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Alicia Viloria-Petit

Researcher at Ontario Veterinary College

Publications -  44
Citations -  4217

Alicia Viloria-Petit is an academic researcher from Ontario Veterinary College. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor A. The author has an hindex of 21, co-authored 40 publications receiving 3793 citations. Previous affiliations of Alicia Viloria-Petit include Women's College, Kolkata & Sunnybrook Health Sciences Centre.

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Exosomes Mediate Stromal Mobilization of Autocrine Wnt-PCP Signaling in Breast Cancer Cell Migration

TL;DR: It is reported that fibroblast-secreted exosomes promote breast cancer cell (BCC) protrusive activity and motility via Wnt-planar cell polarity (PCP) signaling and it is demonstrated that exosome-stimulated BCC protrusions display mutually exclusive localization of the core PCP complexes.
Journal Article

Acquired Resistance to the Antitumor Effect of Epidermal Growth Factor Receptor-blocking Antibodies in Vivo A Role for Altered Tumor Angiogenesis

TL;DR: The results suggest that variants displaying acquired resistance to anti-EGFR antibodies can emerge in vivo and can do so, at least in part, by mechanisms involving the selection of tumor cell subpopulations with increased angiogenic potential.
Journal Article

Oncogenes and Tumor Angiogenesis: Differential Modes of Vascular Endothelial Growth Factor Up-Regulation in ras-transformed Epithelial Cells and Fibroblasts

TL;DR: The data suggest that the stimulatory effect of mutant ras on VEGF expression is executed in a nonautocrine and cell type-dependent manner and that it can be significantly exacerbated by physiological/ environmental influences such as high cell density.
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Possible mechanisms of acquired resistance to anti-angiogenic drugs: implications for the use of combination therapy approaches.

TL;DR: The ultimate target of anti-angiogenic drugs is the genetically stable, activated endothelial cell of a newly forming tumor blood vessel, rather than the genetically unstable tumor cell population per se, which led to the notion that acquired resistance to such drugs may not develop as readily.