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PubMed1975

Cancer and ageing in mice and men.

In an experiment involving 950 mice with a normal lifespan of 2-3 years, in laboratory conditions, regular benzpyrene application to the skin was started at 10, 25, 40 or 55 weeks of age. The incidence rate of malignant epithelial tumours among the survivors in each group increased steeply with time. This increase was associated directly with duration of exposure but, given duration, was independent of age at the start of exposure, as were the growth rates of already established tumours. In our experiment, although age per se was irrelevant, the cancer incidence rate increased approximately as a power of the duration of exposure to benzpyrene. This shows that the observed approximate power-law increase of most human adult cancer incidence rates with age could exist merely because age equals duration of exposure to background and spontaneous carcinogenic stimuli. Thus, no intrinsic effects of ageing (such as failing immunological surveillance or age related hormonal changes) whatever need to postulated to explain the vast increases in old age of the incidence rates of such human cancers. This result can greatly simplify speculation about mechanisms of carcinogenesis.

Age Factors↗
PubMed1977

Effect of ascorbic acid on tumour growth.

The growth of tumours in guinea-pigs was observed for 20 weeks after placing them on various doses of vitamin C. Complete tumour regression occurred in 55% of those animals receiving 0-3 mg/kg/day ascorbic acid, whereas animals given 10 mg/kg/day showed tumour inhibition but no regression. In contrast, tumours in animals maintained on 1 g/kg/day ascorbic acid grew without sign of retardation. When increased amounts of ascorbic acid were restored to the diet of scorbutic tumour-bearing animals, tumours which had not regressed responded with enhanced growth. Likewise, animals previously maintained on 10 mg/kg ascorbic acid responded in turn to the additional vitamin with enhanced tumour growth. In contrast, all tumour-bearing animals maintained on 1 g/kh ascorbic acid died within 3 weeks when this dose was replaced with 0-3 mg/kg.

Animals↗
PubMed1976

Subversion of host defense mechanisms by murine tumors. II. Counter-influence of concomitant antitumor immunity.

Subcutaneous injection of murine tumor cells first resulted in a state of severely suppressed macrophage-mediated antibacterial resistance and then in a contrasting state of greatly enhanced antibacterial resistance. Whereas, the state of suppressed antibacterial resistance corresponded to a state of suppressed resistance to a tumor cell challenge, the generation of enhanced antibacterial resistance corresponded to the acquisition of concomitant antitumor immunity. It was suggested on the basis of this evidence that changes in the level of macrophage-mediated antibacterial resistance that occur during growth of the primary tumor reflected changes in the level of the host's resistance to the tumor itself. It was further suggested that the coincidental suppression of antibacterial and antitumor resistance that occurs during the initial stages of growth of the primary tumor represents the operation of a mechanism that enables the tumor to avoid destruction by macrophages. The results support the view that macrophages play an important role in native and acquired resistance to malignant tumors.

Animals↗
PubMed1978

The immunological basis of endotoxin-induced tumor regression. Requirement for a pre-existing state of concomitant anti-tumor immunity.

It was shown that of four syngeneic, murine tumors investigated, only those that evoked the generation of a state of concomitant anti-tumor immunity were susceptible to endotoxin-induced regression. Moreover, the temporal relationship between the generation of concomitant immunity and the onset of susceptibility to endotoxin-induced regression points to the likely possibility that tumor regression depends on the preceding acquisition of the specifically-sensitized, effector T cells that express concomitant immunity. It is suggested that endotoxin-induced hemorrhagic necrosis which invariably precedes tumor regression serves to create conditions inside the tumor that are conducive to the entry and the functioning of effector T cells. It is also suggested that tumor necrosis factor causes hemorrhagic necrosis rather than tumor regression.

Animals↗
PubMed1976

Induction of tumors by a guinea pig herpesvirus-transformed hamster cell line.

Syrian hamster embryo cells that had been transformed in vitro by guinea pig herpes-like virus (GPHLV) were found to be oncogenic when inoculated into hamster sc or ip. Of 71 animals inoculated, 30 showed tumors at the site of inoculation. Tumors appeared 4-23 weeks after inoculation of the transformed cells at passage 37 or higher. Inbred and randombred hamsters of all ages were susceptible. Upon microscopic examination the tumors were characterized as fibrosarcomas. The cultured hamster tumor cells were easily transplanted into hamsters, but produced no evidence of tumors when inoculated into guinea pigs. Infectious GPHLV was not isolated from the tumor cells, but GPHLV-specific surface antigens were detected in tumor cells by immunofluorescence of GPHLV antiserum produced in rabbits. Sera from tumor-bearing hamsters did not contain GPHLV-neutralizing antibodies, but sera from 4 of 23 hamsters bearing primary tumors and 12 of 41 bearing transplanted tumors produced nuclear fluorescence in cells infected with GPHLV, thus establishing the relationship between the guinea pig herpesvirus and the hamster tumors.

Animals↗
PubMed1977

Isolation of T-lymphocytes from disaggregated tumors, with high purity and good percentage recovery.

A combination of two cell separation methods was utilized for the isolation of thymus-derived lymphocytes (TL) from enzymatically disaggregated tumors. Passage through Sephadex G-10-glass bead columns to remove adherent cell types followed by exposure to IgG-coated sheep red blood cell monolayers for removal of Fc receptor-bearing inflammatory cells provided functional TL suspensions of high purity with good percentage recovery.

Animals↗
PubMed1977

High incidence of ependymomas induced by BK virus, a human papovavirus: brief communication.

Ependymomas were produced in 44 of 50 Syrian golden hamsters and in 9 of 31 outbred Swiss mice inoculated intracerebrally with high-titer, purified BK virus (BKV). Tumors contained a T-antigen that reacted with BKV-specific T-antibody in immunofluorescence and complement-fixation tests. A proportion of tumor-bearing animals had antibodies to BKV T-antigen in their sera. BKV could be rescued from two tumor cell lines by Sendal virus-mediated fusion with Vero cells. A low, or lack of, oncogenic activity was displayed by BKV inoculated sc, ip, or iv.

Animals↗
PubMed1978

Serum haptoglobin levels in mice with 7, 12-dimethylbenz[a]anthracene-induced tumors.

Serum haptoglobin (Hp) levels were determined periodically in mice treated with the carcinogen 7, 12-dimethylbenz[a]anthracene (DMBA). The magnitude and duration of the Hp response to tumors induced by DMBA were dependent on the tumor type; lymphocytic lymphomas elicted a minimal response, whereas mice bearing mammary carcinomas and stomach squamous cell carcinomas had high Hp levels which remained elevated throughout most of the period of tumor development. In the majority of mice with mammary carcinomas, the initial rise in serum Hp coincided fairly closely with the first appearance of palpable masses. Some variation in the magnitude of the Hp response was observed between individual mice bearing chemically-induced tumors of similar histological types.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Augmentation of delayed-type hypersensitivity and resistance against allogeneic or syngeneic methylcholanthrene-induced tumors in mice preimmunized with the tumor extracts.

Delayed-type hypersensitivity (DTH) responses against methylcholanthrene-induced fibrosarcomas in C3H/He and BDF1 mice were developed in BDF1 mice by sc injection of the respective mitomycin C-treated tumor cells. The DTH responses to the allogeneic and the syngeneic tumor cells were accelerated and enhanced tumor-specifically by priming 7 days previously with KCl extracts of the respective tumors. The ability in the mice primed with the tumor extracts enhancing the DTH response against the tumor cells could be transferred to recipient mice by the spleen cells, but not by the T-cell-depleted spleen cells. Rejection of allogeneic tumor was accelerated under the development of accelerated and enhanced DTH response against the allogeneic tumor antigens. Moreover, resistance to syngeneic tumor growth increased significantly with the development of accelerated and enhanced DTH response against the syngeneic tumor antigens. Thus, the augmentation of DTH response by preimmunization with tumor extracts was accompanied by the increased resistance to tumor growth, suggesting that T cells involved in the augmentation of tumor-specific DTH response play some role in increasing the resistance to tumor growth.

Animals↗
PubMed1976

Effects of the removal of the regional lymph nodes on the survival of mice bearing B 16 melanoma or EAkR lymphosarcoma.

This work presents data concerning the effect of tumor excision accompanied or not by the removal of the regional lymph node (RLN) on the survival time of mice bearing the EAkR lymphosarcoma or the B16 melanoma. The operations were performed at various times to study this effect in relation to tumor volume. Early tumorectomy, on day 6 for the EAkR lymphosarcoma, on day 10 for the B16 melanoma, prolonged significantly the survival time. The additional removal of the RLN abolished this beneficial effect. In the case of the EAkR lymphosarcoma, a beneficial effect on the survival time was in contrast observed after a total excision of the tumor accompanied by RLN removal performed on day 8. The two surgical procedures were ineffective in increasing the survival time when they were applied after the 8th day for the EAkR lymphosarcoma and after the 10th day for the B16 melanoma. These results suggest that the preservation of the RLN may be favorable for the host at least at an early stage of the tumor growth.

Abdominal Neoplasms↗