B7-H3-redirected chimeric antigen receptor T cells target glioblastoma and neurospheres.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Sep 2019
Historique:
received: 11 06 2019
revised: 13 08 2019
accepted: 14 08 2019
pubmed: 31 8 2019
medline: 12 2 2020
entrez: 31 8 2019
Statut: ppublish

Résumé

The dismal survival of glioblastoma (GBM) patients urgently calls for the development of new treatments. Chimeric antigen receptor T (CAR-T) cells are an attractive strategy, but preclinical and clinical studies in GBM have shown that heterogeneous expression of the antigens targeted so far causes tumor escape, highlighting the need for the identification of new targets. We explored if B7-H3 is a valuable target for CAR-T cells in GBM. We compared mRNA expression of antigens in GBM using TCGA data, and validated B7-H3 expression by immunohistochemistry. We then tested the antitumor activity of B7-H3-redirected CAR-T cells against GBM cell lines and patient-derived GBM neurospheres in vitro and in xenograft murine models. B7-H3 mRNA and protein are overexpressed in GBM relative to normal brain in all GBM subtypes. Of the 46 specimens analyzed by immunohistochemistry, 76% showed high B7-H3 expression, 22% had detectable, but low B7-H3 expression and 2% were negative, as was normal brain. All 20 patient-derived neurospheres showed ubiquitous B7-H3 expression. B7-H3-redirected CAR-T cells effectively targeted GBM cell lines and neurospheres in vitro and in vivo. No significant differences were found between CD28 and 4-1BB co-stimulation, although CD28-co-stimulated CAR-T cells released more inflammatory cytokines. We demonstrated that B7-H3 is highly expressed in GBM specimens and neurospheres that contain putative cancer stem cells, and that B7-H3-redirected CAR-T cells can effectively control tumor growth. Therefore, B7-H3 represents a promising target in GBM. FUND: Alex's Lemonade Stand Foundation; Il Fondo di Gio Onlus; National Cancer Institute; Burroughs Wellcome Fund.

Sections du résumé

BACKGROUND BACKGROUND
The dismal survival of glioblastoma (GBM) patients urgently calls for the development of new treatments. Chimeric antigen receptor T (CAR-T) cells are an attractive strategy, but preclinical and clinical studies in GBM have shown that heterogeneous expression of the antigens targeted so far causes tumor escape, highlighting the need for the identification of new targets. We explored if B7-H3 is a valuable target for CAR-T cells in GBM.
METHODS METHODS
We compared mRNA expression of antigens in GBM using TCGA data, and validated B7-H3 expression by immunohistochemistry. We then tested the antitumor activity of B7-H3-redirected CAR-T cells against GBM cell lines and patient-derived GBM neurospheres in vitro and in xenograft murine models.
FINDINGS RESULTS
B7-H3 mRNA and protein are overexpressed in GBM relative to normal brain in all GBM subtypes. Of the 46 specimens analyzed by immunohistochemistry, 76% showed high B7-H3 expression, 22% had detectable, but low B7-H3 expression and 2% were negative, as was normal brain. All 20 patient-derived neurospheres showed ubiquitous B7-H3 expression. B7-H3-redirected CAR-T cells effectively targeted GBM cell lines and neurospheres in vitro and in vivo. No significant differences were found between CD28 and 4-1BB co-stimulation, although CD28-co-stimulated CAR-T cells released more inflammatory cytokines.
INTERPRETATION CONCLUSIONS
We demonstrated that B7-H3 is highly expressed in GBM specimens and neurospheres that contain putative cancer stem cells, and that B7-H3-redirected CAR-T cells can effectively control tumor growth. Therefore, B7-H3 represents a promising target in GBM. FUND: Alex's Lemonade Stand Foundation; Il Fondo di Gio Onlus; National Cancer Institute; Burroughs Wellcome Fund.

Identifiants

pubmed: 31466914
pii: S2352-3964(19)30552-3
doi: 10.1016/j.ebiom.2019.08.030
pmc: PMC6796553
pii:
doi:

Substances chimiques

Antigens, Neoplasm 0
B7 Antigens 0
Biomarkers 0
CD276 protein, human 0
Receptors, Antigen, T-Cell 0
Receptors, Chimeric Antigen 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

33-43

Subventions

Organisme : NCI NIH HHS
ID : R03 CA231766
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA226483
Pays : United States
Organisme : NCI NIH HHS
ID : R03 CA223886
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM008719
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007171
Pays : United States

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

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Auteurs

Dean Nehama (D)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.

Natalia Di Ianni (N)

Laboratory of Immunotherapy of Brain Tumors, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; Unit of Molecular Neuro-Oncology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

Silvia Musio (S)

Laboratory of Immunotherapy of Brain Tumors, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; Unit of Molecular Neuro-Oncology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

Hongwei Du (H)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.

Monica Patané (M)

Unit of Neuropathology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

Bianca Pollo (B)

Unit of Neuropathology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

Gaetano Finocchiaro (G)

Unit of Molecular Neuro-Oncology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.

James J H Park (JJH)

Department of Radiation Oncology, Duke University Health System, Durham, NC, USA.

Denise E Dunn (DE)

Department of Radiation Oncology, Duke University Health System, Durham, NC, USA.

Drake S Edwards (DS)

Department of Radiation Oncology, Duke University Health System, Durham, NC, USA; Department of Pharmacology and Cancer Biology, Duke University Health System, Durham, NC, USA.

Jeffrey S Damrauer (JS)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.

Hannah Hudson (H)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.

Scott R Floyd (SR)

Department of Radiation Oncology, Duke University Health System, Durham, NC, USA; Department of Pharmacology and Cancer Biology, Duke University Health System, Durham, NC, USA.

Soldano Ferrone (S)

Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Barbara Savoldo (B)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA; Department of Pediatrics, University of North Carolina, Chapel Hill, NC, USA.

Serena Pellegatta (S)

Laboratory of Immunotherapy of Brain Tumors, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy; Unit of Molecular Neuro-Oncology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. Electronic address: serena.pellegatta@istituto-besta.it.

Gianpietro Dotti (G)

Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA; Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC, USA. Electronic address: gdotti@med.unc.edu.

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Classifications MeSH