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William J. Muller

Researcher at McGill University

Publications -  292
Citations -  29807

William J. Muller is an academic researcher from McGill University. The author has contributed to research in topics: Mammary tumor & Carcinogenesis. The author has an hindex of 86, co-authored 279 publications receiving 27904 citations. Previous affiliations of William J. Muller include McGill University Health Centre & Royal Victoria Regional Health Centre.

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Induction of mammary tumors by expression of polyomavirus middle T oncogene: a transgenic mouse model for metastatic disease.

TL;DR: Results suggest that middle T antigen acts as a potent oncogene in the mammary epithelium and that cells that express it possess an enhanced metastatic potential.
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Expression of the neu protooncogene in the mammary epithelium of transgenic mice induces metastatic disease

TL;DR: Overexpression of the unactivated neu protein can induce metastatic disease after long latency and is associated with elevated neu intrinsic tyrosine kinase activity and the de novo tyrosinesine phosphorylation of several cellular proteins.
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Single-step induction of mammary adenocarcinoma in transgenic mice bearing the activated c-neu oncogene

TL;DR: The results indicate that the combination of activated oncogene and tissue context are major determinants of malignant progression and that expression of the activated form of c-neu in the mammary epithelium has particularly deleterious consequences.
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Progression to Malignancy in the Polyoma Middle T Oncoprotein Mouse Breast Cancer Model Provides a Reliable Model for Human Diseases

TL;DR: The PyMT mouse model is demonstrated to be an excellent one to understand the biology of tumor progression in humans, and its comparison to human breast tumors is compared.
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Coexpression of MMTV/v-Ha-ras and MMTV/c-myc genes in transgenic mice: synergistic action of oncogenes in vivo.

TL;DR: Since these tumors arise stochastically and are apparently monoclonal in origin, additional somatic events appear necessary for their full malignant progression, even in the presence of activated v-Ha-ras and c-myc transgenes.