Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum tyrosinase activity in many persons with metastatic diseases was found to be significantly higher than activity in normal persons. The highest activity was observed in melanoma and breast carcinoma. The electrophoretic patterns of serum tyrosinase, resolved by electrophoresis of a serum tyrosinase fraction followed by incubation of the gel sample with L-dopa, and represented as sets of RF's of melanin bands, were characteristically different in melanoma, breast carcinoma, and certain other diseases. The RF's of melanin and protein bands in the serum enzyme preparations from melanoma patients were concisely defined. Further, some potent serum fractions inhibiting tyrosinase melanogenic activity have been obtained, and the presence of tyrosinase inhibitors in the serum enzyme preparation has also been demonstrated. More detailed exploration of these serum tyrosinase parameters may provide more specific and sensitive detection for certain malignant diseases.
Cancer Res 1979 Sep
PMID:Serum tyrosinase in malignant disease, its activity, and the electrophoretic patterns of the enzyme as carried by immunoglobulins'. 11 92

A rapid microcytotoxicity assay for the detection of HL-A antigens on tissue culture cells derived from human solid tumors is described. Tumor cells were prelabeled with 125Iododeoxyuridine. Isotopically labeled tumor cells were reacted with up to 37 highly selected HL-A antisera and diluted rabbit complement. Results of the HL-A typing of nine human tumor cell lines are reported. Three melanoma cell lines showed individually distinct HL-A profiles at the first HL-A locus which agreed with the antigenic pattern of the tumor donor's autologous lymphocytes. Less reactivity was noted with HL-A antisera defining second locus specificities on the three melanoma cell lines, whereas some other cell lines showed more HL-A reactions than required to present a "full house". This method obviates the necessity for visually enumerating residual tumor target cells.
Transplantation 1975 Sep
PMID:A new micromethod for the detection of HL-A antigens on cultured human tumor cells. 12 40

The ultrastructural morphology of the tumour cycle which has as one of its features the blood-borne tumour embolus associated with thrombosis is illustrated by examples of four phases. (1) The intrinsic vasculature of tumours influences the process of intravasation of tumour cells to form bloodborne emboli. Scanning electron microscopy of melanoma tumours reveals channels containing erythrocytes which are sinusoidal in appearance. (2) The reaction of the circulating blood to the villi and folds of tumour cells is to coat the surface with plasma proteins and platelets. Walker 256 carcinoma cells become encrusted with platelets following agitation with rat platelet rich plasma. (3) Damaged endothelium appears to provide a more secure adhesional site for the tumour embolus. Platelets on a damaged site may provide an active adhesional region for the platelets on the passing embolus. (4) Tumour cells migrate through the endothelial layer from the adherent embolus and can be held up at the level of the basement membrane of the endothelium.
Z Krebsforsch Klin Onkol Cancer Res Clin Oncol 1976 Sep 24
PMID:Some aspects of blood borne tumour emboli associated with thrombosis. 13 7

Mice have been immunosuppressed with cyclophosphamide, cortisone-acetate, irradiation, or Ehrlich ascitic fluid (EAF) and then grafted with Ehrlich tumor or with one of the following strain-specific tumors: thymoma, methylcholanthrene-induced fibrosarcoma, B-16 melanoma, lymphatic leukaemia, and myeloid leukaemia. Immunosuppression of the host influenced very differently the growth of transplanted malignancies. The growth of thymoma and of Ehrlich tumor was regularly enhanced. The growth of fibrosarcoma and of melanoma, on the other hand, was retarded in mice pretreated with EAF and X-rays, or remained unchanged in mice pretreated with drugs. Leukaemia growth was not influenced by any immunosuppressive treatment; the only exception was enhanced growth of lymphoid leukaemia in animals pretreated with EAF. Thus different tumors grew differently in animals immunosuppressed by the same immunosuppressive agent, while different immunosuppressive treatment changed the growth of one particular tumor always in the same way. From this we concluded: (1) there is no rule as to how immunosuppression of the host will influence tumor growth; and (2) the way in which the malignant growth will be changed depends mainly upon the type of the tumor and probably not very much upon the type of immunosuppressive treatment.
Z Krebsforsch Klin Onkol Cancer Res Clin Oncol 1978 Sep 28
PMID:Effect of immunosuppression on the growth of six murine tumors. 15 96

A cyclic nucleotide phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine, promoted the differentiation and maturation of B16 melanoma cells, phenomena associated with biological alterations in the surface properties of the cells. 1-Methyl-3-isobutylxanthien inhibited cell replication and increased the intracellular content of melanin and cyclic adenosine 3':5'-monophosphate. Significantly greater amounts of sialoglycoproteins were associated with 1-methyl-3-isobutylxanthine-treated cells. However, the total amount of [3H] glucosamine incorporated into anionic polysaccharide (both sialoglycopeptide and mucopolysaccharides) was not significantly changed.
Cancer Res 1975 Sep
PMID:Properties of acidic saccharides produced by B16 melanoma cells treated with 1-methyl-3-isobutylxanthine. 16 57

A quantitative, digital-output, whole-body scanner in a low background area has been used in the dosimetry of 32P/131I Lipiodol for intralymphatic radiotherapy. Five patients with malignant melanoma received intralymphatic administrations of Lipiodol labelled with 6 mCi 32P and 1.5 mCi 131I. The 131I is used primarily as a tracer for external measurements and the 32P as the chief therapeutic agent. Whole body scans were made at intervals for up to 15 days using the digital scanner, with the spectrometer set over the 364 keV photopeak of 131I. On the same occasions complete gamma-spectra were obtained for these patients using a 2 m arc, single detector whole body counter. The method used in estimating the activity at various sites in the body from the digital whole body scans is described and problems that arise in using 131I as a tracer for 32P Lipiodol in this work are discussed. For the administered activities mentioned above, maximum absorbed doses to the lymph nodes were found to range from 30-96 krad with a mean value of 51 krad. Uptake of radioactivity was also found in the lungs, resulting in absorbed doses of 350-960 rad with a mean value of 540 rad.
Br J Radiol 1976 Sep
PMID:The application of a digital whole body scanner to the dosimetry of intralymphatic 32P/131I Lipiodol. 18 52

Sera from cancer patients and healthy individuals, obtained from two independent sources, were examined for their abilities to react with herpes simplex virus-associated tumor antigens, AG-4 and NVA-TAA (nonvirion antigen-tumor-associated antigen). Both antigens were prepared by infection of HEp-2 cells with herpes simplex virus type 2, and all antigen-antibody interactions were measured by the micro-complement fixation test. Of sera from 16 patients with cancer of the uterine cervix, 81% (P less than 0.01) reacted with NVA-TAA, whereas 78% (P less than 0.001) of 18 sera examined reacted with AG-4. These values differed significantly from those for normal sera, of which 14% reacted with NVA-TAA and 13% with AG-4. Of sera for 8 patients with squamous cell carcinoma of head and neck or vulva, 75% (P less than 0.02) reacted with NVA-TAA, whereas 63% (P less than 0.05) reacted with AG-4. As a group, other cancers (including adenocarcinoma of lung, breast, ovary, and cervix; liposarcoma; sarcoma; melanoma; and carcinoma of the endometrium) did not differ significantly from controls in reactive patterns with AG-4 or NVA-TAA. These studies partly supported the reported preferential reactivity of AG-4 and NVA-TAA with sera of patients with squamous cell carcinoma, especially of the uterine cervix.
J Natl Cancer Inst 1976 Sep
PMID:Comparative diagnostic aspects of herpes simplex virus tumor-associated antigens. 18 98

Endolymphatic radiotherapy with 4 mCi32P tri-n-octylphosphate and 1 mCi 131 I triolein LIPIODOL UF has been performed in 75 patients suffering from malignant melanoma of the lower extremity. On the average, 13.3% of the radioactive substance remains in the syringes and connecting tubes. In most patients the radioactive material available for therapeutic irradiation is further reduced due to contamination of operation sheets and swabs (mean: 15.3%). There is, however, still sufficient radioactivity remaining for effective internal irradiation of the lymph nodes. The average radiation dose absorbed by the lymphatic tissue is 90.998 rad. The method is limited by the hazard of radiation damage to the lungs. Almost 80% of these patients had detectable concentrations of radioactivity in the lung fields. The average radiation dose was found to be 299 rad. So far radiation induced fibrosis has bot been observed in this series.
Lymphology 1976 Sep
PMID:Distribution pattern of radioactive labelled lipiodol-UF following intralymphatic application for therapy. 18 79

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.
Am J Pathol 1977 Sep
PMID:Macrophage migratory dysfunction in cancer. A mechanism for subversion of surveillance. 19 6

The ability of melanocyte stimulating hormone (MSH), adrenocorticotropic hormone (ACTH), and prostaglandin E1 (PGE1) to stimulate the accumulation of cyclic AMP was examined in intact mouse melanoma cells of varying metastatic potential. F1 cells (low metastatic potential) had significantly greater cyclic AMP levels in response to all three hormones than F5 (intermediate metastatic potential) and F10 (high metastatic potential) cells. The ranking of the response was as follows: MSH, F1 greater than F5 greater than F10, ACTH, F1 greater than F5 greater F10, PGE, F1 greater than F10 greater F5. In contrast to the above, the degree of hormonal stimulation of adenylate cyclase in broken cell preparations was virtually identical in all three melanoma cell lines. Control enzyme activity was depressed in both F5 and F10 relative to F1. The conflicting results between studies of intact vs. broken cell preparations could not be explained by increased cyclic AMP phosphodiesterase activity in F5 and F10 cells. We conclude that as the melanoma cells increase in metastatic potential, there is a significant loss in the ability of their cyclic AMP system to respond appropriately to hormonal stimuli.
J Cell Physiol 1978 Sep
PMID:Hormonal activation of adenylate cyclase in mouse melanoma metastatic variants. 20 54


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