Author

Kentaro Nonaka

Harvard UniversityORCID 0009-0009-1063-8829Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:cell type annotation· 2 Research Focus:drug response / drug discovery· 1 Assay:proteomics· 1

Frequent Co-Authors

Tomoharu YoshizumiiD· 3 shared Atrayee BhattacharyaiD· 2 shared Donald W. KufeiD· 2 shared Mark D. LongiD· 2 shared Naoki HaratakeiD· 2 shared Shinkichi TakamoriiD· 2 shared Tomoyoshi TakenakaiD· 2 shared Aaron N. HataiD· 1 shared

Activity by Year

2026-2026 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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3 shared papersCancer Biology

Tomoharu YoshizumiORCID

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3 papers

Recent·Most cited

Cancer BiologyOncogenePeer-reviewedAug 5, 2026

M1C is a druggable target for NSCLC KRAS G12C mutant tumors resistant to KRAS inhibitors

Shinkichi Takamori, Naoki Haratake, Atrayee Bhattacharya…·Donald W. Kufe

This study identifies M1C as a driver of sotorasib resistance in NSCLC KRAS G12C mutant tumors and shows that targeting M1C improves treatment outcomes.

1 citation

humanproteomics

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Cancer BiologybioRxivPreprintJun 23, 2026

M1C IS NECESSARY FOR DARAXONRASIB RESISTANCE OF NSCLC KRAS(G12C) MUTANT CELLS

Shinkichi Takamori, Naoki Haratake, Kentaro Nonaka…·Donald W. Kufe

This study shows M1C is necessary for daraxonrasib resistance in NSCLC KRAS(G12C) mutant cells and identifies M1C as a potential therapeutic target.

DOI 10.64898/2026.06.20.733526

humanexperimental assay

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Cell BiologybioRxivPreprintMay 9, 2026

Temporal regulation of G2 phase avoids therapy-induced senescence caused by DNA replication stress-inducing drugs and provides synergistic cytotoxicity

Kentaro Nonaka, Takeshi Wakasa, Hiroaki Ochiiwa…·Makoto Iimori

This study shows that shortening the G2 phase enhances cell death from DNA replication stress-inducing drugs, regardless of p53 status.

DOI 10.64898/2026.05.06.723184

humanexperimental assay

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