CD70 is a therapeutic target upregulated in EMT-associated EGFR tyrosine kinase inhibitor resistance

Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface pro...

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Published inCancer cell Vol. 41; no. 2; pp. 340 - 355.e6
Main Authors Nilsson, Monique B., Yang, Yan, Heeke, Simon, Patel, Sonia A., Poteete, Alissa, Udagawa, Hibiki, Elamin, Yasir Y., Moran, Cesar A., Kashima, Yukie, Arumugam, Thiruvengadam, Yu, Xiaoxing, Ren, Xiaoyang, Diao, Lixia, Shen, Li, Wang, Qi, Zhang, Minying, Robichaux, Jacqulyne P., Shi, Chunhua, Pfeil, Allyson N., Tran, Hai, Gibbons, Don L., Bock, Jason, Wang, Jing, Minna, John D., Kobayashi, Susumu S., Le, Xiuning, Heymach, John V.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 13.02.2023
Subjects
Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - genetics
CD27 Ligand - genetics
CD70
Cell Line, Tumor
Drug Resistance, Neoplasm - genetics
EGFR
Epithelial-Mesenchymal Transition - genetics
ErbB Receptors - metabolism
Humans
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Mutation
NSCLC
Tyrosine Kinase Inhibitors - therapeutic use
NSCLC
CD70
EGFR
Online AccessGet full text
ISSN1535-6108
1878-3686
1878-3686
DOI10.1016/j.ccell.2023.01.007

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Abstract Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting chimeric antigen receptor (CAR) T cell and CAR NK cells show potent activity against EGFR TKI-resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation. [Display omitted] •CD70 is upregulated on EGFR mutant NSCLC cells that have undergone EMT•In EGFR inhibitor-resistant cells, CD70 regulates cell survival and invasiveness•CD70 upregulation occurs in drug-tolerant persister cells (DTPCs)•Drug-resistant CD70+ tumors can be targeted with CD70-ADCs, CAR Ts, and NK-CARs Nilsson et al. show that CD70 is highly upregulated in non-small cell lung cancer (NSCLC) tumors with acquired EGFR tyrosine kinase inhibitor (TKI) resistance that occurs independent of MET or secondary EGFR mutations. Anti-CD70 antibody drug conjugates and CD70-targeting CAR T and CAR NK cells have activity against resistant cells and drug-tolerant persister cells.
AbstractList Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting chimeric antigen receptor (CAR) T cell and CAR NK cells show potent activity against EGFR TKI-resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation.Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting chimeric antigen receptor (CAR) T cell and CAR NK cells show potent activity against EGFR TKI-resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation.
Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting chimeric antigen receptor (CAR) T cell and CAR NK cells show potent activity against EGFR TKI-resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation. [Display omitted] •CD70 is upregulated on EGFR mutant NSCLC cells that have undergone EMT•In EGFR inhibitor-resistant cells, CD70 regulates cell survival and invasiveness•CD70 upregulation occurs in drug-tolerant persister cells (DTPCs)•Drug-resistant CD70+ tumors can be targeted with CD70-ADCs, CAR Ts, and NK-CARs Nilsson et al. show that CD70 is highly upregulated in non-small cell lung cancer (NSCLC) tumors with acquired EGFR tyrosine kinase inhibitor (TKI) resistance that occurs independent of MET or secondary EGFR mutations. Anti-CD70 antibody drug conjugates and CD70-targeting CAR T and CAR NK cells have activity against resistant cells and drug-tolerant persister cells.
Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial-to-mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting chimeric antigen receptor (CAR) T cell and CAR NK cells show potent activity against EGFR TKI-resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation.
Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire resistance to EGFR tyrosine kinase inhibitors (TKIs) mediated by epithelial to mesenchymal transition (EMT). We investigate cell surface proteins that could be targeted by antibody-based or adoptive cell therapy approaches and identify CD70 as being highly upregulated in EMT-associated resistance. Moreover, CD70 upregulation is an early event in the evolution of resistance and occurs in drug-tolerant persister cells (DTPCs). CD70 promotes cell survival and invasiveness, and stimulation of CD70 triggers signal transduction pathways known to be re-activated with acquired TKI resistance. Anti-CD70 antibody drug conjugates (ADCs) and CD70-targeting CAR T cell and CAR NK cells show potent activity against EGFR TKI resistant cells and DTPCs. These results identify CD70 as a therapeutic target for EGFR mutant tumors with acquired EGFR TKI resistance that merits clinical investigation. Nilsson et al. show that CD70 is highly upregulated in non-small cell lung cancer (NSCLC) tumors with acquired EGFR tyrosine kinase inhibitor (TKI) resistance that occurs independent of mesenchymal-epithelial transition (MET) or secondary EGFR mutations. Anti-CD70 antibody drug conjugates and CD70-targeting CAR T and CAR NK cells have activity against resistant cells as well as drug tolerant persister cells.
Author Poteete, Alissa
Zhang, Minying
Moran, Cesar A.
Robichaux, Jacqulyne P.
Diao, Lixia
Udagawa, Hibiki
Yang, Yan
Arumugam, Thiruvengadam
Ren, Xiaoyang
Kobayashi, Susumu S.
Gibbons, Don L.
Bock, Jason
Shi, Chunhua
Shen, Li
Minna, John D.
Heeke, Simon
Wang, Jing
Elamin, Yasir Y.
Pfeil, Allyson N.
Nilsson, Monique B.
Kashima, Yukie
Heymach, John V.
Patel, Sonia A.
Tran, Hai
Le, Xiuning
Wang, Qi
Yu, Xiaoxing
AuthorAffiliation 4 Oncology Research BIT, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
3 Department of Thoracic/Head and Neck Medical Oncology, Bioinformatics and Computational Biology
5 Biologics Development, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
7 Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas
1 Department of Thoracic/Head and Neck Medical Oncology
6 Hamon Center for Therapeutic Oncology Research, Simmons Comprehensive Cancer Center, Department of Pharmacology
2 Department of Thoracic/Head and Neck Medical Oncology, Pathology
9 Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
8 Division of Translational Genomics, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/36787696$$D View this record in MEDLINE/PubMed
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Thu Apr 24 23:08:37 EDT 2025
Fri Feb 23 02:38:58 EST 2024
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Issue 2
Keywords NSCLC
CD70
EGFR
Language English
License Copyright © 2023. Published by Elsevier Inc.
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Lead Contact
Conceptualization, M.B.N and J.V.H; Formal analysis, M.B.N, J.V.H, J.W; Investigational studies, M.B.N, Y.Y, J.P.R, S.H, S.A.P, A.P, H.U, Y.K, T.A, X.Y, X.R, L.S, L.D, Q.W, M.Z, C.S, A.P, Y.E. C.M.; Writing, M.B.N, and J.V.H; Supervision, M.B.N, J.V.H, H.T, J.M., J.B, S.S.K., J.W., X.L, and D.L.G.
Currently affiliated with AstraZeneca Pharmaceuticals, Cambridge, Massachusetts
Author Contributions
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/10259078
PMID 36787696
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Snippet Effective therapeutic strategies are needed for non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations that acquire...
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SubjectTerms Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - genetics
CD27 Ligand - genetics
CD70
Cell Line, Tumor
Drug Resistance, Neoplasm - genetics
EGFR
Epithelial-Mesenchymal Transition - genetics
ErbB Receptors - metabolism
Humans
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Mutation
NSCLC
Tyrosine Kinase Inhibitors - therapeutic use
Title CD70 is a therapeutic target upregulated in EMT-associated EGFR tyrosine kinase inhibitor resistance
URI https://dx.doi.org/10.1016/j.ccell.2023.01.007
https://www.ncbi.nlm.nih.gov/pubmed/36787696
https://www.proquest.com/docview/2777011656
https://pubmed.ncbi.nlm.nih.gov/PMC10259078
Volume 41
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