Author

Mai Onishi

Harvard UniversityORCID 0000-0002-6733-0253Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Aaron N. HataiD· 1 shared Atrayee BhattacharyaiD· 1 shared Chendi LiiD· 1 shared Donald W. KufeiD· 1 shared Hiroki KomatsudaiD· 1 shared Hiroki OzawaiD· 1 shared Jiehui DengiD· 1 shared Keisuke ShigetaiD· 1 shared

Activity by Year

2026-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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1 shared paperCancer Biology

Aaron N. HataORCID

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1 paper

Recent·Most cited

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

Shinkichi Takamori, Naoki Haratake, Atrayee Bhattacharya, Hiroki Ozawa, Keisuke Shigeta, Mai Onishi, Kentaro Nonaka, Takefumi Komiya, Hiroki Komatsuda, Tomoyoshi Takenaka, Tomoharu Yoshizumi, Chendi Li, Jiehui Deng, Aaron N. Hata, Kwok‐Kin Wong, , 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.

Oncogene · Aug 5, 2026Peer-reviewedCancer Biology