General Keynote: Expression of Epidermal Growth Factor Receptor Family in Transgenic Mouse Models of Human Breast Cancer

Muller, William J.

doi:10.1006/gyno.2002.6682

Cited by 4 publications

(4 citation statements)

References 38 publications

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“…34 Some transgenic mouse lines have been established that express mutated versions of the EGFreceptor. 35,36 Due to the considerable efforts and time that is inevitable to produce transgenic mice, such animals have been used more to show that mutated, constitutively activated EGFR have the capacity to induce tumorous growth in vivo. A routine, simple and quick whole animal test for tumorigenic potential of mutations detected in human cancers is not possible.…”

Section: Discussionmentioning

confidence: 99%

Activating mutations in the extracellular domain of the melanoma inducing receptor Xmrk are tumorigenic in vivo

Winnemoeller¹,

Wellbrock²,

Schartl³

2005

Intl Journal of Cancer

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Mutated versions or overexpression of receptor tyrosine kinases such as the epidermal growth factor receptor are found frequently in various cancers. In Xiphophorus the formation of hereditary melanoma is caused by the overexpression of the Xmrk oncogene locus. Xmrk is a mutationally altered version of the epidermal growth factor receptor. Two amino acid changes in the extracellular domain of the receptor were shown in vitro to be responsible for a constitutive, ligand-independent activity of Xmrk. To analyze whether these two mutations are indeed responsible for the in vivo oncogenic activity of the receptor, both were independently introduced into the wild-type, non-oncogenic Xiphophorus EGF-receptor and tested in Medaka embryos for their tumorigenic capacity. Both mutations were sufficient to induce tumors after short latency periods and at a comparable frequency as the native Xmrk oncogene. The G359R mutation led to a significantly higher tumor rate than the C578S mutation. Our study shows that subtle point mutations of the EGF-receptor can lead to a highly tumorigenic oncoprotein.

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Section: Discussionmentioning

confidence: 99%

Activating mutations in the extracellular domain of the melanoma inducing receptor Xmrk are tumorigenic in vivo

Winnemoeller¹,

Wellbrock²,

Schartl³

2005

Intl Journal of Cancer

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“…Both ErbB1 and ErbB2 have been implicated in breast cancer through transgenic animals. Mammary expression of the ErbB1 ligand TGFα induces mammary adenocarcinomas [Muller, 2003]. Mammary expression of the ErbB3 ligand neuregulin or of ErbB2 does likewise.…”

Section: Erbb Receptors and Ligandsmentioning

confidence: 99%

Glycoprotein contributions to mammary gland and mammary tumor structure and function: Roles of adherens junctions, ErbBs and membrane MUCs

Carraway

Palau

Carraway

2005

J of Cellular Biochemistry

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Mammary function is dependent on its three-dimensional organization, which is established and maintained by cell adhesive junctions linked through the membrane to the cell cytoskeleton. These junctions serve not only as structural elements, but also function as initiators and integrators of cell signals. In this review we discuss three types of glycoproteins whose interactions impinge on the function of mammary cell-cell junctions, cadherins, ErbB receptor tyrosine kinases and membrane mucins, as a microcosm of events regulating mammary cell behaviors. Actions of these components are integrated by the critical signaling element b-catenin. When functioning properly, these glycoproteins, b-catenin and associated signaling pathways mesh into a highly structured program for development and function of the gland. However, disruption or dysfunction of these glycoproteins or the signaling elements can lead to disorganization of the epithelia and ultimately to neoplasia. J. Cell. Biochem. 96: 914-926, 2005. ß 2005 Wiley-Liss, Inc.

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“…Control of cell proliferation by the EGFR pathway is critical at multiple steps for specification and determination of the correct numbers of specialized cell types in the fly eye (Baker, 2001;Yang and Baker, 2003;Jones and Moses, 2004). In mouse and human, activation of ErbB signals leads to deregulated cell division and formation of various tumors (Muller, 2002;Holbro et al, 2003). The capacity to stimulate cell proliferation by ErbBs seems to hold true in Xenopus as well.…”

Section: Discussionmentioning

confidence: 99%

“…2 and data not shown), indicating that ErbBs may not act as Wnt or BMP inhibitors to convert ventral to dorsal mesoderm to form a partial secondary axis. Since activation of ErbB signaling in epidermal-derived tissues leads to dysregulated cell proliferation and carcinoma formation in human and mouse (Olayioye et al, 2000;Yarden and Sliwkowski, 2001;Muller, 2002;Holbro et al, 2003), we hypothesized that the ectopic structures induced by ErbB overexpression in frogs might represent a tumor-like cell mass formed by increased cell division. We, therefore, examined the number and the distribution of the mitotic cells in these embryos by anti-phosphorylated histone H3 antibody staining in our immunohistochemistry studies.…”

Section: Activation Of Erbb Signaling Stimulates Cell Proliferationmentioning

confidence: 99%

Regulation of early Xenopus development by ErbB signaling

Nie

Chang

2005

Developmental Dynamics

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ErbB signaling has long been implicated in cancer formation and progression and is shown to regulate cell division, migration, and death during tumorigenesis. The functions of the ErbB pathway during early vertebrate embryogenesis, however, are not well understood. Here we report characterization of ErbB activities during early frog development. Gain-of-function analyses show that EGFR, ErbB2, and ErbB4 induce ectopic tumor-like cell mass that contains increased numbers of mitotic cells. Both the muscle and the neural markers are expressed in these ectopic protrusions. ErbBs also induce mesodermal markers in ectodermal explants. Loss-of-function studies using carboxyl terminal-truncated dominant-negative ErbB receptors demonstrate that blocking ErbB signals leads to defective gastrulation movements and malformation of the embryonic axis with a reduction in the head structures in early frog embryos. These data, together with the observation that ErbBs are expressed early during frog embryogenesis, suggest that ErbBs regulate cell proliferation, movements, and embryonic patterning during early Xenopus development. Developmental Dynamics 235:301-314, 2006.

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General Keynote: Expression of Epidermal Growth Factor Receptor Family in Transgenic Mouse Models of Human Breast Cancer

Cited by 4 publications

References 38 publications

Activating mutations in the extracellular domain of the melanoma inducing receptor Xmrk are tumorigenic in vivo

Activating mutations in the extracellular domain of the melanoma inducing receptor Xmrk are tumorigenic in vivo

Glycoprotein contributions to mammary gland and mammary tumor structure and function: Roles of adherens junctions, ErbBs and membrane MUCs

Regulation of early Xenopus development by ErbB signaling

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