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James Dongjoo Ham

Researcher at Massachusetts Institute of Technology

Publications -  5
Citations -  384

James Dongjoo Ham is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 2, co-authored 2 publications receiving 113 citations.

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CAR-NK cells: A promising cellular immunotherapy for cancer

TL;DR: Current challenges and future promise of CAR-NK cells as a novel cellular immunotherapy in cancer are discussed, and they could be engineered to target diverse antigens, enhance proliferation and persistence in vivo, increase infiltration into solid tumours, overcome resistant tumour microenvironment, and ultimately achieve an effective anti-tumour response.
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Memory-like NK cells armed with a neoepitope-specific CAR exhibit potent activity against NPM1 mutated acute myeloid leukemia

TL;DR: Efficient arming of CIML NK cells with a neoepitope-specific chimeric antigen receptor (CAR) significantly enhances their antitumor responses to nucleophosphmin-1 (NPM1)-mutated AML while avoiding off-target toxicity.
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Engineered Memory-like NK Cars Targeting a Neoepitope Derived from Intracellular NPM1c Exhibit Potent Activity and Specificity Against Acute Myeloid Leukemia

TL;DR: This work utilized a new approach to arm NK cells for adoptive immunotherapy based on innate cell memory and overcome the transduction block in primary human and mouse NK cells by utilizing an unconventional pseudotyped lentivirus based on a unique protein with high expression on CIML NK cells.
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Ovarian Cancer Ascites Inhibits Transcriptional Activation of NK Cells Partly through CA125

TL;DR: It is shown that ascites and CA125 inhibit antitumor activity of NK cells at transcriptional levels by suppressing expression of genes involved in NK cell activation and cytotoxicity.
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Integrated multi-omics analyses reveal homology-directed repair pathway as a unique dependency in near-haploid leukemia

TL;DR: In this article , the homologous recombination pathway component RAD51B was identified as an essential gene in near-haploid leukemia, and DNA damage analyses revealed significantly increased sensitivity of RAD51-mediated repair to RAD51b loss in the G2/M stage.