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)

The leukocyte adherence inhibition assay was used to measure cell-mediated immunity in 26 patients with malignant glial neoplasms and 41 control subjects. A significant inhibition of leukocyte adherence was observed in 21 of 26 (80%) glioma patients in the presence of a 3 M KCl extract of glioma tissue, as compared to that of normal brain extract. Among the control group, no significant difference in the percentage of nonadherent leukocytes was noted in the presence of either antigen. To study the specificity of the reaction, a 3 M KCl extract of meningioma, pituitary tumor, carcinomas of breast, and lung, melanoma, brain, and heart tissues were used as nonspecific antigens. Such studies revealed significantly lower values of nonadherent leukocytes. These data indicate that patients with malignant glial neoplasms manifest a cellular immune response to glioma-associated antigens which can be measured by the tube leukocyte adherence inhibition assay and that leukocyte adherence inhibition assay may render additional useful information in diagnostic and prognostic evaluation of malignant glial neoplasms.
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PMID:Specific cellular immune responses in patients with malignant gliomas. 8 87

The leukocyte adherence inhibition assay (LAI) was used to measure cell-mediated immunity in 26 patients with malignant glial neoplasms and in 41 control subjects. A significant inhibition of leukocyte adherence was observed in 21 out of 26 (80%) patients with malignant astrocytic gliomas in the presence of a 3M KC1 extract of glioma tissue compared to that of normal brain extract. Among the control group, no significant difference in the percentage of nonadherent leukocytes (NAL) was noted in the presence of either antigen. To study the specificity of the reaction, 3M KC1 extracts of meningioma, pituitary tumor, carcinoma of breast, carcinomas of lung, melanoma, brain, and heart tissues were employed as non-specific antigens. Such studies revealed significantly lower values of NAL. These data indicate that patients with malignant glial neoplasms manifest a cellularimmune response to glioma-associated antigens that can be measured by the tube LAI assay and that LAI assay may render additional useful information in the diagnostic and prognostic evaluation of malignant glial neoplasms.
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PMID:Preoperative cell-mediated immune status of patients with malignant glial tumors. 23 66

The sensitivity to local tumor hyperthermia (43 degrees, 60 min) of a spectrum of eight different solid mouse tumors (Lewis lung carcinoma, M5076 ovarian carcinoma, colon carcinoma 38, colon carcinoma 26, mammary adenocarcinoma C3HBA, mammary adenocarcinoma 16C, glioma 26, and B16 melanoma) was investigated. A microwave (2.45-GHz) apparatus produced localized heating of the tumors without generation of whole-body hyperthermia. The temperature at the center of the heated tumors was regulated to within +/- 0.1 degrees while the temperature uniformity within the tumor was +/- 0.5 degrees. The local hyperthermia treatments reduced the size and retarded the growth of the treated tumors compared with control values for each of the tumors tested. The faster-growing Lewis lung carcinoma and B16 melanoma were the least responsive to treatment, while the slower-growing colon 38 and M5076 ovarian carcinomas were the most responsive. Multiple treatments resulted in longer grwoth delays and greater tumor growth inhibition than did single treatments. No consistent difference in life span between the control and treated groups was measured, and only five of 188 treated animals were cured.
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PMID:Effects of local tumor hyperthermia on the growth of solid mouse tumors. 49 85

A 57-year-old man had a clinically suspected malignant melanoma in his left eye. On microscopic study, the enucleated eye harbored an unusual choroidal tumor that had extended extraocularly. This tumor had been variously interpreted microscopically as an angiosarcoma, an atpical angioma, a glioma, or a neurilemoma. Electron microscopic examination of deparaffinized tissue established the smooth muscle nature of the tumor cells as well as the presence of numerous pericytes associated with conspicuous vascular channels. This unique myogenous tumor of the choroid probably had a vascular origin.
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PMID:Choroidal leiomyoma of vascular origin. 94 70

From 1969-1974 1000 unselected enucleated globes have been examined histopathologically. 277 derive from the University Eye Hospital in Hamburg, 723 from various Eye Hospitals in northern and southern Germany. They originate from 589 men and 408 women, three times the sex was unknown. 86 globes had to be removed from children less than 15 years old. 6 groups of etiologies have been distinguished: trauma (308), histologically confirmed neoplastic disease (281), ocular manifestations of systemic diseases (diabetes mellitus, occlusions of central retinal vessels presumably following generalized vascular disease etc.: 128), "operative ocular disease" (164), primary inflammatory disease (71), miscellaneous (malformations, high myopia, pseudo-glioma and pseudo-melanoma: 48). The etiology "operative ocular disease" consists of 67 primary glaucomas (57 adults, 10 buphthalmus), 41 idiopathic cataracts (7 of these congenital) and 3 primary corneal dystrophies, as well as 53 cases of primary retinal detachment. Among the 281 neoplastic diseases, there are 238 primary intraocular malignant melanomas of the uvea, 18 retinoblastomas, 4 primary reticulumcellsarcomas of the retina, 2 choroidal nevi, 10 intraocular metastases and 9 orbital tumors. 16 enucleations among the 1000 enucleations have been performed for pseudo-gliomas (5 x Coats disease, 5 x persistent primary hyperplastic vitreous, 2 x retrolental fibroplasia, others 4 x). The manifestations of systemic disease are consisting of 68 central retinal vein-occlusions, 30 complications of diabetes mellitus and 10 central retinal artery occlusions as well as 20 other generalized diseases. A primary inflammatory disease led to enucleation 50 times due to an intraocular process, 5 times due to scleritis and 18 times as a consequence of keratitis (including 13 times herpes simplex). As the final clinical cause for enucleation the following categories have been elaborated: secondary glaucomas (416), clinical diagnosis of "tumor" (275), atrophy and phthisis bulbi (118), inflammation (112), acute trauma to 4 weeks after the accident (72), others (7). In conclusion the central role of rubeosis iridis leading to secondary angle closure glaucoma is emphasized. This process presents a challenge to ophthalmologic research. Finally the significance of early surgery for primary angle closure glaucomas and for complete restoration of the anterior chamber after trauma and any intraocular procedure is stressed.
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PMID:[Etiology and final clinical cause for 1000 enucleations. (A clinico-pathologic study) (author's transl)]. 95 59

Two new murine monoclonal antibodies were prepared by hybridoma technique after immunization with the immature pluripotent leukemia cell line K562. The monoclonal antibody Bra10G (IgG2b) reacted in a non-lineage pattern with all examined hematopoietic neoplastic cell lines and peripheral blood cells (granulocytes, lymphocytes, erythrocytes) of healthy donors, with the exception of monoblastoid cell line U-937 and B lymphoma cell line Daudi. This monoclonal antibody immunoprecipitated an 18-20 kDa cell surface protein expressed also on the cell surface of examined non-hematopoietic (malignant glioma, melanoma and breast carcinoma) cell lines. These properties and the efficient inhibition of Bra10G binding to the cell surface of K562 cells by the reference CD59 monoclonal antibody (MEM-43) indicated that Bra10G belongs to the CD59 cluster of monoclonal antibodies which identify the human protectin molecule. The monoclonal antibody Bra7G (IgM) reacted with a 95 kDa cell surface protein expressed on hematopoietic cells (with the exception of erythrocytes) and was absent on the examined non-hematopoietic neoplastic cell lines. These data together with a partial inhibition of Bra7G binding by the reference CD-43 monoclonal antibody suggested the CD43 (leukosialin, sialophorin) specificity of this monoclonal antibody.
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PMID:Monoclonal antibodies to two adhesive cell surface antigens (CD43 and CD59) with different distribution on hematopoietic and non-hematopoietic tumor cell lines. 128 43

The cytotoxic activity of immunotoxins constructed with human diferric transferrin (Tfn) as the carrier ligand and an abrin variant Pseudomonas exotoxin A (PE) and the diphtheria toxin mutant cross-reacting material (CRM) 107 as the toxin moieties were studied in vitro. Three malignant human cell lines, the glioblastomas multiforme SNB19 and SF295 and the LOX melanoma, and a nonhuman control murine melanoma cell line B16 were assessed. The presence of transferrin receptors on the cell lines was confirmed by direct 125I-Tfn binding assays. The 50% protein synthesis inhibitory concentration (IC50) values for all cell lines demonstrated that Tfn-abrin variant and Tfn-PE had comparable potency and were both more effective than Tfn-CRM 107. Monensin, a carboxylic ionophore, potentiated the effect of Tfn-abrin variant against glioma cells approximately 35-fold with IC50 values of 4.0 x 10(-13) M and 4.7 x 10(-12) M for SNB19 and SF295, respectively. Cytotoxic activity of Tfn-abrin variant (with or without monensin) and Tfn-PE was correlated with the degree of Tfn receptor expression measured on the cell lines. The exquisite in vitro cytotoxicity of Tfn-abrin variant and Tfn-PE immunotoxins against glioma and melanoma cells warrants further in vivo evaluation and future consideration of these agents for potential clinical application against glioblastoma multiforme and leptomeningeal neoplasia.
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PMID:In vitro efficacy of transferrin-toxin conjugates against glioblastoma multiforme. 131 94

Glioblastoma multiforme is one of the most resistant of human tumors to radiation whether used alone or in combination with surgery and/or chemotherapy. This resistance may be caused by one or more of several different factors. These include inherent cellular radiation sensitivity, an efficient repair of radiation damage, an increased number of clonogens per unit of volume, a high hypoxic fraction, high [GSH] concentration, and rapid proliferation between fractions. In the present study, we evaluate the intrinsic radiation sensitivity (surviving fraction at 2 Gy or mean inactivation dose) of malignant human glioma cells in vitro. The in vitro radiation sensitivity of 21 malignant glioma cell lines (early and long term passages) has been measured using colony formation as the end-point of cell viability. The survival curve parameters (SF2 measured and calculated, alpha, beta, D0, n and MID) have been determined for single dose irradiations of exponential phase cells (18-24 hr after plating) under aerobic conditions and growing on plastic. The mean SF2 of the 21 cell lines is 0.51 +/- 0.14 (with a range of 0.19 to 0.76). This value may be compared to the mean SF2 of 0.43-0.47 for SCC, 0.43 for melanoma, and 0.52 for glioblastoma as reported from other authors when using colony formation of cells in exponential phase on plastic. Although glioblastoma is almost invariably fatal, our data demonstrate a very wide range of intrinsic radiosensitivities. These broadly overlap the radiation sensitivities of cell lines from tumors that are often treated successfully. We conclude that standard in vitro measurements of cellular radiation sensitivity (SF2) do not yield values that track in a simple manner with local control probability at the clinical level and that, for at least some of the tumors, other parameters and/or physiological factors are more important.
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PMID:In vitro intrinsic radiation sensitivity of glioblastoma multiforme. 131 13

During the last several decades, immunohistochemical studies of tumors, along with other approaches, have suggested that the clinical and biological progression results, at least in part, from the sequential appearance within the neoplasm of cellular subpopulations whose new characteristics reflect specific somatic genetic changes. However, CNS may provide a different microenvironment for activation and proliferation than other tissues. The tissue-specific distribution of intermediate filament proteins, in particular the keratins, permits their use as marker in histopathology, but several important exceptions are recognized. In this connection, it is of interest that, according to the other reports, glial tumors may be positive for different anti-keratin antibodies. However, the gliomas did not show an immunoreaction in any of the cases when HEA-125 and Ber-EP4 were applied. The great number of multihormonal pituitary adenomas and possible change of the immunohistochemically detectable hormone status in cases of recurrent tumors have particularly re-emphasized the need for new thinking about patterns of classification. The diagnosis of malignant melanoma has been considerably facilitated recently by the introduction of immunohistological labelling with antibodies selective against melanoma antigen (HMB-45). Our results confirmed the necessity of cautious interpretation of HMB-45 immunoreactivity because a HMB-45 expression can be observed in several non-melanotic tumors.
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PMID:[Changes of microenvironment and tumor cell heterogeneity--consequences for bioptic diagnosis]. 137 17

The anti-proliferative activity of human interferon (HuIFN) was enhanced by dipyridamole, 2,6-bis-(diethanolamino)-4,8-dipiperidinopyrimido-[5,4-d]-py rimidine, when tested against various human tumor cell lines, including KT (breast carcinoma), PLC/PRF/5 (hepatoma), MGC-I, U251-SP and T98 (glioma), HAC-2 and SHIN-3 (ovarian carcinoma), and MM-ICB (melanoma). The enhancement occurred irrespective of the kind of HuIFN used (alpha, beta or gamma) and the original degree of susceptibility of the cells to HuIFN. Even low doses down to 0.01 microM of dipyridamole that had no intrinsic anti-proliferative activity could enhance the effect of HuIFN. The enhancement of HuIFN effects seems not to be caused by induction of HuIFN production, because neither anti-viral activity nor HuIFN antigens were detected in culture medium in cells treated with dipyridamole. Mopidamole, a derivative of dipyridamole lacking one piperidine residue, produced little enhancement of the effects of HuIFN. Among ovarian cancer cell lines tested, the enhancement of the activity of HuIFN by dipyridamole for HAC-2 and SHIN-3 cells was equivalent to or greater than that for 3 chemotherapy agents (adriamycin, vincristine, and a camptothecin derivative). However, neither HOC-21 ovarian cancer cells nor HEC-1 endometrial adenocarcinoma cells were susceptible to any combinations. When MGC-1, U251-SP, and HAC-2 cells were injected into nude mice, the growth of tumors was more markedly inhibited by the subcutaneous administration of HuIFN in combination with oral administration of dipyridamole than by the HuIFN alone. Thus, this combination therapy seems to be worth trying for human cancer, although the enhancement of the effects of HuIFN by dipyridamole varied among the cell lines examined.
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PMID:Dipyridamole enhances an anti-proliferative effect of interferon in various types of human tumor cells. 137 1


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