Inducible dimerization of FGFR1 : development of a mouse model to analyze progressive transformation of the mammary gland (original) (raw)

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Article| May 13 2002

Bryan E. Welm,

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

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Kevin W. Freeman,

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

3Department of Immunology, Baylor College of Medicine, Houston, TX 77030

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Mercy Chen,

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

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Alejandro Contreras,

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

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David M. Spencer,

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

3Department of Immunology, Baylor College of Medicine, Houston, TX 77030

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Jeffrey M. Rosen

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

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Bryan E. Welm

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

Kevin W. Freeman

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

3Department of Immunology, Baylor College of Medicine, Houston, TX 77030

Mercy Chen

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

Alejandro Contreras

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

David M. Spencer

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

3Department of Immunology, Baylor College of Medicine, Houston, TX 77030

Jeffrey M. Rosen

1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

2Program in Cell and Molecular Biology, Baylor College of Medicine, Houston, TX 77030

Address correspondence to J.M. Rosen, Dept. of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Tel.: 713-798-6210. Fax: 713-798-8012. E-mail: [email protected]

The online version of this article contains supplemental material.

B.E. Welm's present address is Dept. of Anatomy, University of California, San Francisco, San Francisco, CA 94143.

*

Abbreviations used in this paper: BrdU, 5-bromo-2′-deoxyuridine; ECM, extracellular matrix; FGF, fibroblast growth factor; FGFR, FGF receptor; H&E, hematoxylin and eosin; HA, hemagglutinin; LTR, long terminal repeat; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; MMTV, mouse mammary tumor virus; PR, progesterone receptor; TEB, terminal-end bud; TUNEL, TdT-mediated dUTP-biotin nick end labeling.

Received: July 27 2001

Revision Received: March 22 2002

Accepted: March 22 2002

Online ISSN: 1540-8140

Print ISSN: 0021-9525

The Rockefeller University Press

2002

J Cell Biol (2002) 157 (4): 703–714.

To develop an inducible and progressive model of mammary gland tumorigenesis, transgenic mice were generated with a mouse mammary tumor virus–long terminal repeat–driven, conditional, fibroblast growth factor (FGF)–independent FGF receptor (FGFR)1 (iFGFR1) that can be induced to dimerize with the drug AP20187. Treatment of transgenic mice with AP20187 resulted in iFGFR1 tyrosine phosphorylation, increased proliferation, activation of mitogen-activated protein kinase and Akt, and lateral budding. Lateral buds appeared as early as 3 d after AP20187 treatment and initially consisted of bilayered epithelial cells and displayed apical and basolateral polarity appeared after 13 d of AP20187 treatment. Invasive lesions characterized by multicell-layered lateral buds, decreased myoepithelium, increased vascular branching, and loss of cell polarity were observed after 2–4 wk of treatment. These data indicate that acute iFGFR1 signaling results in increased lateral budding of the mammary ductal epithelium, and that sustained activation induces alveolar hyperplasia and invasive lesions.

The Rockefeller University Press

2002

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