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At least 19 recordsLinked to original sources
PubMed1978

Decreased hepatic nuclear L-triiodothyronine receptors in rats and mice bearing transplantable neoplasms.

The concentration of hepatic nuclear T3 receptors was measured in isolated nuclei from athyreotic mice bearing thyrotrophic tumors and intact rats with Walker 256 carcinoma. Receptor concentration was reduced in all tumor-bearing animals. The mean receptor capacity of the Walker tumor-bearing rats [0.31 +/- 0.05 (SEM) ng/mg DNA] was significantly decreased from simultaneously assayed controls (0.47 +/- 0.04 ng/mg DNA; P less than 0.01). No change in the apparent equilibrium association constant was observed. In individual rats, the magnitude of the decrease in nuclear T3 receptor concentration was highly correlated with the decrease in tumor-free body weight. Additional studies showed that the decrease in nuclear receptors was not due to delayed equilibration of added T3 with nuclear sites in vitro or to an increase in endogenous hepatic T3 concentration. The plasma concentration of total and free T4 and T3 was decreased in tumor-bearing rats. Plasma TSH concentration, however, remained unchanged. Thus, these transplantable neoplasms seem to be associated with decreased hepatic nuclear receptors and low concentrations of plasma thyroid hormones. The unchanged plasma TSH suggests that the animals remained euthyroid.

Animals↗
PubMedDate not supplied

Serum ceruloplasmin concentrations in rats with primary and transplanted sarcomas induced by nickel subsulfide.

Ceruloplasmin (CPN) concentrations were measured by p-phenylenediamine oxidase assay in serums from (a) 30 control Fischer rats; (b) 5 rats with primary sarcomas induced by i.m. injection of nickel subsulfide (alpha Ni3S2), and (c) 12 rats at intervals up to six weeks after s.c. transplantation of four alpha Ni3S2-induced sarcomas. Serum CPN concentrations were not significantly increased in rats with primary sarcomas (mean = 0.38 g per liter) (S.D. +/- 0.05), versus 0.35 g per liter (S.D. +/- 0.04) in controls. In contrast, serum CPN concentrations were increased within 11 to 21 days in all rats with transplanted sarcomas. Maximum concentrations of serum CPN occurred at 31 to 34 days after tumor transplantation, (mean = 0.56 +/- 0.05 g per liter), equivalent to 1.6 +/- 0.2 times the initial CPN concentrations in serums obtained prior to treatment (P less than 0.001). The development of hyperceruloplasminemia in rats with transplanted sarcomas and not in rats with primary sarcomas is attributed to greatly enhanced growth-rates of the transplanted neoplasms.

Animals↗
PubMed1977

Macrophage migratory dysfunction in cancer. A mechanism for subversion of surveillance.

There is considerable evidence to suggest that macrophages participate in host resistance to the development and spread of cancer. We have, therefore, studied monocytemacrophage function in humans and animals with neoplasms. Approximately 60% of patients with various types of cancer were found to have abnormal monocyte chemotactic responsiveness in vitro, and abnormal chemotaxis was an indicator of poor prognosis in patients with melanoma. By studying patients before and after surgery, it was found that abnormal chemotactic responses normalized within weeks after removal of malignant tumors, indicating that a neoplasm itself might affect the host's monocyte chemotactic responsiveness. Subsequent studies using transplantable neoplasms in mice substantiated this hypothesis in that macrophage accumulation in vivo as well as macrophage chemotactic responsiveness in vitro was depressed in animals during the early phases of tumor growth. This depression of macrophage function could be attributed to a low-molecular-weight factor contained in murine neoplasms, which when given to normal mice was extremely potent in depressing peritoneal macrophage accumulation and chemotaxis but, paradoxically, enhanced phagocytosis. The serum of tumor-bearing mice also contained potent inhibitory activity for macrophage accumulation. In contrast to the effects on macrophages, granulocyte accumulation in vivo and chemotaxis in vitro was not depressed by the presence of a neoplasm or the administration of the factor from neoplasms. By releasing factors which depress macrophage migratory function, neoplasms may protect themselves from immunologically mediated host destruction during the early phases of tumor growth.

Animals↗
PubMed1975

Transplantation of adenocarcinomas of the colon in mice.

1, 2-Dimethylhydrazine treatment induced multiple colon tumors in 100% of NMRI mice. Many of these tumors were transplanted and yielded five serially transplantable tumor lines. These subcutaneously transplanted neoplasms were all adenocarcinomas varying in degree of differentiation and mucin production. No evidence of dedifferentiation or change in growth rate has been seen in up to six transplant generations. These tumor lines appeared to provide relatively stable, well-differentiated models for colorectal cancer.

Adenocarcinoma↗
PubMed1975

BCG-induced protection against malignant melanoma: possible immunospecific effect in a murine system.

This report documents for the first time BCG-induced protection against a murine malignant melanoma. Adult Balb/C mice recieved 0.1-cm3 doses of BCG prior to intramuscular challenge with 1 x 10-6 S-91 melanoma cells. A 65% reduction in melanoma incidence was noted in BCG-pretreated mice. The possibility of specific protection induced by the BCG against the melanoma exists, since the BCG pretreatment did not protect against challenge with 1 x 10-5 mammary carcinoma cells or 1 x 10-4 MCA fibrosarcoma cells in the same strain of mice. Lack of immunogenicity was not a factor in the inability of the carcinoma and sarcoma to be inhibited by BCG. The strenght of the BCG-induced protection against the S-91 melanoma was demonstrated by significantly decreased tumor incidence following three different log challenge doses of the melanoma. However, reduction of the sarcoma challenge dose to as few as 10-2 cells administered to BCG pretreated mice did not result in decreased tumor incidence. It was further discovered that as few as two doses of 0.1 cm3 of BCG were sufficient to produce a 70% reduction in melanoma incidence compared with the incidence in control animals (P less than .001). Lymphocyte-mediated cytotoxicity studies paralleled the results of the in vivo experiments. Lymphocytes immune to each of the three tumors showed significant cytotoxicity against their respective tumor target cells (p less than .001), while the only tumor cells that lymphocytes from BCG-pretreated mice showed significant cytotoxicity against were S-91 target cells (p less than .01). Nonspecific cytotoxicity was not a factor in the effect of BCG-immune lymphocytes against S-91 target cells, since BCG-immune lymphocytes were not cytotoxic to Balb/C fibroblasts.

Animals↗
PubMed1978

Effects of ultraviolet light on nude mice: cutaneous carcinogenesis and possible leukemogenesis.

Squamous cell carcinomas were induced by ultraviolet irradiation in the skin of all T-cell deficient nude mice rendered sufficiently long-lived by reconstitution with syngeneic splenic or thymic cells. All homozygous hairless mice similarly exposed developed squamous cell carcinomas. Striking granulocytic proliferation was provoked in one hairless and in five reconstituted nude mice; two of the latter were interpreted as having true granulocytic leukemia.

Animals↗
PubMed1979

Discrepant effects of interferon murine syngeneic ascites tumors and their solid metastasizing counterparts.

The effects of interferon on mice with syngeneic tumors growing either intraperitoneally or as solid tumors were analyzed. The same dose that depressed the growth of ascites tumors, enhanced growth and in one case metastasizability of the corresponding solid tumors. The possibility that this was due to some host reaction is discussed. It seems important to develop animal models for analyzing interferon effects before treatment is initiated in human tumor disease.

Animals↗