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At least 19 recordsLinked to original sources
PubMed1978

Glomerulonephritis in malignant extra-renal neoplasms. Experimental study on mice using the method of immunofluorescence.

Histologic and immunofluorescence studies were done in the murine kidneys (strain C3HAvy) suffering a spontaneous cancer of the liver. Proliferative glomerulonephritis has been found in 17 animals and memranproliferative glomerulonephritis with "wire loop" appearance in 6 animals. The glomeruli of all animals presented immune complex deposition in the mesangium and along the glomerular basement membrane. Furthermore, heavy intensity of IgG complex deposition was observed in animals with membranproliferative glomerulonephritis. The latter animals had developed a poorly differentiated liver cancer.

Animals↗
PubMed1978

[Thrombocytic reactions in experimentally induced neoplasms (author's transl)].

Strain XVII mice with Graffi virus induced leukemia of various hematological types showed a pronounced thrombocytopenia which was severe in erythroblastic leukemia and weaker in lymphatic ones. The thrombocytic reactions shortly following Friend and Rauscher virus applications and occurred 3 weeks after birth in AKR mice are not found in Graffi virus system. A significant preleukemic thrombocytopenia did appear only 8 weeks after Graffi virus infection. The origin of both the preleukemic and the secondary thrombocytic reactions are discussed. (XVII X AKR) F1 hybrids, neonatally treated with N-nitroso-N-methylurea (NMU), resulted also in a decline in the number of thrombocytes after manifestation of leukemia. In contrast to the expection following NMU treatment a preleukemic thrombocytopenia appeared as in viral leukemogenesis too. The possibility of a co-operation of oncogenic viruses in chemical carcinogenesis is considered.

Animals↗
PubMed1978

Islet cells as a component of pancreatic ductal neoplasms. I. Experimental study: ductular cells, including islet cell precursors, as primary progenitor cells of tumors.

The ductular complex of the Syrian hamster pancreas represents a system of conduit which encompasses intercalated (intralobular), periinsular, and intrainsular ductules. The intercalated (intralobular) ductules comprise centroacinar and intercalated cells. A meshwork of small ductules (invisible by usual histologic procedures) surrounds islets (periinsular ductules) and extends in the form of often ramified tiny channels within the islet (intrainsular ductules). Although the function of the latter ductules is obscure, their cells seem to make up one of the undifferentiated cellular units of the pancreas, and as such are also the progenitors of beta-cells of the islets (islet cell precursor = IP). Systematic histologic examination of the pancreas in this species treated with pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine indicated that ductular cells, especially those of periinsular and intrainsular origin, are the most responsive to this carcinogen. The neoplastic process was initiated with hyperplasia of intercalated (intralobular) ductular and interlobular ductal cells associated with newly formed islets (nesidioblastosis). This process was followed by excess formation of mature but especially of immature islet cells and their precursors (IP) in the islet periphery, as well as with the appearance, distention, and multiplication of periinsular and particularly of intrainsular ductules. The hyperplasia, metaplasia, and malignant alteration of these periinsular and intrainsular ductules (including IP) and, to a lesser degree, of intercalated ductules indicated their histogenetic relationship and their potency for reproducing embryonic tissue on carcinogenic stimulus. The similarity of some induced lesions to diabetes has been emphasized.

Animals↗
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↗
PubMed1979

Inhibitory effect of prostaglandin F2 alpha on the growth of a hormone-dependent rat mammary tumor.

Growth of the rat hormone-dependent mammary adenocarcinoma MTW-9 was inhibited by prostaglandin F2alpha (PGF2alpha) This inhibition of tumor growth was associated with a marked reduction in serum progesterone concentrations. The inhibitory effect of PGF2alpha on tumor growth was abolished by concomitant injections of progesterone. The growth rates of coimplanted prolactin-secreting pituitary tumor MtTW-5 and plasma concentrations of prolactin and estradiol were not affected significantly by PGF2alpha. Our data imply that the effect of PGF2alpha on growth of rat mammary adenocarcinoma is mediated by progesterone.

Adenocarcinoma↗
PubMed1979

Synergism of diethylstilbestrol and radiation in mammary carcinogenesis in female F344 rats.

One compressed 20-mg pellet containing cholesterol only or cholesterol mixed with 0.98, 1.6, 2.6, or 3.9 mg of diethylstilbestrol (DES) was implanted into each of 203 female F344 rats. Two days later, half the animals in each group were exposed to 150 R of X-rays, and the other half were sham irradiated. The rats were maintained until 350 days post implantation. Mortality increased with the higher doses of DES, with or without X-rays. DES at all dose levels, with or without X-rays, produced pituitary tumors and pyometritis. Only rats that received both DES and X-rays had mammary adenocarcinomas (AC). A synergistic AC response was found in the group that received 2.6 mg DES plus X-rays. Synergism was defined as a significantly greater incidence of rats with mammary neoplasia resulting from DES plus X-ray treatment when compared to the summed incidence from comparable individual treatments. For all other groups of rats that received both treatments, synergism was detected only when their data were combined. Synergism was not detected among rats that had fibroadenomas (FA). Both types of neoplasms were independent phenomena because no significant relationship was found between the incidences of FA and AC.

Adenocarcinoma↗
PubMed1976

Treatment of transplanted rat tumours with double-stranded RNA(BRL 5907). II. Treatment of pleural and peritoneal growths.

Intrapleural growth of transplanted rat tumours was prevented or retarded by intrapleural administration of double-stranded RNA. A similar suppression of growth was achieved with peitoneal tumours by the intraperitoneal injection of the compound. These studies indicate the possible potential of this form of treatment of thoracic and peritoneal tumours for clinical application in the treatment of mesothelioma.

Animals↗