Open AccessGrowth Inhibition of CD20‐positive B Lymphoma Cell Lines by IDEC‐C2B8 Anti‐CD20 Monoclonal Antibody
Author(s) -
Taji Hirohumi,
Kagami Yoshitoyo,
Okada Yasutaka,
Andou Manabu,
Nishi Yoshimi,
Saito Hidehiko,
Seto Masao,
Morishima Yasuo
Publication year - 1998
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1998.tb03280.x
Subject(s) - cd20 , cell culture , monoclonal antibody , cell growth , growth inhibition , apoptosis , biology , lymphoma , mantle cell lymphoma , microbiology and biotechnology , antibody , flow cytometry , programmed cell death , cancer research , cell , chemistry , immunology , biochemistry , genetics
Treatment with IDEC‐C2B8 (C2B8), the chimeric anti‐CD20 antibody, was shown in a phase I‐II study to be very effective for the treatment of low‐grade B‐cell lymphoma, in contrast to the results of most previous immunotherapies with monoclonal antibodies. In a study designed to elucidate the reason for this efficacy, two cell lines derived from lymphomas with BCL2 gene rearrangement (SU‐DHL‐4 and SU‐DHL‐6) showed remarkable growth inhibition and cell‐death, and two other cell lines derived from a diffuse lymphoma (RC‐K8) and a mantle cell lymphoma (SP‐49) showed moderate growth inhibition, but neither a CD20 weakly positive cell line (NALL‐1) nor a negative cell line (MOLT‐4) showed any growth inhibition. An examination of the intensity of cell‐surface CD20 expression showed no correlation between intensity and degree of growth inhibition among the four cell lines showing growth inhibition. Morphological examination revealed condensed and fragmented nuclei and budding of the plasma membrane, both characteristic of apoptosis, with some cells in these cell lines showing growth inhibition by C2B8. Such apoptosis was also confirmed by flow cytometric analysis, suggesting that, at least in part, apoptosis plays a role in this growth inhibition. This growth‐inhibitory mechanism may thus account for the effectiveness of C2B8 antibody therapy.