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Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse
BACKGROUND: During pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect. METHODS: We have asked whether functional Id2 expression is necessary for Wnt induced mammary hyperplasi...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2004
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC544352/ https://www.ncbi.nlm.nih.gov/pubmed/15601467 http://dx.doi.org/10.1186/1471-2407-4-91 |
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author | Marino, Susan Romelfanger, Claire Yokota, Yoshifumi Nusse, Roel |
author_facet | Marino, Susan Romelfanger, Claire Yokota, Yoshifumi Nusse, Roel |
author_sort | Marino, Susan |
collection | PubMed |
description | BACKGROUND: During pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect. METHODS: We have asked whether functional Id2 expression is necessary for Wnt induced mammary hyperplasia, side branching, and cancer, by generating mice expressing a Wnt1 transgene in an Id2 mutant background. RESULTS: We show in this work that forced expression of Wnt1 in the mammary gland is capable of overcoming the block to proliferation caused by the absence of Id2. We also show that Wnt1 expression is able to cause mammary tumors in an Id2 mutant background. CONCLUSIONS: We conclude that functional Id2 expression is not required for Wnt1 to induce mammary hyperplasia and mammary tumors. |
format | Text |
id | pubmed-544352 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2004 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-5443522005-01-14 Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse Marino, Susan Romelfanger, Claire Yokota, Yoshifumi Nusse, Roel BMC Cancer Research Article BACKGROUND: During pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect. METHODS: We have asked whether functional Id2 expression is necessary for Wnt induced mammary hyperplasia, side branching, and cancer, by generating mice expressing a Wnt1 transgene in an Id2 mutant background. RESULTS: We show in this work that forced expression of Wnt1 in the mammary gland is capable of overcoming the block to proliferation caused by the absence of Id2. We also show that Wnt1 expression is able to cause mammary tumors in an Id2 mutant background. CONCLUSIONS: We conclude that functional Id2 expression is not required for Wnt1 to induce mammary hyperplasia and mammary tumors. BioMed Central 2004-12-15 /pmc/articles/PMC544352/ /pubmed/15601467 http://dx.doi.org/10.1186/1471-2407-4-91 Text en Copyright © 2004 Marino et al; licensee BioMed Central Ltd. |
spellingShingle | Research Article Marino, Susan Romelfanger, Claire Yokota, Yoshifumi Nusse, Roel Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title | Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title_full | Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title_fullStr | Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title_full_unstemmed | Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title_short | Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
title_sort | wnt1 is epistatic to id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC544352/ https://www.ncbi.nlm.nih.gov/pubmed/15601467 http://dx.doi.org/10.1186/1471-2407-4-91 |
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