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Jedd D. Wolchok

Researcher at Memorial Sloan Kettering Cancer Center

Publications -  795
Citations -  154490

Jedd D. Wolchok is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Ipilimumab & Immune system. The author has an hindex of 140, co-authored 713 publications receiving 123336 citations. Previous affiliations of Jedd D. Wolchok include Ludwig Institute for Cancer Research & University of York.

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Ipilimumab efficacy and safety in patients with advanced melanoma: a retrospective analysis of HLA subtype from four trials

TL;DR: P pooled efficacy and safety data are presented according to HLA-A*0201 status and dose from pretreated patients randomized to 0.3, 3, or 10 mg/kg ipilimumab in four phase II trials to support the hypothesis that ipILimumab-treated patients with advanced melanoma have similar outcomes regardless of their HLA*0 201 status.
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18F-FDG PET/CT for Monitoring of Ipilimumab Therapy in Patients with Metastatic Melanoma.

TL;DR: In patients with metastatic melanoma treated with ipilimumab, tumor response according to PERCIST was associated with OS and the data suggest that PMD should not be defined by the appearance of new lesions, but rather by an increase in the sum of SULpeak.
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A Single Heteroclitic Epitope Determines Cancer Immunity After Xenogeneic DNA Immunization Against a Tumor Differentiation Antigen

TL;DR: In this model of xenogeneic DNA immunization, the presence of an hgp100 heteroclitic epitope with a higher affinity for MHC created by three amino acid substitutions at predicted minor anchor residues was necessary and sufficient to induce protective tumor immunity in H-2b mice with melanoma.
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Targeting myeloid-derived suppressor cells with colony stimulating factor-1 receptor blockade can reverse immune resistance to immunotherapy in indoleamine 2,3-dioxygenase-expressing tumors

TL;DR: It is shown that MDSCs are the critical cell population in IDO-expressing B16 tumors in mediating accelerated tumor outgrowth and resistance to immunotherapy, and inhibition of CSF-1R signaling can functionally block tumor-infiltrating M DSCs and enhance anti-tumor T cell responses.