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Cheryl A. London

Researcher at University of California, Davis

Publications -  30
Citations -  3664

Cheryl A. London is an academic researcher from University of California, Davis. The author has contributed to research in topics: Cytotoxic T cell & T cell. The author has an hindex of 24, co-authored 30 publications receiving 3495 citations. Previous affiliations of Cheryl A. London include Brigham and Women's Hospital & Harvard University.

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Journal ArticleDOI

Biochemical Mechanisms of IL-2–Regulated Fas-Mediated T Cell Apoptosis

TL;DR: The ability of IL-2 to enhance expression of a pro-apoptotic molecule, FasL, and to suppress an inhibitor of Fas signaling, FLIP, likely accounts for the role of this cytokine in potentiating T cell apoptosis.
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Functional Responses and Costimulator Dependence of Memory CD4+ T Cells

TL;DR: The findings suggest that the threshold for activation of memory CD4+ cells is lower than that of naive cells, which would permit memory cells to rapidly express their effector functions in vivo earlier in the course of a secondary immune response, when the levels of Ag and the availability of costimulation may be relatively low.
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Multi-center, Placebo-controlled, Double-blind, Randomized Study of Oral Toceranib Phosphate (SU11654), a Receptor Tyrosine Kinase Inhibitor, for the Treatment of Dogs with Recurrent (Either Local or Distant) Mast Cell Tumor Following Surgical Excision

TL;DR: Palladia has biological activity against canine MCTs and can be administered on a continuous schedule without need for routine planned treatment breaks, and shows that spontaneous tumors in dogs are good models to evaluate therapeutic index of targeted therapeutics in a clinical setting.
Journal Article

Phase I Dose-Escalating Study of SU11654, a Small Molecule Receptor Tyrosine Kinase Inhibitor, in Dogs with Spontaneous Malignancies,

TL;DR: This study provides the first evidence that p.o. administered kinase inhibitors can exhibit activity against a variety of spontaneous malignancies in dogs, and it is likely that such agents will demonstrate comparable antineoplastic activity in people.
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Spontaneous canine mast cell tumors express tandem duplications in the proto-oncogene c-kit.

TL;DR: It is demonstrated that although c-kit derived from canine MCT did not contain the previously described activating point mutations, 5 of the 11 tumors analyzed possessed novel mutations consisting of tandem duplications involving exons 11 and 12, suggesting that these mutations may contribute to the development or progression of canine M CT.