| First Author | Bascom JL | Year | 2005 |
| Journal | Cancer Res | Volume | 65 |
| Issue | 19 | Pages | 8617-21 |
| PubMed ID | 16204027 | Mgi Jnum | J:101605 |
| Mgi Id | MGI:3604312 | Doi | 10.1158/0008-5472.CAN-05-1985 |
| Citation | Bascom JL, et al. (2005) Epimorphin overexpression in the mouse mammary gland promotes alveolar hyperplasia and mammary adenocarcinoma. Cancer Res 65(19):8617-21 |
| abstractText | Epimorphin/syntaxin-2 (EPM) is a plasma membrane-anchored protein that has at least two distinct functions depending on its membrane topology: vesicle fusion when localized to the cytoplasmic surface and morphogenic signaling when localized to the extracellular surface. Transgenic mice that express full-length extracellular EPM fused to the NH2-terminal signal sequence of interleukin-2, under the control of the whey acidic protein (WAP) gene promoter, exhibit aberrant mammary gland morphogenesis associated with increased expression of CCAAT enhancer binding protein beta (C/EBPbeta). Here we report that aged nulliparous and uniparous female WAP-EPM transgenic mice develop alveolar hyperplasias and well-differentiated adenocarcinomas that express high levels of C/EBPbeta, keratin-14, matrix metalloproteinase-3, and beta-catenin. This study reveals another pathway in which overexpression and alteration of a normal morphogenic process promote the development of cancer in the mammary gland. |
