Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.

Resistance to the cytocidal action of Adriamycin (ADR) was induced in rat hepatocytes by incorporation of the carcinogen 2-acetylaminofluorene (AAF) into the rat diet. Using a quantitative assay in primary monolayer culture, it was demonstrated that resistance to ADR is an early phenotypic change th...

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Detalles Bibliográficos
Autores principales: Carr, B. I., Laishes, B. A.
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1981
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2010790/
https://www.ncbi.nlm.nih.gov/pubmed/7295513
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author Carr, B. I.
Laishes, B. A.
author_facet Carr, B. I.
Laishes, B. A.
author_sort Carr, B. I.
collection PubMed
description Resistance to the cytocidal action of Adriamycin (ADR) was induced in rat hepatocytes by incorporation of the carcinogen 2-acetylaminofluorene (AAF) into the rat diet. Using a quantitative assay in primary monolayer culture, it was demonstrated that resistance to ADR is an early phenotypic change that is induced during chemical carcinogenesis in the rat, and appears to be stable.
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spelling pubmed-20107902009-09-10 Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis. Carr, B. I. Laishes, B. A. Br J Cancer Research Article Resistance to the cytocidal action of Adriamycin (ADR) was induced in rat hepatocytes by incorporation of the carcinogen 2-acetylaminofluorene (AAF) into the rat diet. Using a quantitative assay in primary monolayer culture, it was demonstrated that resistance to ADR is an early phenotypic change that is induced during chemical carcinogenesis in the rat, and appears to be stable. Nature Publishing Group 1981-10 /pmc/articles/PMC2010790/ /pubmed/7295513 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Research Article
Carr, B. I.
Laishes, B. A.
Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title_full Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title_fullStr Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title_full_unstemmed Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title_short Resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
title_sort resistance to the cytocidal effects of adriamycin is an early phenotypic change induced during hepatocarcinogenesis.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2010790/
https://www.ncbi.nlm.nih.gov/pubmed/7295513
work_keys_str_mv AT carrbi resistancetothecytocidaleffectsofadriamycinisanearlyphenotypicchangeinducedduringhepatocarcinogenesis
AT laishesba resistancetothecytocidaleffectsofadriamycinisanearlyphenotypicchangeinducedduringhepatocarcinogenesis

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