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Kathleen Graham

Researcher at University of Pennsylvania

Publications -  8
Citations -  717

Kathleen Graham is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Macrophage & Pancreatic cancer. The author has an hindex of 5, co-authored 7 publications receiving 443 citations.

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IFNγ and CCL2 Cooperate to Redirect Tumor-Infiltrating Monocytes to Degrade Fibrosis and Enhance Chemotherapy Efficacy in Pancreatic Carcinoma

TL;DR: It is reported that CD40 agonists improve chemotherapy efficacy in pancreatic carcinoma by redirecting tumor-infiltrating monocytes/macrophages to induce fibrosis degradation that is dependent on MMPs.
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Metabolic rewiring of macrophages by CpG potentiates clearance of cancer cells and overcomes tumor-expressed CD47−mediated ‘don’t-eat-me’ signal

TL;DR: It is shown that stimulation with a CpG oligodeoxynucleotide, a Toll-like receptor 9 agonist, evokes changes in the central carbon metabolism of macrophages that enable antitumor activity, including engulfment of CD47+ cancer cells.
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Genetically Engineered Mouse Models of Pancreatic Cancer: The KPC Model (LSL-Kras(G12D/+) ;LSL-Trp53(R172H/+) ;Pdx-1-Cre), Its Variants, and Their Application in Immuno-oncology Drug Discovery.

TL;DR: The value of genetic mouse models for characterizing the immunobiology of PDAC and for investigating novel immunotherapeutics are considered and several variants of these models are described, which may be used in drug development and for providing information on unique aspects of disease biology and therapeutic responsiveness.
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A rational mouse model to detect on-target, off-tumor CAR T cell toxicity.

TL;DR: A mouse model with stable and tunable human HER2 (hHER2) expression on normal hepatic tissue and compared toxicity between affinity-tuned HER2 CAR T cells outperformed the HA-CARTs with superior antitumor efficacy in vivo highlights the importance of T cell targeting in reducing toxicity of normal tissue and also in preventing off-tumor sequestration of CARTs, which reduces their therapeutic potency.