Evolution of cell‐mediated antitumor immunity in mice bearing a syngeneic chemically induced tumor. Influence of tumor growth, surgical removal and treatment with irradiated tumor cells

Belehradek, Jean; Barski, G; Thonier, M.

doi:10.1002/ijc.2910090302

Cited by 80 publications

(36 citation statements)

References 20 publications

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“…Evidence by Benjamini et al (1977) and Wu & Kearney (submitted for publication) revealed that the development of MCTinduced immunity was paralleled by the development of specific cell-mediated cytotoxicity without the formation of detectable anti-tumour antibodies. On the other hand, specific immunity acquired by tumour excision is mediated by both cytotoxic cells (Belehradek et al, 1972) and antibody (Pilch & Riggins, 1966). By using a modification of the method described by Brown et al (1977), sera from Hf1 tumour-bearing mice and from mice immunized by tumour excision were found to possess specific antibody to the HI tumour (Kearney, to be published).…”

Section: Discussionmentioning

confidence: 99%

Effects of carrageenan, PVP and tumour-bearer serum on immunity induced by excision or mitomycin C-treated tumour cells in mice

Kearney¹,

Wu²,

Orr³

1979

Br J Cancer

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Summary.-Carrageenan (Cg) was tested for its effects on the growth of, and immunity to, 2 methylcholanthrene-induced syngeneic murine fibrosarcomas (HI and H2). The tumours were found not to share major tumour-specific transplantation antigens. H2 appeared more immunogenic than HI. In contrast to HI, immunity induced by H2 was not affected by Cg, nor was its growth in Cg-treated normal mice augmented. We propose that TBS does not inhibit CMI in vivo provided that macrophages remain functional, but may do so when macrophages are rendered defective by antimacrophage agents or by products of neoplastic cells. Increasing the levels of specific effector cells can over-ride the inhibiting effects of TBS, even when defective macrophages are present.

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Section: Discussionmentioning

confidence: 99%

Effects of carrageenan, PVP and tumour-bearer serum on immunity induced by excision or mitomycin C-treated tumour cells in mice

Kearney¹,

Wu²,

Orr³

1979

Br J Cancer

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“…The LPB cell line, a methylcholanthrene-induced C57Bl/6 mouse sarcoma cell line (Belehradek et al, 1972), and the B16 F0 melanoma cells (ATCC CRL 6322) were cultured using classical procedures and minimum essential medium culture medium (Gibco BRL, Cergy-Pontoise, France) supplemented with 100 U ml À1 penicillin, 100 mg ml À1 streptomycin (Sarbach, France) and 8% fetal calf serum (Gibco). These two cell lines had been previously used in the laboratory in preclinical trials of the ECT (Mir et al, , 1992Sersa et al, 1994) as well as for analysing in vivo cell electrofusion (Mekid and Mir, 2000).…”

Section: Tumour Cells Culture and Tumour Productionmentioning

confidence: 99%

“…Of course, this could result from different kinetics in the generation and disappearance of the apoptotic cells in both tumours, but it cannot be excluded that the infiltrating immune system cells present in the LPB tumours at these time points could contribute to the generation of apoptotic cells. As a matter of fact, it is known that LPB cells are immunogeneic (Belehradek et al, 1972) while the B16F0 are not. In parallel, it must be noted that a large fraction (up to 60%) of LPB tumours can be cured after one single ECT session using 10 mg of BLM per mice (Mir et al, 1992) while, using exactly the same protocol, only 16% of the B16F0 tumours could be cured (Sersa et al, 1995).…”

Section: In Vivo Blm Causes Mitotic Cell Death or Pseudoapoptosismentioning

confidence: 99%

In vivo evolution of tumour cells after the generation of double-strand DNA breaks

et al. 2003

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In vitro, the ratio of single-to double-strand DNA breaks (DSB) and their absolute values determine the cell death pathway. The consequences of the generation of various numbers of DSB generated in vivo in tumour cells have been analysed in two different experimental tumour models. Synchronisation of DSB generation and control of their number have been achieved using different doses of bleomycin (BLM) and tumour cell permeabilisation by means of locally delivered electric pulses. According to BLM dose, different cell death pathways are observed. At a low therapeutic dose, a mitotic cell death pathway is detected. It is characterised by the appearance of 'atypical mitosis', TUNEL and caspase-3 positive, 24 h after the treatment, and later by the presence of typical apoptotic figures, mainly TUNEL positive but caspase-3 negative. Caspase-3 is thus an early marker of apoptosis. Mitotic cell death is also followed by lymphocytic infiltration reaction. At high doses of BLM, pseudoapoptosis is detected within a few minutes after the treatment. These cell death pathways are discussed as a function of the number of DSB generated, by comparison with previous results obtained in vitro using BLM or ionising radiation.

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“…It can be induced by both immunogenic and non-immunogenic tumours but the mechanisms involved have been reported to be different. In effect, concomitant resistance induced by strongly immunogenic tumours has been described as tumour specific and mainly mediated by T-cell-dependent cytotoxic mechanisms, not different from a classical immunological rejection (Belehradek et al, 1972;Chandradasa, 1973;Tuttle et al, 1983;North, 1984;Akporiaye et al, 1988). On the other hand, concomitant resistance induced by weakly or non-immunogenic tumours has been described as non-specific and mediated by a cytostatic mechanism presumably unrelated to any known conventional immunological mechanism (Gorelik et al, 1981;Gorelik, 1983;Ruggiero et al, 1985;Meiss et al, 1986;Bonfil et al, 1988).…”

mentioning

confidence: 99%

A serum-mediated mechanism for concomitant resistance shared by immunogenic and non-immunogenic murine tumours

Franco

Bustuoabad²,

Gianni³

et al. 1996

Br J Cancer

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Summary Resistance of tumour-bearing mice to a second tumour challenge, that is concomitant resistance, was evaluated in euthymic and nude mice using nine tumours with widely different degrees of immunogenicity. Two temporally separate peaks of concomitant resistance were detected during tumour development. The first one was exhibited only by small immunogenic tumours; it was tumour specific and mediated by classical immunological T-cell-dependent mechanisms. The second peak was shared by both immunogenic and nonimmunogenic large tumours; it was non-specific, thymus independent and correlated with the activity of a serum factor (neither antibody nor complement) that inhibited the in vitro proliferation of tumour cells. This factor was eluted from a Sephadex G-15 column at fractions corresponding to a molecular weight of approximately 1000 Da and it was recovered from a high-performance liquid chromatography column in one peak presenting maximum absorption at 215 and 266 nm. The data presented in this paper suggest for the first time, to our knowledge, that in spite of the differences between immunogenic and non-immunogenic tumours, a common serum-mediated mechanism seems to underlie the concomitant resistance induced by both types of tumours at late stages of tumour development.

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Evolution of cell‐mediated antitumor immunity in mice bearing a syngeneic chemically induced tumor. Influence of tumor growth, surgical removal and treatment with irradiated tumor cells

Abstract: The evolution of the specific cell-mediated immune status was studied in C57BL/6 mice bearing a chemically induced syngeneic savcoma, the TBL CL2 tumor. Peritoneal cells ( P C )

Cited by 80 publications

References 20 publications

Effects of carrageenan, PVP and tumour-bearer serum on immunity induced by excision or mitomycin C-treated tumour cells in mice

Effects of carrageenan, PVP and tumour-bearer serum on immunity induced by excision or mitomycin C-treated tumour cells in mice

In vivo evolution of tumour cells after the generation of double-strand DNA breaks

A serum-mediated mechanism for concomitant resistance shared by immunogenic and non-immunogenic murine tumours

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