Search PubMed⌕ Search

Biomedical subjects

M Pollard

Publications and source records attributed to M Pollard.

At least 109 records · Page 6Linked to original sources
PubMed1980

Animal models for prostate cancer.

Four model systems for prostate adenocarcinomas have been developed in rats: they are designated Dunning, Noble, ACI, and Pollard tumors. They have attributes that make them valuable sources of information, of relevance to the disease in man. The development and use of the Pollard tumors as in vitro and in vivo model systems are reviewed, especially on the phenomenon of metastasis. Specific agents either accelerate or retard the rate and extent of metastatic spread of the prostate tumor cells from extravascular sites to specific target organs. Specific enzymes may be involved in the phenomenon of metastasis.

Animals↗
PubMed1980

Metastasis-enhancing effect of heparin and its relationship to a lipoprotein factor.

The effect of low-dose heparin on spontaneous metastasis formation was studied with the PA-III rat prostate adenocarcinoma cell line model system. In LW rats given heparin iv at a dose of 1,000 U/kg body weight (three times/wk), the metastatic spread of implanted PA-III cells from the footpad through ipsilateral lymphatics to the lungs was enhanced. The weights of the draining lymph nodes (popliteal, inguinal, and axillary) and the number of lung tumor colonies were significantly increased compared with those in the saline-treated control tumor-bearing rats. The growth of the primary tumor was also enhanced. Heparin alone did not induce enlarged lymph nodes in rats nor did it change the growth pattern of PA-III cells in vitro. The accelerated metastatic spread of the PA-III cells was possibly related to the destruction of the oncolytic activity of the very low-density lipoprotein by the lipoprotein lipases induced by the iv administration of heparin. However, the possibility that other mechanisms could be operative in this phenomenon has not been ruled out.

Adenocarcinoma↗
PubMed1980

Indomethacin treatment of rats with dimethylhydrazine-induced intestinal tumors.

Intestinal tumors were induced in male Sprague-Dawley rats following the administration of five weekly doses of 1,2-dimethylhydrazine (DMH) by gavage. At intervals thereafter, groups of rats were given indomethacin (IND) in the drinking water. In three trials, the incidence of rats with tumors was significantly reduced by 40% below the control rats which did not receive IND and there was no significant difference in body weights. Also, in those IND-treated rats which developed tumors, the tumors were generally smaller in numbers and sizes compared to the control rats. A group of DMH-treated rats was treated with crude IND by gavage and the differences between them and untreated control rats were not significant. It is likely that the treatment was directed at the tumors and not at the DMH which induced them.

Animals↗
PubMed1979

Patterns of spontaneous metastasis manifested by three rat prostate adenocarcinomas.

Three transplantable rat prostate adenocarcinoma cell lines were assessed for patterns of metastasis, ie, routes of dissemination and larger organ(s) selected for implantation. Two lines (I and III) were disseminated only through ipsilateral lymphatic channels to the lungs. The third cell line (II) was disseminated through lymphatic and blood channels to lungs, liver, and kidneys. The pattern of spontaneous metastasis is a characteristic of the tumor cell; but there is evidence that the rate and extent of metastasis can be modified experimentally.

Adenocarcinoma↗
PubMed1979

Ozonation of mutagenic and carcinogenic polyaromatic amines and polyaromatic hydrocarbons in water.

The Salmonella-microsome assay for mutagenesis was used to determine the effect of ozone on the mutagenesis of selected carcinogens and mutagens in water. Short periods of ozonation were shown to completely inactivate the mutagenicity of several polyaromatic amine mutagens including acriflavine, proflavine, and beta-naphthylamine. Selected polyaromatic hydrocarbons were also sensitive to ozonation. Kinetic studies revealed that the mutagenicity of benzo(a)pyrene, 3-methylcholanthrene, and 7,12-dimethylbenz(a)anthracene was destroyed after short periods of ozonation. To correlate loss of mutagenicity with loss of carcinogenicity, two polyaromatic hydrocarbons were treated with ozone, extracted from water with hexane, and tested for carcinogenicity in mice. When 7,12-dimethyl-benz(a)anthracene and 3-methyl-cholanthrene were treated with ozone, there was a substantial reduction in carcinogenicity compared to control groups treated with oxygen alone. However, a small number of tumors developed in the group of animals receiving a hexane extract of ozonated 7,12-dimethylbenz(a)anthracene. This activity may be due to breakdown products of 7,12-dimethylbenz(a)anthracene that are not mutagenic.

2-Naphthylamine↗
PubMed1979

Spontaneous liver tumors in aged germfree Wistar rats.

Liver tumors, ranging from benign nodules to carcinomas, developed spontaneously in 115 (87%) of 132 germfree Wistar rats beyond the age of 30 months. In addition, the rats developed a high incidence of benign adenomas of endocrine glands and of the breasts.

Adenoma↗
PubMed1979

Ozonation of mutagenic and carcinogenic alkylating agents, pesticides, aflatoxin B1, and benzidine in water.

The effect of ozonation on the mutagenicity of selected chemicals in water was determined. The use of the Salmonella-microsome assay for mutagensis allowed kinetic studies to be performed on the ozonation of all chemicals tested. The results indicate that the mutagenicity of certain pesticides, including captan and Dexon, was inactivated by short periods of ozonation. The mutagenicity of certain alkylating agents including bis(2-chloroethyl)amine and sodium azide was rapidly inactivated by ozonation while other alkylating agents such as beta-propiolactone, propanesultone, and N-methyl-N'-nitro-N-nitrosoguanidine were unaffected by treatment with ozone. The mutagenicity of aflatoxin B1 was rapidly inactivated by treatment with ozone. Three chemicals were shown to be converted to direct mutagens by ozone treatment. Under certain conditions, dimethylhydrazine could be converted to a mutagen that was stable for 3 weeks. A similar chemical, 2-hydroxyethylhydrazine, was converted to an unstable mutagen that was inactive after 24 hr at room temperature. When benzidine was treated with ozone, there was a transient increase in mutagenicity which was lost after longer treatment with ozone.

Aflatoxins↗
PubMed1979

Promotional effect of sodium barbiturate on intestinal tumors induced in rats by dimethylhydrazine.

Noninbred Sprague-Dawley rats were administered 1,2-dimethylhydrazine hydrochloride (DMH) by gavage or methylazoxymethanol acetate by sc inoculation. Thereafter, one group was given water to which 0.1% sodium barbiturate was added, and the other was given drug-free water. They were examined 20 weeks after onset of the experiments. A direct relationship was noted between dosage of DMH and numbers of intestinal tumors induced in the rats. The rats provided with sodium barbiturate-supplemented water developed more intestinal tumors than did those that drank drug-free water.

Animals↗
PubMed1978

In vitro effects of lipoprotein-associated cytotoxic factor on rat prostate adenocarcinoma cells.

As assayed by the colony inhibition technique, sera from rats at an advanced stage of pregnancy were cytotoxic to a number of tumorigenic and "nontransformed" cell lines. The cytotoxic effect is not species specific. Primary fetal rat kidney cells were not susceptible to this cytotoxic effect. The level of demonstrable cytotoxicity in sera rose gradually as gestation advanced; it peaked at 48 hr before parturition and disappeared thereafter. Sera from control nonpregnant rats were not cytotoxic. The cytotoxic factor(s) in sera was demonstrable only in the very low-density lipoprotein (VLDL) (hydrated density less than 1.006 g/ml) fraction. Reconstitution studies suggest that: (a) inhibitors which usually mask the cytotoxic actitivity of VLDL in whole serum, are present; and (b) pregnancy initiates enhanced VLDL synthesis, which exceeds the masking effect. The possible role of this cytotoxic VLDL in host defense against neoplasia is discussed.

Adenocarcinoma↗
PubMed1978

Induction of colon tumors in 1,2-dimethylhydrazine-resistant Lobund Wistar rats by methylazoxymethanol acetate.

Sprague-Dawley and Lobund Wistar rats, which were sensitive and resistant to induction of colon tumors by 1,2-dimethylhydrazine (DMH), respectively, were treated with methylazoxymethanol (MAM), the product of DMH metabolism by the microsomal mixed-function oxidase system. Although the colon tissue in both stocks of rats had similar NAD+-dependent dehydrogenase activities that are considered necessary to activate MAM to an ultimate carcinogen, still a sevenfold greater incidence of colon tumors was found in the Sprague-Dawley rats, and their tumors were more extensive. The results indicated that the difference in susceptibility to colon tumor induction between the rat stocks was partially related to metabolic activation of the DMH and to other, as yet undetermined, endogenous factors.

Adenocarcinoma↗
PubMed1977

The Erlangen magnetic colostomy control device: technique of use and results in 22 patients.

The evolution and general principle of the Erlangen magnetic ring colostomy device are described and its practical use illustrated by reference to a personal series of 22 patients treated with the device. Analysis of the functional results obtained in 13 of these cases, who were assessed after at least 3 months' trial, shows that only 3, or at most 4, could be considered to have achieved worth-while continence, but there are grounds for believing that these results might be improved a little by more stringent selection of patients for the procedure and by employing a more meticulous technique for implanting the rings.

Colostomy↗
PubMed1977

Investigations on prostatic adenocarcinomas in rats.

Metastatic prostate adenocarcinomas, derived from aging germfree Wistar rats, have been propagated in rats and in tissue culture. A protocol has been developed and demonstrated for assay of treatments which retard or which accelerate the rate and extent of tumor growth and of metastasis in tumor-bearing rats. The pattern of spread has been retarded by cyclophosphamide, aspirin, indomethacin, and Corynebacterium parvum. The spread pattern has been accelerated by oral administrations of sodium barbiturate.

Adenocarcinoma↗
PubMed1977

In vitro propagation of prostate adenocarcinoma cells from rats.

Two rat adenocarcinomas were physically dispersed and propagated in vitro. Epithelial and fibroblast cell lines were cloned from them and the monolayer cell lines derived therof were further characterized. The cells produced acid phosphatase in early in vitro cell passages, and later they turned negative. Fibroblast-like cells produced no tumors when implanted in syngeneic Lobund Wistar rats, but as few as 10 epithelial cells produced metastasizing adenocarcinomas in them. A third prostate tumor has yielded a line of epithelial cells which reproduced the original tumor type in inoculated rats, but the cells have not yet been characterized. Rat prostate adenocarcinomas provided a useful model system for in vitro and in vivo studies on prostate cancer and on metatasis.

Acid Phosphatase↗