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Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid

All nucleated mammalian cells synthesize protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA). The response to exogenous ALA under standard conditions (the ALA phenotype) is characteristic for each cell type. Significantly more PpIX accumulates in malignant and premalignant...

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Autores principales: Li, G, Szewczuk, M R, Raptis, L, Johnson, J G, Weagle, G E, Pottier, R H, Kennedy, J C
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1999
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362266/
https://www.ncbi.nlm.nih.gov/pubmed/10360643
http://dx.doi.org/10.1038/sj.bjc.6690409
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author Li, G
Szewczuk, M R
Raptis, L
Johnson, J G
Weagle, G E
Pottier, R H
Kennedy, J C
author_facet Li, G
Szewczuk, M R
Raptis, L
Johnson, J G
Weagle, G E
Pottier, R H
Kennedy, J C
author_sort Li, G
collection PubMed
description All nucleated mammalian cells synthesize protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA). The response to exogenous ALA under standard conditions (the ALA phenotype) is characteristic for each cell type. Significantly more PpIX accumulates in malignant and premalignant cells than in the normal cells from which they were derived. A rodent fibroblast model was developed to study the mechanisms responsible for this phenomenon. Exogenous ALA induced the accumulation of substantial concentrations of PpIX in fibrosarcoma cells, and in immortalized fibroblasts transfected with the oncogene c-myc, IGF-1 receptor, IGF-1 and its receptor, v-fos, v-raf, v-Ki-ras, v-abl, or polyomavirus middle T antigen with G418 resistance selection. Much lower concentrations of PpIX accumulated in primary fibroblast cultures, in immortalized fibroblast cell lines, and in immortalized fibroblasts transfected with the G418-resistance gene only. The mechanisms responsible for the increased accumulation of ALA-induced PpIX by transformed cells (the malignant ALA phenotype) therefore appear to be closely linked to the mechanisms responsible for malignant transformation. Identification of the nature of that linkage may lead to new approaches to cancer therapy. © 1999 Cancer Research Campaign
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spelling pubmed-23622662009-09-10 Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid Li, G Szewczuk, M R Raptis, L Johnson, J G Weagle, G E Pottier, R H Kennedy, J C Br J Cancer Regular Article All nucleated mammalian cells synthesize protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA). The response to exogenous ALA under standard conditions (the ALA phenotype) is characteristic for each cell type. Significantly more PpIX accumulates in malignant and premalignant cells than in the normal cells from which they were derived. A rodent fibroblast model was developed to study the mechanisms responsible for this phenomenon. Exogenous ALA induced the accumulation of substantial concentrations of PpIX in fibrosarcoma cells, and in immortalized fibroblasts transfected with the oncogene c-myc, IGF-1 receptor, IGF-1 and its receptor, v-fos, v-raf, v-Ki-ras, v-abl, or polyomavirus middle T antigen with G418 resistance selection. Much lower concentrations of PpIX accumulated in primary fibroblast cultures, in immortalized fibroblast cell lines, and in immortalized fibroblasts transfected with the G418-resistance gene only. The mechanisms responsible for the increased accumulation of ALA-induced PpIX by transformed cells (the malignant ALA phenotype) therefore appear to be closely linked to the mechanisms responsible for malignant transformation. Identification of the nature of that linkage may lead to new approaches to cancer therapy. © 1999 Cancer Research Campaign Nature Publishing Group 1999-05 /pmc/articles/PMC2362266/ /pubmed/10360643 http://dx.doi.org/10.1038/sj.bjc.6690409 Text en Copyright © 1999 Cancer Research Campaign 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 Regular Article
Li, G
Szewczuk, M R
Raptis, L
Johnson, J G
Weagle, G E
Pottier, R H
Kennedy, J C
Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title_full Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title_fullStr Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title_full_unstemmed Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title_short Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
title_sort rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362266/
https://www.ncbi.nlm.nih.gov/pubmed/10360643
http://dx.doi.org/10.1038/sj.bjc.6690409
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