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At least 199 records · Page 11Linked to original sources
PubMed1981

Normal levels of natural cytotoxic cells against solid tumours in NK-deficient beige mice.

Natural cell-mediated cytotoxicity (NCMC) capable of in vitro lysis of various lymphoid and non-lymphoid tumours has been described in mice and other species, including man. NCMC has been proposed as a first level of defence against tumour growth in vivo, one which does not need the priming of the conventional immunological response. The effector cells of NCMC seem to belong to a special category of lymphoid cells, being neither classical T or B cells nor macrophages; natural killer (NK) cells have been proposed as the prototype effector cell, although some heterogeneity among effector cells seems to exist, depending on the target cells used for testing. Two main subgroups of NCMC effector cells have been defined: NK cells directed against lymphoma targets and natural cytotoxic (NC) cells directed against solid non-lymphoid tumours. We describe here another distinction between the two systems: while NK activity is low in mice homozygous for the beige (bg) gene NC activity in spleen cell preparations from these animals is comparable with that observed in the appropriate controls (bg/+ and +/+ littermates). The bg syndrome of mice affects lysosome, melanosome and enzymatic functions and is a homologue of the Chediak--Higashi syndrome of man. Defective NK activity in blood lymphocytes has also been reported in patients with Chediak--Higashi syndrome. We also show that several mouse strains which have low NK activity, have normal or high levels of NC functions, expanding our previous observation that NC and NK cells are under distinct genetic control.

Animals↗
PubMed1972

Carcinogenic activity of some benz(a)anthracene derivatives in newborn mice.

Equimolar doses of 7-methylbenz(a)anthracene and 3 of its derivatives were given to newborn male and female Swiss mice. All 4 substances tested increased the risk of tumour development compared with that seen in control mice given the vehicle, arachis oil, only.7-Methylbenz(a)anthracene itself was the most actively tumorigenic of the compounds studied, giving rise to subcutaneous sarcomata at the site of injection, and multiple lung tumours and liver tumours. 7-Bromomethyl-12-methylbenz(a)-anthracene was similarly active in the lung and liver but evoked fewer subcutaneous sarcomata. 7-Bromomethylbenz(a)anthracene was seemingly slightly less active than either 7-methylbenz(a)anthracene or 7-bromomethyl-12-methylbenz(a)anthracene. 4-Chloro-7-bromomethylbenz(a)anthracene exhibited only marginal activity in that it slightly increased the risk of liver tumour development in male mice.

Animals↗
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↗
PubMed1987

Specific (EMT6) and non-specific (WEHI-164) cytolytic activity by host cells infiltrating tumour spheroids.

The development of a serum-free, low-protein culture medium has allowed the detection of tumour-specific cytolytic cells in EMT6 immunized mice bearing EMT6 multicellular tumour spheroids. Spheroid associated (SAC) and peritoneal (PC) effector cells were specific to EMT6 as the target cell, not killing line 1, P815 or RIF-1. The natural killer (NK) cell sensitive target YAC-1 was also not lysed by SAC or PC, indicating undetectable levels of NK cells present within infiltrated spheroids. In contrast, high levels of cytolytic activity were present in SAC, PC and spleen cells against WEHI-164, a line sensitive to natural cytotoxic (NC) and macrophage mediated killing. The EMT6 specific activity was mediated by Thyl+, Lyt2+ cells. The anti-WEHI-164 effector cell population was Thyl-, Lyt2-. The WEHI-164 killer cells were present in SAC and PC from unimmunized mice while the EMT6 specific effector cells were not. After separation of SAC and PC by size using centrifugal elutriation, anti-EMT6 activity was present only in the lymphocyte fraction while anti-WEHI-164 activity was enriched in the macrophage fraction.

Animals↗
PubMed1989

Conversion of xanthine dehydrogenase to xanthine oxidase as a possible marker for hypoxia in tumours and normal tissues.

The enzyme activities of endogenous xanthine dehydrogenase (XDH) and xanthine oxidase (XO) have been measured in 10 different types of mouse tumour and seven normal tissues. The conversion of XDH to XO has been observed in two tumour types upon the prolonged clamping off of the blood supply to the tumours. It is proposed that a similar conversion might also occur naturally in chronically hypoxic cells and that the ratio of the XO activity to the combined XO + XDH activities (%XO activity) could well serve as a marker for tissue hypoxia. A qualitative relationship exists between the %XO activity and literature values of the hypoxic fraction for some tumours measured by radiobiological assays. The influence of tumour size (about 0.2-1.8 g) on %XO activity is presented for all 10 tumours as well as %XO activity determinations for four of the normal tissues.

Animals↗