All three projects of the proposed program involve the study of the consequences of loss-of-function mutations generated by targeting of genes encoding tumor suppressors in mice. These studies require expert and efficient pathological analyses of large number of specimens (embryos, tissues and tumors), to investigate phenotypic manifestations affect normal murine development and/or contributing to tumorigenesis. The diagnostic procedures that are central to the development of the program include macroscopic anatomic examination, microscopic histology, in situ hybridization and immunohistochemistry.
The aim of this Core facility is to provide murine pathology serve by an experienced pathologist combining uniquely in his background expertise in both human clinical pathology and mouse development and pathology, including oncogenesis. Quality control in the Core will be secured by optimizing, standardizing nd streamlining the procedures involved, to [provide interpretations rapidly and efficiently. Active interactions with the program participants are anticipated and should enhanced the development of the projects involving mouse models.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Research Program Projects (P01)
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Columbia University (N.Y.)
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Politi, Katerina; Szabolcs, Matthias; Fisher, Peter et al. (2004) A mouse model of uterine leiomyosarcoma. Am J Pathol 164:325-36
Politi, Katerina; Kljuic, Ana; Szabolcs, Matthias et al. (2004) 'Designer' tumors in mice. Oncogene 23:1558-65
Mason, Jeffrey L; Xuan, Shouhong; Dragatsis, Ioannis et al. (2003) Insulin-like growth factor (IGF) signaling through type 1 IGF receptor plays an important role in remyelination. J Neurosci 23:7710-8
Chiao, Eric; Fisher, Peter; Crisponi, Laura et al. (2002) Overgrowth of a mouse model of the Simpson-Golabi-Behmel syndrome is independent of IGF signaling. Dev Biol 243:185-206
Zhang, Mei; Xuan, Shouhong; Bouxsein, Mary L et al. (2002) Osteoblast-specific knockout of the insulin-like growth factor (IGF) receptor gene reveals an essential role of IGF signaling in bone matrix mineralization. J Biol Chem 277:44005-12
Podsypanina, K; Lee, R T; Politis, C et al. (2001) An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/- mice. Proc Natl Acad Sci U S A 98:10320-5
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Simpson, L; Li, J; Liaw, D et al. (2001) PTEN expression causes feedback upregulation of insulin receptor substrate 2. Mol Cell Biol 21:3947-58
Ludwig, T; Fisher, P; Murty, V et al. (2001) Development of mammary adenocarcinomas by tissue-specific knockout of Brca2 in mice. Oncogene 20:3937-48
Dietrich, P; Dragatsis, I; Xuan, S et al. (2000) Conditional mutagenesis in mice with heat shock promoter-driven cre transgenes. Mamm Genome 11:196-205

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