Abstract
As in the development of many human cancers, in a transgenic mouse model of beta-cell carcinogenesis (Rip1Tag2), expression of neural cell adhesion molecule (NCAM) changes from the 120-kDa isoform in normal tissue to the 140/180-kDa isoforms in tumors. NCAM-deficient RiplTag2 mice, generated by crossing Rip1Tag2 mice with NCAM knockout mice, develop metastases, a tumor stage that is not seen in normal Rip1Tag2 mice. In contrast, overexpression of NCAM 120 in NCAM-deficient Rip1Tag2 mice prevents tumor metastasis. The results indicate that the loss of NCAM-mediated cell adhesion is one rate-limiting step in the actual metastatic dissemination of beta tumor cells.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Disease Progression
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Gene Dosage
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Gene Expression Regulation, Neoplastic*
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Humans
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Insulinoma / genetics
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Insulinoma / metabolism
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Insulinoma / physiopathology*
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Islets of Langerhans / cytology
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Islets of Langerhans / metabolism
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Mesoderm
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mice, Transgenic
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Neoplasm Metastasis
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Neural Cell Adhesion Molecules / genetics*
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Neural Cell Adhesion Molecules / physiology
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Pancreatic Neoplasms / genetics
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Pancreatic Neoplasms / metabolism
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Pancreatic Neoplasms / physiopathology*
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Protein Isoforms
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Tumor Cells, Cultured
Substances
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Neural Cell Adhesion Molecules
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Protein Isoforms