ROR1-targeting switchable CAR-T cells for cancer therapy.


Journal

Oncogene
ISSN: 1476-5594
Titre abrégé: Oncogene
Pays: England
ID NLM: 8711562

Informations de publication

Date de publication:
08 2022
Historique:
received: 10 01 2022
accepted: 08 07 2022
revised: 07 07 2022
pubmed: 22 7 2022
medline: 24 8 2022
entrez: 21 7 2022
Statut: ppublish

Résumé

The success of chimeric antigen receptor T cell (CAR-T) therapy in the treatment of hematologic malignancies has prompted the development of numerous CAR-T technologies, including switchable CAR-T (sCAR-T) systems that combine a universal CAR-T with bispecific adapter proteins. Owing to their controllability and versatility, sCAR-Ts have received considerable attention. To explore the therapeutic utility of sCAR-Ts targeting the receptor tyrosine kinase ROR1, which is expressed in hematologic and solid malignancies, and to identify bispecific adaptor proteins that efficiently mediate universal CAR-T engagement, a panel of switches based on ROR1-targeting Fabs with different epitopes and affinities was compared in in vitro and in vivo models of ROR1-expressing cancers. For switches targeting overlapping or identical epitopes, potency correlated with affinity. Surprisingly, however, we identified a switch targeting a unique epitope with low affinity but mediating potent and selective antitumor activity in vitro and in vivo. Converted to a conventional CAR-T, the same anti-ROR1 mAb (324) outperformed a clinically investigated conventional CAR-T that is based on an anti-ROR1 mAb (R12) with ~200-fold higher affinity. Thus, demonstrating therapeutic utility on their own, sCAR-Ts also facilitate higher throughput screening for the identification of conventional CAR-T candidates for preclinical and clinical studies.

Identifiants

pubmed: 35859167
doi: 10.1038/s41388-022-02416-5
pii: 10.1038/s41388-022-02416-5
pmc: PMC9398970
mid: NIHMS1824060
doi:

Substances chimiques

Epitopes 0
Receptors, Chimeric Antigen 0
ROR1 protein, human EC 2.7.10.1
Receptor Tyrosine Kinase-like Orphan Receptors EC 2.7.10.1

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4104-4114

Subventions

Organisme : NCI NIH HHS
ID : R21 CA229961
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA204484
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA174844
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA263240
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA181258
Pays : United States

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Haiyong Peng (H)

Department of Immunology and Microbiology, UF Scripps Biomedical Research, University of Florida, Jupiter, FL, 33458, USA. h.peng@ufl.edu.

Thomas Nerreter (T)

Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Oberdürrbacher Strasse 6, 97080, Würzburg, Germany.

Katrin Mestermann (K)

Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Oberdürrbacher Strasse 6, 97080, Würzburg, Germany.

Jakob Wachter (J)

Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Oberdürrbacher Strasse 6, 97080, Würzburg, Germany.

Jing Chang (J)

Department of Immunology and Microbiology, UF Scripps Biomedical Research, University of Florida, Jupiter, FL, 33458, USA.

Michael Hudecek (M)

Medizinische Klinik und Poliklinik II, Universitätsklinikum Würzburg, Oberdürrbacher Strasse 6, 97080, Würzburg, Germany.

Christoph Rader (C)

Department of Immunology and Microbiology, UF Scripps Biomedical Research, University of Florida, Jupiter, FL, 33458, USA. c.rader@ufl.edu.

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Classifications MeSH