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Query: UMLS:C0025202 (melanoma)
69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viable human melanoma cells are known to rapidly release cell surface macromolecules and tumor-associated antigens. To study whether this is a phenomenon related to malignant transformation, the release of surface macromolecules by human and murine melanoma cells was compared to that by normal allogeneic cells. Following lactoperoxidase radioiodination of cell surfaces, it was found that the proportion of labeled macromolecules released by human melanoma cells in 3 hr (60.0 +/- 9.9% (S.D.)] did not differ significantly from that released in the same time by normal allogeneic keratinocytes (56.0 +/- 10.0%) or fibroblasts (42.1 +/- 11.1%). Likewise in mice, the release of labeled surface macromolecules by B16 melanoma cells (36% in 3 hr) was no faster than that by normal syngeneic fibroblasts (56% in 3 hr). Control experiments excluded the possibilities that release was the result of cell death or of artifacts of the radioiodination procedure or that it represented release of fetal calf serum proteins adhering to the cells. These results suggest that rapid release of membrane macromolecules is not an expression of malignant transformation but rather a normal process which involves a major portion of macromolecules on the external surface of melanoma and normal cells and which occurs at a similar rate in both instances.
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PMID:Release of surface macromolecules by human melanoma and normal cells. 745 77

Malignant fibrous histiocytoma was diagnosed in seven cats from biopsy specimens received at the University of Missouri Veterinary Medical Diagnostic Laboratory during a 4-year period from 1987-1991. Tissue blocks from formalin-fixed specimens were resectioned and stained for type I (AE1) and type II (AE3) cytokeratins, desmin, S100 protein, vimentin, and alpha 1-antitrypsin by the avidin biotin peroxidase complex method with diaminobenzidine (DAB) chromogen. None of the tumors stained positively for alpha 1-antitrypsin. Four of seven of the tumors had similar immunohistochemical staining results, with positive staining for type I and type II cytokeratins, desmin, S100 protein, and vimentin. Of the remaining three, one stained positively only for S100 protein and vimentin; one stained positively for vimentin only; and one was negative for all six antigens. Based only on immunohistochemical staining results, three of the tumors could possibly be reclassified: one as a melanoma, one as a probable fibrosarcoma, and one as unknown. These results also indicate that feline malignant fibrous histiocytomas show a diversity of intermediate filament expression, as do human tumors. Our results also do not support the theory that malignant fibrous histiocytomas are of histiocytic origin.
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PMID:Immunohistochemical staining of feline malignant fibrous histiocytomas. 751 36

In order to determine epithelial markers in malignant melanoma in routinely processed paraffin sections and to compare the staining of primary (cutaneous) malignant melanomas and their metastases, we stained formalin-fixed paraffin sections of 13 primary and 18 metastatic malignant melanomas using the streptavidin-biotin peroxidase method by antibodies to S-100, vimentin, HMB-45, polyclonal carcinoembryonic antigen (CEA), monoclonal CEA, cytokeratins (CAM 5.2 and broad-spectrum CKKES), and epithelial membrane antigen (EMA). All primary and most metastatic malignant melanomas showed positive staining with anti-S-100, HMB-45, and anti-vimentin. Reactivity with polyclonal CEA was observed in 15 (48%) of the 31 lesions; 14 of them were metastatic. No lesion was reactive with monoclonal CEA. Significant cytokeratin (CK) staining was evident in only three (9.7%) lesions (all metastatic), which also stained specifically with anti-CK 18. EMA was observed only focally in two (6.5%) lesions. There was no correlation between epithelial markers staining of the primary tumours and their metastases. All lesions with CK or EMA staining showed concomitant extensive staining for S-100, HMB-45, and vimentin. We conclude that (a) polyclonal CEA staining in malignant melanoma is not rare and is probably due to CEA-related molecules; (b) significant CK reactivity is rare and related to simple CK, such as CK 18; (c) epithelial marker reactivity is more common in metastases of malignant melanomas and is not correlated to the reactivity in their primary tumors. Considering our results and reports of positive S-100, vimentin, and HMB-45 in epithelial tumors, a wide panel of antibodies is recommended for the study of undifferentiated tumors.
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PMID:Epithelial markers in malignant melanoma. A study of primary lesions and their metastases. 752 76

Alterations of cell-surface glycoconjugates have been associated with invasiveness and metastatic capacity in a number of experimental and human tumors (bladder and colon cancer). We have recently shown that human melanoma cells from variants selected for high metastatic potential in an animal model bind the lectin peanut agglutinin (PNA), and that human melanoma cell populations enriched for PNA binding cells generated a higher frequency of metastases when xenografted into immune suppressed neonatal rats. We have therefore sought cells binding PNA in biopsied human melanocytic tumors and compared frequencies of PNA binding by cells from benign nevi, early and late primary melanomas, and metastatic melanomas. Sections of conventionally processed tissues were deparaffinised and exposed to biotinylated PNA; PNA fixation was revealed by the avidine/peroxidase/AEC technique. In 51 specimens tested, PNA appears to react electively with invasive tumors, since only one of the 7 early primary melanomas (Clark I-II) reacted while 13/23 late primary melanomas (Clark III-V), and 4/21 melanoma metastases were reactive. In addition, only 1/17 benign nevi bound PNA. In primary tumors, the reactive cells were exclusively invasive tumors cells in the dermis. PNA reactive material was observed in the cytoplasm and plasma membrane of reactive cells. Hence, alterations in composition and cellular localisation of glycoconjugates detectable by lectin histochemistry in melanoma cells may be markers of metastatic potential that may be applicable on an individual patient basis.
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PMID:Selective expression of PNA-binding glycoconjugates by invasive human melanomas: a new marker of metastatic potential. 776 55

Post-surgical macular oedema results from blood-retinal barrier breakdown, but it is not accompanied by structural abnormalities in the retinal vessels or retinal pigmented epithelium. Previous studies, using horseradish peroxidase in a primate model, suggested that leakage occurs primarily through this epithelium. This study was conducted to localize sites of the barrier breakdown in humans following different types of intra-ocular surgery and to compare them with eyes affected with ocular inflammatory disease, ocular infection, and choroidal melanoma. Paraffin sections of eyes were immunohistochemically stained for albumin to localize extravascular albumin, which was graded in a masked study. With aphakia/pseudophakia, penetrating keratoplasty, ocular inflammatory disease, ocular infection, and choroidal melanoma, barrier breakdown occurred primarily at the inner blood-retinal barrier (retinal vasculature), but leakage also occurred at the outer barrier (retinal pigmented epithelium). After retinal re-attachment surgery, the inner and outer blood-retinal barriers were equally compromised. Vascular leakage in the optic nerve head coincided with barrier failure in these disorders. The widespread pattern of blood-retinal barrier compromise with leakage at multiple sites suggests that soluble mediators are likely to play a role in postsurgical macular oedema, ocular inflammatory disease, and choroidal melanoma.
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PMID:Immunohistochemical localization of blood-retinal barrier breakdown sites associated with post-surgical macular oedema. 798 91

Oxidative tissue damage and inflammatory reaction were investigated in the neurosensory retina of five eyes with malignant choroidal melanoma and correlated to the distance from the tumour. The results showed elevated levels of both lipid peroxides (expressed as thiobarbituric acid reactive substances) and myeloperoxidase in the retina adjacent to the tumour. The values declined with distance from the tumour. The results indicate that production of oxygen free radicals contributes to tumour associated retinopathy.
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PMID:Increased lipid peroxides and inflammatory parameters in the retina adjacent to choroidal melanoma. 812 21

A 53-year-old Japanese male noticed pigmented lesions on his right upper gingiva and hard palate in February of 1986. Histological examination revealed in situ malignant melanoma. Chemotherapy, beta-interferon, and oral BCG were given. However, tumors subsequently developed in the nasal cavity in March of 1989. The patient died in April of 1990 after developing Garcin's syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Autopsy revealed aggressively infiltrating, whitish tumor masses invading the hard palate, the nasal cavity, the paranasal sinuses, the base of the skull, cranial nerves I-X, and the pituitary body, as well as severe necrosis of the soft palate. However, there was no evidence of malignant melanoma. Instead, these oval tumor cells had atypical nuclei and scanty cytoplasm. They contained no melanin granules, were negative for S-100 protein, and were also negative for various melanoma-associated antigens. They were positive for CD2, CD3, and CD8 by avidin-biotin-peroxidase complex immunohistochemistry. It was concluded that the patient had CD8+ non-Hodgkin's malignant lymphoma (diffuse, large cell type) of the nasopharyngeal region, which was preceded by in situ malignant melanoma of the palate.
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PMID:A case of CD8+ T cell lymphoma occurring during treatment for in situ malignant melanoma of the palate. 834 26

In B16a melanoma cells, protein kinase-C-alpha (PKC alpha) is immunomorphologically associated with cytoplasmic vesicles in addition to the previously observed locations (plasma membrane, cytoskeleton, nucleus), as detected with monoclonal antibody (MAb) MC3a. Subcellular fractionation indicated that the authentic 80-KD protein as well as PKC activity can be detected in several particulate fractions except for L2, which contains dense lysosomes. The highest PKC activity is associated with the cytosol-ultralight vesicles and the L1 fraction (containing plasma membrane, endosomes, and the Golgi apparatus). Both of these fractions contained the fluid-phase endocytosis marker peroxidase, indicating that PKC alpha, in addition to other subcellular structures, is most probably associated with endosomal membranes in B16a melanoma cells.
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PMID:Association of protein kinase-C-alpha with cytoplasmic vesicles in melanoma cells. 860 74

We used several biotinylated neoglycoproteins as tumor markers to detect and localize endogenous carbohydrate-binding proteins in cultured hepatoblastoma, melanoma, and bladder carcinoma tumor cells. The neoglycoproteins used consisted of cellobiose, fucose, N-acetyl-galactosamine, N-acetyl-glucosamine, lactose, maltose, mannose, melibiose, and xylose. In addition, naturally occurring asialofetuin that was chemically disialylated was also used. Binding to the cultured tumor cells was made visible with the avidin-peroxidase technique. Depending on the type of neoglycoprotein used, markedly different expression of cytoplasmic and nuclear receptors for sugars (endogenous lectins) was obtained from rat hepatoblastoma, human melanoma, and bladder carcinoma tumor cells. The most pronounced staining differences were documented for asialofetuin and the neoglycoproteins containing fucose, N-acetyl-galactosamine, and lactose.
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PMID:Potential usefulness of biotinylated neoglycoproteins as tumor markers. 874 39

The ability of iron chelates to promote hydroxyl radical (.OH) formation from hydrogen peroxide (H2O2) via Fenton chemistry was exploited to detect H2O2 produced during the oxidations of the eumelanin precursors 5,6-dihydroxyindole (DHI) and 5,6-dihydroxyindole-2-carboxylic acid (DHICA). H2O2 generation during the autooxidations of DHI and DHICA was confirmed on the basis of the electrochemical detection of three hydroxylation products of salicylate [2,3 and 2,5-dihydroxybenzoic acid (DHBA) and catechol], which was used as an .OH indicator. The oxidations of both 5,6-dihydroxyindoles were augmented by tyrosinase and peroxidase without the addition of H2O2. The partial inhibitions by catalase of the auto-oxidations and tyrosinase- and peroxidase-mediated oxidations of DHI and DHICA provide additional evidence of an endogenous origin of H2O2 during the final stages of eumelanogenesis. The mechanism proposed for the formation of H2O2 involves the semiquinones of DHI and DHICA in the univalent transfer of electrons to molecular oxygen. The observations described in this study support previous reports suggesting that factors modulating the levels of H2O2 in melanocytes and melanoma cells play critical roles in directing the course of melanogenesis and influencing the potential cytotoxicity of the biosynthetic pathways.
Melanoma Res 1996 Oct
PMID:Hydrogen peroxide generation associated with the oxidations of the eumelanin precursors 5,6-dihydroxyindole and 5,6-dihydroxyindole-2-carboxylic acid. 890 94


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