Anti-Fas/Apo-1 monoclonal antibody CH-11 depletes glutathione and kills multidrug-resistant human leukemic cells

Publication type:
Journal article
Metadata:
Autoren
  • T Efferth
  • U Fabry
  • R Osieka
Autoren-URL
https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:A1996TU63100002&DestLinkType=FullRecord&DestApp=WOS_CPL
DOI
10.1006/bcmd.1996.0002
Externe Identifier
  • Clarivate Analytics Document Solution ID: TU631
  • PubMed Identifier: 8807081
ISSN
1079-9796
Ausgabe der Veröffentlichung
1
Zeitschrift
BLOOD CELLS MOLECULES AND DISEASES
Schlüsselwörter
  • apoptosis
  • Fas/APO-1
  • glutathione
  • drug resistance
  • leukemia
Paginierung
2 - 9
Datum der Veröffentlichung
1996
Status
Published
Titel
Anti-Fas/Apo-1 monoclonal antibody CH-11 depletes glutathione and kills multidrug-resistant human leukemic cells
Sub types
  • Article
Ausgabe der Zeitschrift
22

Data source: Web of Science (Lite)

Other metadata sources:
Autoren
  • Thomas Efferth
  • Ursula Fabry
  • Rainhardt Osieka
DOI
10.1006/bcmd.1996.0002
ISSN
1079-9796
Ausgabe der Veröffentlichung
1
Zeitschrift
Blood Cells, Molecules, and Diseases
Sprache
en
Paginierung
2 - 9
Datum der Veröffentlichung
1996
Status
Published
Herausgeber
Elsevier BV
Herausgeber URL
http://dx.doi.org/10.1006/bcmd.1996.0002
Datum der Datenerfassung
2019
Titel
Anti-Fas/Apo-1 Monoclonal Antibody CH-11 Depletes Glutathione and Kills Multidrug-Resistant Human Leukemic Cells
Ausgabe der Zeitschrift
22

Data source: Crossref

Abstract
Apoptosis is a common pathway by which cells respond to noxious insults or growth regulatory factors. Since cellular glutathione (GSH) content has long been known to govern response to antineoplastic treatment we have compared induction of apoptosis in drug sensitive (HL-60 and K562/WT) and drug resistant (KG-1a and K562/ADM) human leukemic cell lines by the monoclonal antibody CH-11 (anti-Fas/Apo-1). Fraction of apoptotic cells and cellular GSH were determined by flow cytometry. All cell lines were induced to undergo apoptosis by exposure to mAb CH-11 independent of resistance to conventional antineoplastic treatment. In conjunction with exposure to daunorubicin, vincristine, carboplatin, cytosine arabinoside, dexamethasone, or ionizing irradiation the effect of mAb CH-11 on induction of apoptosis was no more than additive. In contrast, preincubation with IFN-gamma markedly enhanced the induction of apoptosis by mAb CH-11 due to an increase of Fas-receptor expression. In each instance, GSH content decreased with increasing fraction of apoptotic cells indicating a crucial role of GSH in the apoptotic pathway.
Addresses
  • Medizinische Klinik IV, RWTH Aachen, Germany.
Autoren
DOI
10.1006/bcmd.1996.0002
eISSN
1096-0961
Externe Identifier
  • PubMed Identifier: 8807081
Open access
false
ISSN
1079-9796
Ausgabe der Veröffentlichung
1
Zeitschrift
Blood cells, molecules & diseases
Schlüsselwörter
  • Tumor Cells, Cultured
  • Humans
  • Leukemia
  • Glutathione
  • Antineoplastic Agents
  • Antibodies, Monoclonal
  • Flow Cytometry
  • Drug Resistance, Multiple
  • Apoptosis
  • Cytotoxicity, Immunologic
  • Drug Resistance, Neoplasm
  • Interferon-gamma
  • fas Receptor
Sprache
eng
Medium
Print
Paginierung
2 - 10
Datum der Veröffentlichung
1996
Status
Published
Datum der Datenerfassung
1996
Titel
Anti-Fas/Apo-1 monoclonal antibody CH-11 depletes glutathione and kills multidrug-resistant human leukemic cells.
Sub types
  • Research Support, Non-U.S. Gov't
  • Journal Article
Ausgabe der Zeitschrift
22

Data source: Europe PubMed Central

Abstract
Apoptosis is a common pathway by which cells respond to noxious insults or growth regulatory factors. Since cellular glutathione (GSH) content has long been known to govern response to antineoplastic treatment we have compared induction of apoptosis in drug sensitive (HL-60 and K562/WT) and drug resistant (KG-1a and K562/ADM) human leukemic cell lines by the monoclonal antibody CH-11 (anti-Fas/Apo-1). Fraction of apoptotic cells and cellular GSH were determined by flow cytometry. All cell lines were induced to undergo apoptosis by exposure to mAb CH-11 independent of resistance to conventional antineoplastic treatment. In conjunction with exposure to daunorubicin, vincristine, carboplatin, cytosine arabinoside, dexamethasone, or ionizing irradiation the effect of mAb CH-11 on induction of apoptosis was no more than additive. In contrast, preincubation with IFN-gamma markedly enhanced the induction of apoptosis by mAb CH-11 due to an increase of Fas-receptor expression. In each instance, GSH content decreased with increasing fraction of apoptotic cells indicating a crucial role of GSH in the apoptotic pathway.
Autoren
  • T Efferth
  • U Fabry
  • R Osieka
Autoren-URL
https://www.ncbi.nlm.nih.gov/pubmed/8807081
DOI
10.1006/bcmd.1996.0002
ISSN
1079-9796
Ausgabe der Veröffentlichung
1
Zeitschrift
Blood Cells Mol Dis
Schlüsselwörter
  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Apoptosis
  • Cytotoxicity, Immunologic
  • Drug Resistance, Multiple
  • Drug Resistance, Neoplasm
  • Flow Cytometry
  • Glutathione
  • Humans
  • Interferon-gamma
  • Leukemia
  • Tumor Cells, Cultured
  • fas Receptor
Sprache
eng
Country
United States
Paginierung
2 - 9
PII
S1079-9796(96)90002-9
Datum der Veröffentlichung
1996
Status
Published
Datum, an dem der Datensatz öffentlich gemacht wurde
1996
Titel
Anti-Fas/Apo-1 monoclonal antibody CH-11 depletes glutathione and kills multidrug-resistant human leukemic cells.
Sub types
  • Journal Article
  • Research Support, Non-U.S. Gov't
Ausgabe der Zeitschrift
22

Data source: PubMed

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