In addition to these changes, the unamplified c‐myc oncogene was found to be lost in 12 cases out of the 17 sarcomas with the amplification.
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spelling pubmed-59187132018-05-11 Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas Niwa, Ohtsura Kominami, Ryo Jpn J Cancer Res Article Sarcomas were induced in Fl mice between C57BL/6N and C3H/He strains by subcutaneous injection of methylcholanthrene. The c‐myc oncogene was found to be amplified in 16 cases among 43 sarcomas of C57BL/6N × C3H/He mice and 1 case among 5 sarcomas of the reciprocal cross. The origin of the amplified allele was determined by the polymerase chain reaction single strand conformation polymorphism analysis. Among the 17 sarcomas, only one had both of the alleles amplified. The rest of the tumors carried the amplified c‐myc allele coming either from C57BL/6N (9 cases) or from C3H/He (8 cases). These results indicate that the c‐myc allele is amplified randomly in methylcholanthrene‐induced mouse sarcomas irrespective of its origin, such as paternal or maternal allele and C57BL/6N or C3H/He allele. In addition to these changes, the unamplified c‐myc oncogene was found to be lost in 12 cases out of the 17 sarcomas with the amplification. Blackwell Publishing Ltd 1992-11 /pmc/articles/PMC5918713/ /pubmed/1483933 http://dx.doi.org/10.1111/j.1349-7006.1992.tb02744.x Text en
spellingShingle Article
Niwa, Ohtsura
Kominami, Ryo
Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title_full Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title_fullStr Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title_full_unstemmed Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title_short Lack of Allelic Preference in Amplification and Loss of the c‐myc Oncogene in Methylcholanthrene‐induced Mouse Sarcomas
title_sort lack of allelic preference in amplification and loss of the c‐myc oncogene in methylcholanthrene‐induced mouse sarcomas
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918713/
https://www.ncbi.nlm.nih.gov/pubmed/1483933
http://dx.doi.org/10.1111/j.1349-7006.1992.tb02744.x
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