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At least 811 records · Page 45Linked to original sources
PubMed1979

Investigation of the human macrophage. II. The in vitro cytotoxicity of macrophages.

Macrophage-mediated cytotoxicity in vitro was studied by a tritiated thymidine incorporation inhibition assay as well as by microscopic examination and optical transmitance determination. It was found that macrophages from patients with malignant diseases showed cytotoxic effects on two malignant human cell lines. The cytotoxic activity was more marked in patients who were clinically tumor-free. Some patients with benign diseases and normal subjects also exhibited cytotoxic macrophages. Macrophage-mediated cytotoxicity (MMC) was thus nonspecific in nature. Cell-free exudate from cancer patients did not influence MMC appreciably. The experimental methods and the possible significance of MMC are discussed.

Animals↗
PubMed1994

Effect of shock waves and cisplatin on cisplatin-sensitive and -resistant rodent tumors in vivo.

The effect of a combination of shock waves with cisplatin was examined in vivo with subcutaneously implanted amelanotic melanomas (A-Mel 3) in Syrian golden hamsters and cisplatin-sensitive or cisplatin-resistant fibrosarcoma (SSK2/0 and SSK2/R2) in C3H mice. In all 3 tumor models, 4 treatment modalities were compared: control, cisplatin treatment, shock waves and the combination of shock waves and cisplatin. Shock waves significantly delayed tumor growth in all 3 tumor models when compared to the respective control group. Cisplatin alone delayed the growth of A-Mel 3 and SSK2/0, whereas SSK2/R2 remained uninfluenced by the drug. In all 3 tumor models the combined treatment with shock waves and cisplatin additively and significantly delayed tumor growth. In A-Mel-3-bearing animals the combined treatment significantly increased survival time. The growth of SSK2/0 and SSK2/R2 tumors was delayed to a similar extent by the combined treatment modality as compared to shock-wave treatment alone. This indicates that the cisplatin resistance of SSK2/R2 tumors has been overcome by the simultaneous shock wave treatment. An increased intracellular cisplatin accumulation in the tumors due to shock wave exposure is suggested as the mechanism of interaction between shock waves and cisplatin.

Animals↗
PubMed1994

31P MRS of tumour metabolism in anaesthetized vs conscious mice.

The injectable anaesthetics Hypnorm/Hypnovel, chloral hydrate and etomidate, were examined for their effects on C3H/He mouse core temperature and on the in vivo 31P MR spectra of KHT and SCCVII/Ha transplantable tumours, compared with conscious mice gently restrained in jigs. Hypnorm/Hypnovel at 0.1 mL/mouse i.p. reduced core temperature by 6 degrees C at 30 min after injection, returning to control levels by 100 min, but did not significantly alter the 31P MR spectra of either KHT or SCCVII/Ha tumours. Chloral hydrate at 300 mg/kg i.p. produced a 5 degrees C fall in mouse core temperature, at 25 min after injection, again returning to control levels by 100 min. This agent increased the Pi/total ratio to 155% of control at 15 min after injection in the KHT tumour, and to 170% of control at 45 min in SCCVII/Ha. Etomidate at 25 mg/kg i.p. reduced mouse core temperature by 7.5 degrees C by 20 min after injection, returning to only 84% of control by 100 min. This agent increased the Pi/total ratio by 260% in the KHT tumour 15 min after injection, without recovery to control values by 100 min. In SCCVII/Ha, a maximum increase in Pi/total of 360% was observed at 15 min after injection, with a return to control levels by 60 min. In addition, etomidate caused convulsions in the mice during the induction phase, and myoclonic jerking within 15 min of anaesthesia.

Anesthetics↗
PubMed2005

Possible protective effects of alpha-tocopherol on enhanced induction of reactive oxygen species by 2-methoxyestradiol in tumors.

Several non-surgical tumor treatment modalities produce their cytotoxic activity by generating reactive oxygen species (ROS). Anti-oxidative enzymes such as superoxide dismutase (SOD) or exogenously supplied antioxidants may therefore reduce the efficacy of these treatments. The aim of the present study was to analyze the impact of (i) inhibiting SOD using 2-methoxyestradiol (2-ME), or (ii) application of alpha-tocopherol, on the cellular damage induced by hyperthermia (HT) in experimental tumors. DS-sarcoma cells grew either in culture or as solid tumors subcutaneously implanted in rats. In vitro, DS-cells were incubated with 2-ME, and cell proliferation, ROS formation, lipid peroxidation and apoptosis were measured. In vivo, DS-sarcomas were treated with a ROS-generating hyperthermia combined with 2-ME or alpha-tocopherol application. Inhibition of SOD by 2-ME in vitro induced pronounced oxidative injury resulting in reduced proliferation. In vivo, ROS-generating hyperthermia led to local tumor control in 23% of the animals. The additional inhibition of SOD by 2-ME increased the control rate by approximately 50%. Application of alpha-tocopherol was found to have no effect on local tumor control, either in combination with ROS-generating hyperthermia or when 2-ME was additionally applied. Inhibition of SOD during ROS-generating hyperthermia results in pronounced cell injury and an improved local tumor control whereas exogenously applied vitamin E seems not to have an impact on oxidative stress.

2-Methoxyestradiol↗
PubMed1982

Mononuclear phagocytes in the control of primary and secondary tumor growth.

In a variety of defined experimental host/tumor situations there is now considerable evidence that mononuclear phagocytes are critically involved in the control of tumor cell nidation and their establishment as primary tumors. The factors which determine secondary tumor cell spread and the establishment of metastases are clearly complex and make it highly unlikely that tumor cell dissemination is under the control of a single host defense mechanism. Nonetheless, findings in various experimental models suggest a critical role for mononuclear phagocytes in the surveillance of tumor cell dissemination.

Animals↗
PubMed1984

Considerations in the use of nude mice for cancer research.

Transplants of human tumors in nude mice have shown a progressive increase during the past 15 years as an experimental model for cancer research. A variety of factors, including relatively fragile health, have been identified that require appropriate experimental controls if the investigator is obtain consistent results. Not all tumors grow in nude mice. The frequency of tumor 'take' varies according to tumor origin, tumor type, inoculation site, age and conditioning of the mouse host, and a variety of other factors. Manipulation of these variables has led to successful propagation of almost every known variety of human malignancy. Following transplant, changes in characteristics have been documented, but the frequency and degree of such changes remains uncertain. Tumor growth rate probably increases after transplantation, requiring great care in the interpretation of chemotherapy experiments, but biochemical characteristics may be more stable. The nude mouse offers great interest as a model for the in vivo study of metastasis, as a number of experimental variables, mainly immunological, have been shown to affect this process. Spontaneous tumors have been shown to arise in these animals, but the controversy over their frequency relative to the thymus-bearing background strain is unresolved. We conclude that the nude mouse/tumor xenograft model, while requiring meticulous experimental controls, is nevertheless an extremely useful tool for cancer research.

Animal Husbandry↗
PubMed1979

Vincristine-methotrexate combination chemotherapy and the influence of weight loss on experimental tumour growth.

According to pharmacokinetic reports, vincristine administration should precede methotrexate therapy. Our sequential treatment of L1210 leukaemic mice, in which vincristine was administered before methotrexate therapy, was as effective as treatment with the two drugs given simultaneously. In solid tumour experiments we were unable to show any increase in the antitumour effect of methotrexate when vincristine was injected before methotrexate administration. Consequently, we advocate the re-evaluation of the practice of vincristine leads to methotrexate therapy as used in many clinical protocols for the treatment of patients with osteosarcoma. Pretreatment with vincristine resulted in methotrexate-induced weight loss and sometimes in toxic death of the mice. Since the growth of tumours can be modified by regulation of the caloric intake of the host, this aspect was investigated in more detail. The effect of starvation, which was comparable to the effect of drug-induced weight loss, had a retarding effect on tumour growth. The growth rates of smaller tumour volumes were less severely affected than were those of large tumour masses.

Animals↗