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At least 181 records · Page 10Linked to original sources
PubMed1981

Modification of radiation carcinogenesis by marihuana.

Male, female, and ovariectomized female Sprague-Dawley rats were irradiated with 400 rads, 150 rads, or 300 rads, respectively, of 60Co gamma rays when they were between 40 and 50 days of age. The animals were injected three times weekly with either marihuana extract or with alcohol-emulphor carrier. Comparable unirradiated groups were similarly injected. Mean survival time in males was significantly shorter in the 400 rad + marihuana group compared with the three other groups whose mean survival times did not differ. Through the 546 days that the males were observed, the total number of tumors other than fibrosarcomas was significantly greater following radiation and marihuana (22) than radiation alone (6). Fifteen of the tumors were of breast or endocrine tissues. No differences were seen in the unirradiated groups. In the females, which were observed for 635 days, the total number of breast tumors was greater with the combined treatment (38) compared with radiation alone (22). This was entirely due to a marked difference in the adenocarcinoma incidence, which was 21 (radiation + marihuana) compared with four (radiation alone). The number of adenofibromas was similar in the two groups. In the unirradiated female groups the breast adenocarcinoma incidence was eight in the marihuana group and two in the control group. Ovariectomy resulted in a lower breast tumor incidence in all groups. Nonbreast tumors were more frequent in the ovariectomized-irradiated groups. Radiation plus marihuana produced more nonbreast tumors (25) than radiation alone (17) in the ovariectomized females.

Adenocarcinoma↗
PubMed1970

The possible carcinogenic effects of radiations on the uterus.

The carcinogenic effects of radium and X-rays on the rat uterus have been investigated. Malignant endometrial tumours, usually adenocarcinomas, were produced in a small proportion of treated rats. One rat treated with X-rays developed an adeno-sarcoma (possibly carcino-sarcoma) of the endometrium. Benign mixed polypoidal endometrial tumours occurred also in radium and X-ray treated rats and in non-radiated controls; radiation increased the incidence of these tumours and may have induced malignant transformation in some. The incidence of lymphosarcomas and mammary tumours in the strain of rat used appeared to be influenced by radiation treatment.Review of the literature of human cases of mixed uterine tumours showed that in women over 40 years, more than one-fifth of the reported cases had a history of previous pelvic radiation; with other kinds of uterine malignancy a history of prior radiation treatment was considerably less. The results of our experiments enhance the suspicion that radiations are one factor in the causation of uterine cancer, especially mixed tumours.

Adenocarcinoma↗
PubMed1978

Estrogen induction of growth factors specific for hormone-responsive mammary, pituitary, and kidney tumor cells.

The problem of estrogen-promoted tumor cell growth has been studied extensively in an attempt to establish the direct mitogenic role of these steroid hormones. We have developed cell lines from three estrogen-responsive tumors or cell populations: the H-301 kidney tumor cells established from a parent estrogen-dependent hamster kidney tumor, the GH3/C14 rat pituitary tumor cell line established as a subline of the original GH3 population, and the MTW9/PL mammary cell line developed from a parent estrogen- and prolactin-responsive MT-W9A carcinogen-induced rat tumor. With all three of these cell lines, we have encountered a paradox: although estrogens are obligatory for tumor formation in vivo, no direct mitogenic effect of estrogens can be shown in culture when assayed by an increase in cell number. We have thus considered the possibility that estrogens may induce growth factors in vivo that are then responsible for tumor formation by the three cell lines described. Experiments presented in this report show that extracts of rodent uterus, kidney, or liver contain growth activity for these three tumor cell lines, that estrogen treatment causes an increase in tissue content of these activities, and that the estrogen-induced activities are specific for the estrogen-responsive cells. These studies suggest that estrogen-responsive tumor growth in vivo includes the mechanism of estrogen leads to uterus, kidney, or liver leads to specific growth factors leads to estrogen-responsive tumor cells.

Animals↗
PubMed1998

Cytofluorometric DNA analysis by stathmokinetic method of experimental thyroid neoplasms in rats.

Thyroid neoplasms were induced in rats by the intraperitoneal injection of N-bis(2-hydroxy-propyl)nitrosamine as a carcinogenic substance and by the oral administration of KCIO4 as a promoter. The nuclear DNA content was measured in tissue sections of the tumors by the stathmokinetic method with the use of vincristine, and was correlated with the histopathological findings in the process of tumorigenesis and progression. Histological examination showed various types of lesions were produced in 47 surviving rats. A diploid pattern was seen in 82 (92%) of 89 tumors and an aneuploid pattern in 7 (8%) of 89 tumors. Papillary carcinomas and mixed carcinomas only had a diploid pattern, while two of 17 follicular carcinomas and five of 13 anaplastic carcinomas had an aneuploid pattern. On the other hand, benign proliferative nodules only had a diploid pattern. DNA heterogeneity was noted in seven malignant tumors. In four of them it was associated with the histopathological evidence of change, but in three there was no histological difference between the aneuploid and diploid areas other than a difference in the mitotic index. Mitotic indices were significantly higher in the aneuploid than in the diploid areas. These findings suggest that changes in the DNA ploidy cause histological abnormalities and/or affect the mitotic index. It is hypothesized that a change occurs in some diploid cells in a region of a tumor, and that aneuploid cells develop from the diploid cells which then acquire high proliferative activity.

Aneuploidy↗