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Kevin M. McBride

Researcher at University of Texas MD Anderson Cancer Center

Publications -  15
Citations -  1782

Kevin M. McBride is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Somatic hypermutation & Immunoglobulin class switching. The author has an hindex of 7, co-authored 15 publications receiving 990 citations.

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B cells and tertiary lymphoid structures promote immunotherapy response

TL;DR: B cell markers were the most differentially expressed genes in the tumours of responders versus non-responders and insights are provided into the potential role of B cells and tertiary lymphoid structures in the response to ICB treatment, with implications for the development of biomarkers and therapeutic targets.
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Mechanism of suppression of chromosomal instability by DNA polymerase POLQ

TL;DR: The experiments show that Polq-null murine cells are selectively hypersensitive to DNA strand breaking agents, and that damage resistance requires the DNA polymerase activity of POLQ, and depart from the prevailing view that alternative end joining processes are generically translocation-prone.
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Arginine methylation facilitates the recruitment of TOP3B to chromatin to prevent R-loop accumulation

TL;DR: By reducing negative supercoiling and resolving R loops, TOP3B promotes transcription, protects against DNA damage, and reduces the frequency of chromosomal translocations.
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Identification of a fragment-like small molecule ligand for the methyl-lysine binding protein, 53BP1.

TL;DR: This work has targeted the DNA damage response protein, 53BP1, which uses its tandem tudor domain to recognize histone H4 dimethylated on lysine 20 (H4K20me2), a modification related to double-strand DNA breaks and shows cellular activity by suppressing class switch recombination.
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Defining the mutation signatures of DNA polymerase θ in cancer genomes

TL;DR: The POLQ-associated mutation signatures in human cancers are defined, characterized by short insertions and deletions in a specific range of microhomologies, and it is shown that TMEJ dominates end joining of two separated DSBs (distal EJ), which will aid in identifying tumors relying on POLQ activity.