Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0278883 (metastatic melanoma)
 6,224 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have immunised BALB/c mice with a melanoma antigen obtained after papain solubilisation of the membranes of a metastatic melanoma tumour and fused the immune spleen cells to the mouse myeloma line P3-NS1/1-Ag4.1. The produced hybridoma antibodies (Mel-PV antibodies) recognised the initial melanoma antigen in haemagglutination, but did not react with any of the HLA phenotypes tested by cytotoxicity on a panel of B lymphocytes with known HLA-A and B phenotypes. We rosetted red blood cells coated with protein A with dispersed cells from fresh melanoma tumours, and a high degree of specificity for human malignant melanocytes was observed. Purified Mel-PV antibodies were also tested by indirect immunofluorescence and found to be oriented towards cytoplasmic components of malignant melanoma cells. These results indicate that the use of melanoma antigens for preparing monoclonal antibodies maintained a satisfactory degree of specificity and may be an adequate starting point for defining common and specific antigenic determinants on human melanoma.
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PMID:Antimelanoma hybridoma antibodies against partially purified melanoma antigen. 633 53

Nitric Oxide (NO) and Reactive oxygen species (ROS) are endogenous regulators of angiogenesis-related events as endothelial cell proliferation and survival, but NO/ROS defect or unbalance contribute to cancers. We recently designed a novel photoactive inhibitor of NO-Synthases (NOS) called NS1, which binds their NADPH site in vitro. Here, we show that NS1 inhibited NO formed in aortic rings. NS1-induced NO decrease led to an inhibition of angiogenesis in a model of VEGF-induced endothelial tubes formation. Beside this effect, NS1 reduced ROS levels in endothelial and melanoma A375 cells and in aorta. In metastatic melanoma cells, NS1 first induced a strong decrease of VEGF and blocked melanoma cell cycle at G2/M. NS1 decreased NOX(4) and ROS levels that could lead to a specific proliferation arrest and cell death. In contrast, NS1 did not perturb melanocytes growth. Altogether, NS1 revealed a possible cross-talk between eNOS- and NOX(4) -associated pathways in melanoma cells via VEGF, Erk and Akt modulation by NS1 that could be targeted to stop proliferation. NS1 thus constitutes a promising tool that modulates NO and redox stresses by targeting and directly inhibiting eNOS and, at least indirectly, NADPH oxidase(s), with great potential to control angiogenesis.
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PMID:Regulation of NADPH-dependent Nitric Oxide and reactive oxygen species signalling in endothelial and melanoma cells by a photoactive NADPH analogue. 2529 75