Abstract |
In this study, we compared the ability of different bispecific monoclonal antibodies (BsmAb) and immunotoxins to deliver the type 1 ribosome-inactivating proteins (RIP) saporin and gelonin through the CD25 or CD30 target molecules to Hodgkin's lymphoma cells. An anti-CD25/antisaporin and an anti-CD30/antisaporin BsmAb enhanced the toxicity of the relevant RIP against the CD25+CD30+ L540 Hodgkin's lymphoma cell line, although targeting by anti-CD30 BsmAb appeared eight times more efficient. Two anti-CD30/antigelonin BsmAb, reacting with different epitopes of the gelonin molecule, were able to enhance gelonin toxicity against L540 cells and had a synergistic effect when used in combination. Among CD25-CD30+ Hodgkin's lymphoma lines, which were resistant to targeting by anti-CD25/ saporin BsmAb, one (L428) was sensitive to both gelonin and saporin delivered by anti-CD30 BsmAb. Another CD25-CD30+ cell line (COLE) was completely resistant to the toxic effect of gelonin targeted by the two synergistic BsmAb, as well as to an anti-CD30/ gelonin immunotoxin. However, these cells were partially sensitive to saporin delivered by an anti-CD30/anti- saporin BsmAb, and they were efficiently killed by an anti-CD30/ saporin immunotoxin. These results indicate that heterogeneity in the sensitivity to certain RIP, such as gelonin, exists among tumor cells of the same histotype.
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Authors | S Sforzini, A Bolognesi, R Meazza, S Marciano, P L Tazzari, H Stein, F Stirpe, S Ferrini |
Journal | Journal of hematotherapy
(J Hematother)
Vol. 4
Issue 5
Pg. 429-32
(Oct 1995)
ISSN: 1061-6128 [Print] United States |
PMID | 8581380
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antibodies, Monoclonal
- Antigens, Neoplasm
- Immunotoxins
- Ki-1 Antigen
- Plant Proteins
- Receptors, Interleukin-2
- Ribosome Inactivating Proteins, Type 1
- GEL protein, Gelonium multiflorum
- N-Glycosyl Hydrolases
- Saporins
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Topics |
- Animals
- Antibodies, Monoclonal
(administration & dosage, immunology)
- Antibody Specificity
- Antigens, Neoplasm
(metabolism)
- Burkitt Lymphoma
(pathology)
- Drug Synergism
- Hodgkin Disease
(pathology)
- Humans
- Immunotoxins
(administration & dosage)
- Ki-1 Antigen
(metabolism)
- Mice
- N-Glycosyl Hydrolases
- Plant Proteins
(administration & dosage, immunology)
- Receptors, Interleukin-2
(metabolism)
- Ribosome Inactivating Proteins, Type 1
- Saporins
- Tumor Cells, Cultured
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