P
Peter A. Forsyth
Researcher at University of Calgary
Publications - 176
Citations - 10507
Peter A. Forsyth is an academic researcher from University of Calgary. The author has contributed to research in topics: Medicine & Glioma. The author has an hindex of 52, co-authored 141 publications receiving 9488 citations. Previous affiliations of Peter A. Forsyth include Alberta Health Services & Tom Baker Cancer Centre.
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Journal ArticleDOI
Metalloproteinases in biology and pathology of the nervous system
TL;DR: Some of the beneficial functions of MMPs during neural development are considered and their roles in repair after brain injury are speculated, as well as a family of proteins known as ADAMs, as some of the properties previously ascribed to M MPs are possibly the result of ADAM activity.
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Reovirus Therapy of Tumors with Activated Ras Pathway
TL;DR: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells and treatment of severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells resulted in regression of tumors.
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Matrix metalloproteinases and diseases of the CNS.
TL;DR: Both the identity of the MMP and its cellular origin could determine whether disease pathogenesis or regeneration occurs, and thus synthetic MMP inhibitors might be valuable for treating some CNS diseases.
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Gelatinase-A (MMP-2), gelatinase-B (MMP-9) and membrane type matrix metalloproteinase-1 (MT1-MMP) are involved in different aspects of the pathophysiology of malignant gliomas
Peter A. Forsyth,Peter A. Forsyth,H Wong,T D Laing,N B Rewcastle,Don Morris,Don Morris,Huong Muzik,Kevin J. Leco,Kevin J. Leco,Randal N. Johnston,Penny M. A. Brasher,Garnette R. Sutherland,Dylan R. Edwards +13 more
TL;DR: The data suggest that gelatinase-A, -B and MT1-MMP are important in the pathophysiology of human gliomas, although the primary role of gelatin enzyme-B may lie in remodelling associated with neovascularization, whereas gelatinase’s role may be involved in both glial invasion and angiogenesis.
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Neutrophils Recruited to Sites of Infection Protect from Virus Challenge by Releasing Neutrophil Extracellular Traps
Craig N. Jenne,Connie H.Y. Wong,Franz J. Zemp,Braedon McDonald,Masmudur M. Rahman,Peter A. Forsyth,Grant McFadden,Paul Kubes +7 more
TL;DR: It is shown that systemic administration of virus analogs or poxvirus infection induces neutrophil recruitment to the liver microvasculature and the release of NETs that protect host cells from virus infection.