MODULATION OF THE RAT TUMOR-ASSOCIATED SHEDDING ANTIGEN (CE7) AND AUGMENTATION OF IMMUNOGENICITY BY IRRADIATION

Citation
T. Shibata et al., MODULATION OF THE RAT TUMOR-ASSOCIATED SHEDDING ANTIGEN (CE7) AND AUGMENTATION OF IMMUNOGENICITY BY IRRADIATION, Anticancer research, 16(1), 1996, pp. 99-104
Citations number
20
Categorie Soggetti
Oncology
Journal title
ISSN journal
02507005
Volume
16
Issue
1
Year of publication
1996
Pages
99 - 104
Database
ISI
SICI code
0250-7005(1996)16:1<99:MOTRTS>2.0.ZU;2-B
Abstract
We have previously reported that rat fibrosarcoma KMT-17 cells and the ir in vitro counterparts, cloned A3 cells, shed a tumor-associated ant igen (TAA), termed CE7, from the cell surface on vesicular membranes, under growth-enhancing conditions. This study shows that irradiation ( 1 similar to 60Gy) from a Co-60 source, inhibited A3 cell growth dose- dependently and correspondingly increased CE7 expression by A3 cells a s determined by anti-CE7 monoclonal antibody using flow cytometry. CE7 expression gradually increased with increasing doses of irradiation a nd reached a peak level at 30Gy. After 30Gy irradiation, CE7 expressin g A3 cells were fixed with 1% paraformaldehyde and were used to intrad ermally immunize syngenic rats. Immunized rats developed transplantati on resistance to the parent KMT-17 cells as compared to rats immunized with unirradiated A3 cells. Rat MHC class 1 antigen expression was sl ightly decreased by irradiation and therefore, resistance to tumor tra nsplantation appeared to arise solely due to the enhancing effect of i rradiation on TAA expression which increases the antigenicity of the t umor cells coverting them to an effective stimulator of antitumor effe ctor cells. This phenomenon may offer a posibility of the resistance t o the re-emergence and metastasis of the tumor like a KMT-17 through t he induction of antitumor memory cells.