The insulin receptor content is increased in breast cancers initiated by three different oncogenes in transgenic mice

The Insulin Receptor (IR) is a potential oncogene for mammary epithelial cells since its content is increased in most human breast cancer specimens, and both ligand-dependent malignant transformation and ligand-dependent enhanced growth occurs in cultured breast cells overexpressing the IR. To bette...

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Bibliographic Details
Published in:Breast cancer research and treatment 1997-09, Vol.45 (2), p.141-147
Main Authors: FRITTITTA, L, CERRATO, A, SACCO, M. G, WEIDNER, N, GOLDFINE, I. D, VIGNERI, R
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Breast cancer
Cancer research
Carcinogenesis, carcinogens and anticarcinogens
Female
Foods and miscellaneous
Gynecology. Andrology. Obstetrics
Ligands
Male
Mammary gland diseases
Mammary Glands, Animal - chemistry
Mammary Neoplasms, Animal - chemistry
Mammary Neoplasms, Animal - genetics
Mammary Neoplasms, Animal - pathology
Medical sciences
Mice
Mice, Transgenic
Oncogenes - genetics
Proteins
Radioimmunoassay
Receptor, Insulin - analysis
Rodents
Tumors
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Summary:The Insulin Receptor (IR) is a potential oncogene for mammary epithelial cells since its content is increased in most human breast cancer specimens, and both ligand-dependent malignant transformation and ligand-dependent enhanced growth occurs in cultured breast cells overexpressing the IR. To better understand whether the IR plays a role in mammary carcinogenesis which is independent of other initiation factors, we measured IR content in transgenic mouse models of breast cancer induced by 3 known oncogenes (Wnt-1, Neu, and Ret). Insulin receptor content was measured by a specific radioimmunoassay. In normal mammary gland tissues IR content was 14.6 +/- 1.4 ng/mg of protein (mean +/- SEM, n = 6). In the 3 cancers IR content was elevated (Neu = 36.1 +/- 4.6, n = 8, p < 0.002; Wnt-1 = 38.3 +/- 2.6, n = 13, p < 0.001; and Ret = 53.6 +/- 7.1, n = 7, p < 0.001). These data indicate that IR overexpression, in addition to being a potential oncogene, is increased in mouse tumors initiated by other oncogenes, and therefore may also play a supportive role in the growth of breast cancers.
ISSN:0167-6806
1573-7217
DOI:10.1023/A:1005801713713