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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several in vitro properties of two variant cell lines of the B16 melanoma (B16-F10 and B16-BL6) with markedly different spontaneous metastatic behavior were examined. The two cell lines were compared with regard to their in vitro growth rate, ability to migrate, ability to adhere to a variety of substrata, detachment rates, production of plasminogen activator, and cell surface proteins as determined by lactoperoxidase-catalyzed iodination. Growth rates in vitro, attachment rates, and qualitative patterns of cell surface proteins were almost identical. B16-F10 cells (the less spontaneously metastatic line) produced greater amounts of plasminogen activator, were more motile in vitro, and detached more readily from plastic than the more invasive B16-BL6 cells. The study of tumor cell variants, selected for different biologic behavior, is a valuable approach to the elucidation of those mechanisms responsible for their malignant activity.
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PMID:The selection and characterization of an invasive variant of the B16 melanoma. 50 92

We have developed an experimental model of spinal cord compression in rats. Tumor injected anterior to the T-12 vertebral body grows through the intervertebral foramina to compress the cord and produces paraplegia in 3 to 4 weeks. Evidence for vasogenic edema in spinal cord compressed by tumor includes increased water content, leakage of horseradish peroxidase into gray matter, and histologic evidence of edema. The vascular supply to the cord overlying the tumor appears to be compromised. Both spinal cord edema and clinical symptoms are lessened by treating symptomatic animals with dexamethasone.
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PMID:Experimental spinal cord compression by epidural neoplasm. 55 45

Peritoneal macrophages from C3H/HeN mice treated i.p. with T cell mitogens or viable BCG organisms were cytotoxic to syngeneic tumor cells in vitro. Macrophages from endotoxin-unresponsive C3H/HeJ mice treated with BCG or T cell mitogens, however, were not tumoricidal. Furthermore, unlike cells from C3H/HeN mice, macrophages from C3H/HeJ mice could not be activated for tumor cytotoxicity after in vitro treatment with bacterial endotoxins or with lymphokine-rich supernatants. The subnormal induction of cytotoxic macrophages after in vitro or in vivo treatments in C3H/HeJ mice appears to be a highly selective defect. Macrophage responses (yield, phagocytosis, or peroxidase staining) in inflammatory exudates induced by BCG, T cell mitogens, or heterologous serum in C3H/HeJ or C3H/HeN mice were identical. C3H/HeJ macrophages also responded normally in vitor to chemotactic lymphokines. Thus, C3H/HeJ macrophages possess a profound and selective defect in tumoricidal capacity. This defect was not dependent upon exogenous endotoxins. Defective macrophage cytotoxic responses may reflect non-LPS related functions regulated by the LPS gene.
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PMID:Defective tumoricidal capacity of macrophages from C3H/HeJ mice. 62 23

Taking into account the conception of metabolic immunosuppression, arising in the case when fatty acids but no glucose serves as the basic energetic substrate, the authors have studied the effect of miscleron (clofibrate, athromid-S) on a number of hormonal-metabolic and immune indices. It is shown that miscleron in addition to decreasing the blood level of cholesterol, beta-lipoproteids, triglycerids, free fatty acids, cortisol and reducing 17-ketosteroids excretion, produces higher indices of the blasttransformation reaction, induced by FHA, an increased phagocytic index of monocytes, a rise in the level of peroxidase and lysosomal activity of monocytes. Miscleron and other substances lowering the lipid level in blood should be examined in patients with nonlymphoid types of tumors both with the aim to eliminate metabolic immunosuppression and to retard the rate of tumor cells growth due to a reduced level of low density lipoproteins.
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PMID:[Improvement in the functional and morphological mononuclear blood cell indices under the influence of miscleron]. 65 76

Immunocytochemical localization of GFA protein in formalin-fixed, paraffin-embedded tissue sections by the peroxidase-antiperoxidase method of Sternberger was used to study experimental murine CNS tumors. Transplacental tumor induction in rats by ethylnitrosourea produced oligodendrogliomas and mixed gliomas in the cerebrum and spinal cord, and malignant Schwannomas of the trigeminal nerve. A methylcholanthrene-induced mouse "ependymoblastoma" inoculated intracerebrally in normal and in toxoplasma-infected mice was also studied. A positive reaction of GFA protein antibody was seen in the astrocytic portion of the mixed gliomas; the oligodendrogliomas, the malignant Schwannomas and the mouse "ependymoblastoma" were negative. Staining for GFA protein delineated the astrocytic reaction of neural tissue adjacent to the tumors. The reaction was markedly intensified in the brains of mice infected with toxoplasma. Additionally, ependymal cells near the tumors stained positively for GFA protein; normal ependyma at a distance from tumor remained negative. The technique, which combines a high degree of specificity with great sensitivity and is readily adaptable to routinely processed tissue, should prove a valuable tool in experimental oncology of the central nervous system.
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PMID:The immunocytochemical localization of GFA protein in experimental murine CNS tumors. 76 Mar 68

Lymph nodes were obtained from 28 patients with non-Hodgkin's lymphoma and 24 patients without hematologic malignancy. Cases of undifferentiated lymphoma, diffuse histiocytic lymphoma, diffuse and nodular mixed histiocytic-lymphocytic lymphoma, nodular poorly differentiated lymphocytic lymphoma, and diffuse well differentiated lymphocytic lymphoma were analyzed. Touch preparations were stained for nonspecific esterases, peroxidase, Sudan black B activity and with periodic acid-Schiff and Wright-Giemsa reagents. Mononuclear cell suspension from lymph nodes and, in some cases, peripheral blood were tested for spontaneous rosette formation with sheep erythrocytes and for the presence of surface immunoglobulin. The remainder of the lymph node was examined after staining with hematoxylin and eosin. Analysis of the lymphocyte surface markers indicated that 15 cases of various histologic types of lymphoma were B cell proliferations. However, three out of four cases of diffuse poorly differentiated lymphocytic lymphoma and one of seven cases of diffuse histiocytic lymphoma appeared to represent T cell neoplasia. Lymph nodes from four cases of lymphoma representing diverse histologic types were replaced by neoplastic cells devoid of discernible cell markers. In five cases, the distribution of cell surface markers in the malignant lymph node failed to differ from data obtained in the analysis of non-neoplastic lymph nodes. The study indicates that the histopathologic entities recognized in the currently employed classification of lymphoreticular malignancies are heterogeneous. Alterations in the distribution of cell surface markers in the peripheral blood from five of 12 patients indicated involvement prior to demonstrable morphologic evidence of peripheral blood involvement in four patients and bone marrow infiltration in two patients.
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PMID:Immunologic and cytochemical cell markers in non-Hodgkin's lymphomas. 79 63

A triple-bridge, indirect peroxidase-antiperoxidase method for demonstrating carcinoembryonic antigen (CEA) in frozen, ethanol-fixed or formalin-fixed, paraffin-embedded specimens was evaluated. Examination of 359 tissue specimens--234 malignant tumors, 37 benign neoplasms, 41 nonneoplastic diseased tissues, and 47 normal specimens--showed that CEA could usually be demonstrated in a group of cancers. We could detect CEA in carcinomas of the stomach, colon, rectum, pancreas, lung, and cervix. However, malignant tumors of the breast, prostate, kidney, larynx, brain, lymphoreticular system, soft tissues, and skin proved negative for CEA by the immunoperoxidase test. CEA could be detected in ethanol- or formalin-fixed sections. The only nonmalignant specimens showing CEA staining were a few benign tumors, the mucosae of some cases of colitis, and the resection margins of 2 cases of colon cancer; however, these were commonly very weak reactions. Measurement of tumor CEA content by radioimmunoassay revealed two causes for this relative specificity of the immunoperoxidase test for CEA:1) a quantitative difference existed in tissue CEA among the various specimens, and 2) the threshold for CEA staining in malignant specimens was usually above that in nonmalignant specimens. An analysis of the formalin-paraffin-treated sections showed that immunoperoxidase-tested CEA positivity reflected CEA levels in tissue of at least 3.0-5.0 mug/g; this permitted retrospective estimates of minimal tissue CEA concentrations in older histopathologic specimens by the immunoperoxidase reaction method. Formalin-paraffin-treated sections as old as 10 years still had demonstrable CEA. Although tumor CEA concentration correlated well with immunoperoxidase staining for CEA, plasma CEA titer did not necessarily reflect tumor CEA content. CEA positivity in primary and secondary tumors was strongly correlated; it was less strongly correlated with level of tumor differentiation.
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PMID:Carcinoembryonic antigen in histopathology: immunoperoxidase staining of conventional tissue sections. 79 93

The peroxidase and estradiol-metabolizing activities of mammary tumors induced by 7,12-dimethylbenz(a)anthracene were determined in fresh and stored tissue. In both cases, a wide variation in peroxidase activity was observed in 47 different tumors tested. The properties of the enzyme found in the tumors were similar to those of lactoperoxidase. It is suggested that the amount of peroxidase present might reflect the ability of tumor cells to differentiate in response to hormonal stimulation and be indicative of the degree of tumor progression.
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PMID:Metabolism of (4-14C)estradiol by 7,12-dimethylbenz(a) anthracene-induced mammary tumor peroxidase. 81 11

The enzymatic destruction of oxidizing products produced during metabolic reduction of oxygen in the cell (such as singlet oxygen, H2O2 and OH radical) involves the concerted action of superoxide dismutase-which removes O-2 and yields H2O2-and H2O2 removing enzymes such as catalase and glutathione peroxidase. A difference in distribution or ratio of these enzymes in various tissues may result in a different reactivity of oxygen radicals. It was found that in red blood cells superoxide dismutase and catalase are extracted in the same fraction as hemoglobin, while glutathione peroxidase appears to be "loosely" bound to the cellular structure. This suggests that in red blood cells catalase acts in series with superoxide dismutase against bursts of oxygen radicals formed from oxyhemoglobin, while glutathione & peroxidase may protect the cell membrane against low concentrations of H2O2. On the other hand, catalase activity is absent in various types of ascites tumor cells, while glutathione peroxidase and superoxide dismutase are found in the cytoplasm. However, the peroxidase/dismutase ratio is lower than in liver cells, and this may provide an explanation for the higher susceptibility of tumor cells to treatments likely to involve oxygen radicals.
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PMID:Enzyme defense against reactive oxygen derivatives. II. Erythrocytes and tumor cells. 81 6

Surface proteins and fibrinolysis were investigated in a variety of cell types. A large external transformation-sensitive protein was demonstrated by lactoperoxidase-catalyzed iodination. Electron microscope autoradiography confirmed that the technique labeled surface material only. The protein was present in explants of normal tissues was well as in nontumor-producing cultured cell lines. It was not lost during long-term culture. Neoplastic transformation in vitro, whether spontaneous or induced by a chemical carcinogen or virus, led to the loss of the material in most but not all cases. The protein was also absent from many but not all spontaneous and induced tumors of the different types tested. Elevated fibrinolytic activity was demonstrated in a number of normal tissues and non-tumor-producing cell lines. It was also present in most sarcomas but absent from most carcinomas that we have examined, except for a cell line from a well-differentiated bladder tumor. The correlation between absence of large external transformation-sensitive protein and fibrinolysis was examined, and it was found that activation of plasminogen was not sufficient to cause the absence of this surface protein.
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PMID:Surface proteins and fibrinolytic activity of cultured mammalian cells. 81 65


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