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Kellner, M. ; von Neubeck, B. ; Czogalla, B.* ; Feederle, R. ; Vick, B. ; Jeremias, I. ; Zeidler, R.

A novel anti-CD73 antibody that selectively inhibits membrane 2 CD73 shows antitumor activity and induces tumor immune escape.

Biomedicines 10:825 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
CD73 catalyzes the conversion of ATP to adenosine, which is involved in various physiological and pathological processes, including tumor immune escape. Because CD73 expression and activity are particularly high on cancer cells and contribute to the immunosuppressive properties of the tumor environment, it is considered an attractive target molecule for specific cancer therapies. In line, several studies demonstrated that CD73 inhibition has a significant antitumor effect. How-ever, complete blocking of CD73 activity can evoke autoimmune phenomena and adverse side ef-fects. We developed a CD73-specific antibody, 22E6, that specifically inhibits the enzymatic activity of membrane-tethered CD73 present in high concentrations on cancer cells and cancer cell-derived extracellular vesicles but has no inhibitory effect on soluble CD73. Inhibition of CD73 on tumor cells with 22E6 resulted in multiple effects on tumor cells in vitro, including increased apoptosis and interference with chemoresistance. Intriguingly, in a xenograft mouse model of acute lymphocytic leukemia (ALL), 22E6 treatment resulted in an initial tumor growth delay in some animals, followed by a complete loss of CD73 expression on ALL cells in all 22E6 treated animals, indicating tumor immune escape. Taken together, 22E6 shows great potential for cancer therapy, favorably in combination with other drugs.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Adenosine ; Cancer Therapy ; Cd73 ; Extracellular Vesicles ; Immune Evasion ; Therapeutic Antibody
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2227-9059
e-ISSN 2227-9059
Zeitschrift Biomedicines
Quellenangaben Band: 10, Heft: 4, Seiten: , Artikelnummer: 825 Supplement: ,
Verlag MDPI
Verlagsort Basel, Switzerland
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Gene Vector (AGV)
CF Monoclonal Antibodies (CF-MAB)
Research Unit Apoptosis in Hematopoietic Stem Cells (AHS)
POF Topic(s) 30203 - Molecular Targets and Therapies
30201 - Metabolic Health
30204 - Cell Programming and Repair
Forschungsfeld(er) Immune Response and Infection
Helmholtz Diabetes Center
Stem Cell and Neuroscience
PSP-Element(e) G-501501-001
G-501500-001
G-502210-001
G-506600-001
A-631900-001
Förderungen Helmholtz Zentrum Munchen
DOI 10.3390/biomedicines10040825
WOS ID WOS:000785541300001
Scopus ID 85128329206
PubMed ID 35453575
Erfassungsdatum 2022-08-31
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