Author

Michael R. Schlabach

ORCID 0009-0004-2729-7614Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Approach:genetic perturbation / CRISPR· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:drug response / drug discovery· 1

Frequent Co-Authors

Christopher Wrocklage· 2 shared Conor Calnan· 2 shared Frank ThompsoniD· 2 shared Gregory V. KryukoviD· 2 shared Hugh GannoniD· 2 shared Isabelle Le MercieriD· 2 shared Jason J. MerkiniD· 2 shared Louise CadzowiD· 2 shared

Activity by Year

2023-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersImmunology

Christopher Wrocklage

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2 papers

Recent·Most cited

ImmunologybioRxivPreprintJan 23, 2026

Dual-inactivation of Regnase-1 and SOCS1 rewires exhausted CD8+ T cell fate to enhance anti-tumor functionality

Isabelle Le Mercier, David Monteiro, Katarina Halpin-Veszeleiova…·Micah J. Benson

This study identifies Regnase-1 and SOCS1 dual-inactivation as a strategy to enhance anti-tumor functionality of CD8+ T cells by rewiring their differentiation and effector state.

2 citations

mousegenetic perturbation / CRISPR

𝕏 PostBluesky

ImmunologybioRxivPreprintSep 5, 2023

Rational design of a SOCS1-edited tumor infiltrating lymphocyte therapy for solid tumors using CRISPR/Cas9 screens

Michael R. Schlabach, Sharon Lin, Zachary Collester…·Micah J. Benson

This study uses CRISPR/Cas9 screens to identify SOCS1 as a target for enhancing T cell therapy, leading to the development of an engineered TIL therapy with improved anti-tumor function.

DOI 10.1101/2023.09.05.555798

mousegenetic perturbation / CRISPR

𝕏 PostBluesky