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)

Three predominantly CD8+ CTL lines, TIL 501, TIL 620, and TIL 660, were generated from three HLA-A2+ melanoma patients by culturing tumor-infiltrating lymphocytes in 1000 U/ml IL-2. These tumor-infiltrating lymphocytes lysed 12 of 18 HLA-A2+ autologous and allogeneic melanomas, but none of 20 HLA-A2-negative melanomas. They also did not lyse the MHC class I negative lymphoma-leukemia cell lines, Daudi, K562, or HLA-A2+ non-melanoma cell lines including PHA or Con A-induced lymphoblast, fibroblast, EBV-transformed B cell, Burkitt's B cell lymphoma, and colon cancer cell lines. Autologous and allogeneic melanoma lysis was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag among melanoma cell lines in a TCR-dependent, HLA-A2-restricted manner. Six HLA-A2-negative melanoma cell lines obtained from five HLA-A2-negative patients were co-transfected with the HLA-A2.1 gene and pSV2neo. All 17 cloned transfectants expressing cell surface HLA-A2 molecules, but none of 12 transfectants lacking HLA-A2 expression, were lysed by these three HLA-A2-restricted, melanoma-specific CTL. Lysis of the HLA-A2+ transfectants was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag on transfectants in a TCR-dependent, HLA-A2-restricted manner. These results identify the HLA-A2.1 molecule as an Ag-presenting molecule for melanoma Ag. They also suggest that common melanoma Ag are expressed among melanoma patients regardless of HLA type. These findings have implications for the development of melanoma vaccines that would induce antitumor T cell responses.
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PMID:Shared human melanoma antigens. Recognition by tumor-infiltrating lymphocytes in HLA-A2.1-transfected melanomas. 172 79

Immunization of C57BL/6 mice with syngeneic tumor cells, MBL-2, resulted in the generation of antitumor effector cells in vivo. The immunized C57BL/6 mice permanently rejected viable MBL-2 lymphoma cells, but not B16 melanoma cells. Cytotoxic T cells obtained from MBL-2-immunized mouse peritoneal cells (PEC) showed specific cytotoxicity against MBL-2, but not to YAC-1, RDM-4 and Meth A cells. By sorting with FACStar, the specific CTL were characterized as TCR alpha beta+ CD8+ T cells. Moreover, the cytoplasm of in vivo-induced CTL was stained with a monoclonal antibody against perforin. The localization of perforin in cytoplasmic granules of CTL was demonstrated by electron microscope analysis. This experiment presented the first evidence that in vivo-induced CD8+ CTL against syngeneic tumor cells expressed significant amounts of perforin.
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PMID:Perforin is expressed in CTL populations generated in vivo. 174 Mar 53

Clinical and experimental evidence explaining and supporting the role of UV radiation as a causal factor for the induction and promotion of nonmelanoma and malignant melanoma skin cancer are presented. While there is excellent animal experimental data and human epidemiologic evidence supporting the causal relationship of UVR (UVB, as well as UVA radiation) for basal and squamous cell carcinomas, the data establishing a direct causal relationship between melanoma and exposure to sunlight appear to be complex. They do, however, suggest a definite promotional role of sunlight in the causation of melanoma. Using a hairless pigmented mouse strain (Skh-hr2), experiments were initiated to examine the role of UVR in the induction of melanoma. A single application of DMBA as an initiator and subsequent thrice-weekly exposures to either UVB (290-320 nm) or UVA (320-400 nm) or the combined exposures of UVA and UVB resulted in the formation of blue nevus-like lesions. Repeated UVR exposures for over 30 weeks resulted in the development of melanoma (38%), as well as lymphoma and squamous cell carcinoma only in those mice that were pretreated with DMBA and had developed nevi. Mice receiving UVB, UVA, or the combination treatments of UVB plus UVA without DMBA pretreatment developed papillomas and squamous cell carcinoma but no melanoma. These studies indicate that some initiation event is essential to transform melanocytes to blue nevus-like lesions before UVR (UVB + UVA) can act as a promoter and accelerate the development of malignant melanoma, as as well as lymphoma.
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PMID:Ultraviolet radiation and the development of non-melanoma and melanoma skin cancer: clinical and experimental evidence. 176 52

The cytomorphological features of cells from 52 cases of metastatic melanoma obtained by fine needle aspiration cytodiagnosis were studied. Morphologically, 11, 19 and 22 cases were classified as spindle, epithelial, and mixed cell types of metastatic melanoma respectively. There were 34 melanotic and 18 amelanotic melanomas. Besides melanin, the presence of intranuclear cytoplasmic inclusions, eosinophilic macronucleoli and giant cells were helpful in the diagnosis of a melanoma. Where attempted, staining for S-100 protein was positive in all the 19 cases (eight amelanotic and 11 sparsely pigmented melanomas). In addition eight cases of metastatic tumour where a differential diagnosis of poorly differentiated carcinoma or large cell lymphoma was entertained, were also studied for localization of S-100 protein and all were found to be negative. Electron microscopy was performed in five cases and showed the presence of melanosomes and/or premelanosomes.
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PMID:Cytomorphology of metastatic melanoma--use of S-100 protein in the diagnosis of amelanotic melanoma. 178 61

Axillary lymph node enlargement can be the first and only manifestation of malignancy. Although lymphoma and metastasis from melanoma, breast and lung cancers are known causes, the primary tumour may remain undetected in some cases despite exhaustive investigations. Therefore, once the diagnosis of malignancy is confirmed by clinical examination followed by histology, further investigations should be limited to a search for treatable malignancies only. Extensive investigations with a hope of discovering the primary is useless and not cost effective. Close follow up may occasionally reveal new clinical signs when further investigations can be justified. This paper reports the clinical approach to diagnosis and management of such cases with examples of illustrative cases.
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PMID:Malignant axillary lymphadenopathy--a problem for management. 178 98

Data were obtained for all deaths registered between 1979-1983, and for all new cancers recorded at the Victorian Cancer Registry between 1982-1983, in residents of Melbourne. A socioeconomic status (SES) measure had been produced for each local government area (LGA) by principal components analysis of sociodemographic variables recorded at the 1981 census. A SES score from 1 to 10 was assigned to each death and cancer. Population data from the census were similarly scored. Age standardised rates for all cause mortality, for mortality from all causes other than cancer and for both incidence and mortality of total cancers, cancer of the stomach, colon, rectum, lung, female breast, cervix, uterus, prostate and bladder, and for melanoma, lymphoma and leukaemia were analysed as a function of SES decile using weighted linear regression. Despite the limited number of years of data and the misclassification of the SES score, analyses showed there were inequitable distributions of mortality, and of some major cancers, across social strata in Melbourne during the early 1980s. The incidences of cancer of the breast, colon, prostate and melanoma were all positively associated with SES, while the incidences of cancer of the stomach, lung and cervix demonstrated negative SES gradients. For cancers where incidence showed a significant SES gradient there was a similar SES gradient with mortality. These patterns are consistent with the literature and implicate SES differences in education and access to services. Implications for health policy are discussed.
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PMID:Socioeconomic status and cancer mortality and incidence in Melbourne. 183 29

We describe three patients who experienced several types of visual problems while receiving interleukin 2 therapy for melanoma or lymphoma. Their symptoms included diplopia, binocular negative scotomata, scintillating scotomata, and palinopsia. All symptoms eventually resolved following discontinuation of therapy. It appears that focal neurologic deficits that affect the visual system may complicate interleukin 2 administration.
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PMID:Neuro-ophthalmic complications of interleukin 2 therapy. 184 74

In order to determine the value of immunohistochemical staining methods for the morphologic diagnosis, we studied 949 histologic specimens sent for consultation to the Immunohistochemistry Laboratory of Department of Pathology of the Medical School of Botucatu in the period 1984-1989. All case were submitted to the immunoperoxidase staining with the methods PAP or ABC. Immunohistochemical stains confirmed the original morphologic diagnosis in 468 cases (49.3%); made the definitive diagnosis from a list of differential diagnostic possibilities in 244 cases (25.7%); provided contributory information in 74 cases (7.8%); were non-contributory in 114 cases (12%) and rendered an unsuspected diagnosis in 49 cases (5.2%). In some cases with non-contributory information the differences in methods of fixation might have led to suboptimal preservation of tissue antigens. The immunohistochemical staining may provide important and sometimes essential informations for definitive diagnosis. This technique was particularly useful for differential diagnosis between carcinoma, lymphoma and melanoma.
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PMID:[The usefulness of immunohistochemical methods for the anatomopathologic diagnosis]. 184 1

The immunohistochemical distribution of alpha and beta subunits of S-100 protein (S-100 alpha, S-100 beta, respectively) in 138 cases of human brain tumors was investigated by the avidin-biotin immunoperoxidase method. Brain tumors can be divided into four groups: group 1 [S-100 alpha (+) and/or S-100 beta (+)]; astrocytoma, glioblastoma, ependymoma, subependymoma, oligodendroglioma, choroid plexus papilloma, gangliocytoma, meningioma, chordoma, malignant melanoma. Group 2 [S-100 alpha (+) and S-100 beta (-)]; pineoblastoma, pituitary adenoma, craniopharyngioma, rhabdomyosarcoma. Group 3 [S-100 alpha (-) and S-100 beta (+)]; acoustic Schwannoma. Group 4 [S-100 alpha (-) and S-100 beta (-)]; medulloblastoma malignant lymphoma, germinoma. The S-100 beta immunoreactivity pattern in brain tumors was similar to those obtained using conventional anti-S-100 protein sera. In the first group of brain tumors both the number of positively stained tumor cells and the staining intensity were generally greater for S-100 beta than for S-100 alpha with a few exceptions including one gemistocytic astrocytoma, one subependymoma, one malignant melanoma, and some cases of glioblastomas. As to the relationship between malignancy and S-100 protein in glioma, S-100 beta immunoreactivity decreased according to degree of malignancy, while that of S-100 alpha varied, suggesting a heterogeneity of tumor cells in glioblastomas. Immunostaining for S-100 alpha and S-100 beta might become a useful diagnostic procedure in brain tumors and may give us more detailed and precise data of S-100 protein in brain tumors.
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PMID:Immunohistochemical study on the distribution of alpha and beta subunits of S-100 protein in brain tumors. 188 40

Herein we describe the isolation, physicochemical characterization and preclinical evaluation of a water-soluble biologic response modifier extracted from Sclerotium glucanicum. Alkaline extraction of insoluble S. glucanicum exopolymers produced a soluble scleroglucan composed of a triple-helical beta-1,3-linked glucopyranose backbone with single beta-1,6-linked glucopyranosyl branches every third subunit. Scleroglucan has a weight average molecular mass of 1.56 x 10(6) Da, a weight average root mean square distance from the center of gravity of the molecule to its farthest elements of 51.8 nm, a polydispersity (weight-average molecular mass/number average molecular mass) of 1.83 and intrinsic viscosity of 3.081 dl/g. Scleroglucan (250 mg/kg, intravenously) stimulated in vivo murine macrophage phagocytic activity (66%, P less than .001) and increased in vitro macrophage tumor cytotoxicity against syngeneic tumor targets by 124% (P less than .05). Scleroglucan enhanced (P less than .001) murine bone marrow proliferation in a biphasic manner by up to 328%. Scleroglucan therapy increased survival of mice challenged with syngeneic lymphoma, melanoma or adenocarcinoma. AKR/J mice bearing syngeneic lymphoma (1 x 10(3) cells, intraperitoneally) demonstrated increased (P less than .001) long-term survival (100% vs. 0%, greater than 64 days). C57Bl/6J mice bearing syngeneic melanoma B16 (5 x 10(5) cells, subcutaneously) demonstrated increased long-term survival (64% vs. 0%, P less than .05). C57Bl/6J mice bearing syngeneic adenocarcinoma BW10232 (1 x 10(5) cells, subcutaneously) demonstrated increased (P less than .05) median survival time. In addition, scleroglucan prophylaxis increased resistance of mice to challenge with Staphylococcus aureus, Candida albicans and mouse hepatitis virus A-59. Scleroglucan did not induce toxicity or hepatomegaly. We conclude that: 1) a branched, water-soluble beta-1,3-linked scleroglucan biologic response modifier can be extracted from S. glucanicum; 2) scleroglucan will stimulate immunity, modify experimental neoplastic disease and increase resistance to microbial challenge; and 3) scleroglucan shows promise as an immunopotentiating drug.
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PMID:Isolation, physicochemical characterization and preclinical efficacy evaluation of soluble scleroglucan. 190 59


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