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IgG fractions from serum of patients with transitional-cell carcinoma of the urinary bladder (TCC), patients with carcinoma of the prostate (CC) and healthy donors (HD) were tested for their capacity to induce antibody-dependent lymphocyte-mediated cytotoxicity (ADCC) to tumor cells in vitro. Lymphocytes from healthy donors were selected for low natural cytotoxicity to the target cells from established cell lines of TCC or other origins. IgG was prepared by adsorption of serum to Sepharose-bound protein A from Staphylococcus aureus and subsequent acid elution. When tested against a panel of six different target cells, most individual IgG preparations from all three donor groups contained antibodies inducing ADCC to some of the target cells. When IgG preparations from II untreated TCC patients were studied for ADCC induction to the TCC target T24 and the colon carcinoma HT29, cytotoxicity to T24 was, on an average, significantly higher than that to HT29. For IgG preparations from 18 TCC patients, treated with radiotherapy, a similar difference was seen but was not statistically significant. IgG preparations from II patients with carcinoma of the prostate and from 12 healthy donors did not show this differences. Moreover, while individual IgG preparations from untreated TCC patients were, on the average, significantly more cytotoxic to T24 than those from either of the two control groups, no such differences were seen when HT29 was the target. On the contrary, IgG preparations from patients with prostatic carcinoma were significantly more cytotoxic to HT29 than those from healthy donors. The results suggest that TCC patients develop a disease-related humoral immune response, superimposed on a "natural" immunity to a variety of antigens on the target cells used. The nature of the antigens involved in these reactions remains to be established. However, the results are compatible with previous findings, in these patients, of a bladder-tumor-related cellular cytotoxicity, to a large extent caused by the patients' own antibodies.
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
June 1971,
Journal of the National Cancer Institute,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
December 1972,
National Cancer Institute monograph,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
June 1984,
Journal of immunology (Baltimore, Md. : 1950),
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
October 1977,
International journal of cancer,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
January 1990,
Annali dell'Istituto superiore di sanita,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
December 1982,
Annals of the rheumatic diseases,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
January 1982,
Springer seminars in immunopathology,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
July 1992,
The British journal of surgery,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
March 1978,
Cellular immunology,
M Troye, and
Y Hansson, and
S Paulie, and
P Perlmann, and
H Blomgren, and
B Johansson
October 1988,
Archives of surgery (Chicago, Ill. : 1960),
