Disease relevance of Melanoma, Amelanotic

• In vivo, polyclonal monospecific anti-mouse von Willebrand factor antibody inhibited pulmonary metastases induced by CT26 tumor cells by 53-64%, B16a amelanotic melanoma cells by 45% and T241 Lewis bladder cells by 46% without induction of thrombocytopenia [1].
• The effect of a combination of shock waves with cisplatin was examined in vivo with subcutaneously implanted amelanotic melanomas (A-Mel 3) in Syrian golden hamsters and cisplatin-sensitive or cisplatin-resistant fibrosarcoma (SSK2/0 and SSK2/R2) in C3H mice [2].
• The derivative 2i, referred to by the name carmethizole, was also shown to be active against the MX-1 mammary xenograft, the human amelanotic melanoma cell line (LOX) xenograft, the M5076 sarcoma, and L1210 lymphocytic leukemia [3].
• Ribonucleotide reductase in melanoma tissue. EPR detection in human amelanotic melanoma and quenching of the tyrosine radical by 4-hydroxyanisole [4].
• Albinism and amelanotic melanoma: occurrence in a child with positive test results for tyrosinase [5].

High impact information on Melanoma, Amelanotic

• Prostacyclin is a powerful antimetastatic agent against B16 amelanotic melanoma cells [6].
• Simultaneous high-resolution measurement of adenosine triphosphate levels and blood flow in the hamster amelanotic melanoma A-Mel-3 [7].
• Most MNNG-induced tumors were considered amelanotic melanomas on the basis of histologic findings and a positive dopa reaction in selected samples [8].
• In this study, we investigated the regulation of PKC-alpha in murine B16 amelanotic melanoma (B16a) cells by the monohydroxy fatty acids 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] and 13(S)-hydroxyoctadecadienoic acid [13(S)-HODE] [9].
• LF inhibited PE binding to C32 amelanotic melanoma cells in a dose-dependent manner [10].

Chemical compound and disease context of Melanoma, Amelanotic

• The isolated fractions consisting of necrotic tumor cells and inflammatory cells (alpha fraction) apparently contain a cysteine proteinase inhibitor, since both cathepsin B-like and cathepsin H activities in the beta fraction of B16 amelanotic melanomas could be inhibited by addition of the alpha fraction [11].
• In order to resolve this controversy, the alpha IIb beta 3-like integrin in murine B16 amelanotic melanoma (B16a) cells was characterized at DNA, RNA, and protein levels [12].
• Exposure to hyperoxia generally failed to induce either the activity of GSH peroxidase (GPx) or the manganese-containing form of superoxide dismutase (MnSOD) after 48 h, although at 605 mm Hg oxygen, small inductions of MnSOD activity were observed in adult lung fibroblasts and amelanotic melanoma [13].
• We first investigated the effects of cell source and culture conditions on lung colony formation by i.v. injected B16a (B16 amelanotic melanoma) cells and inhibition of tumor colony formation by the thromboxane A2 synthase inhibitor, CGS14854 [14].
• Using an amelanotic melanoma (A-Mel-3) grown subcutaneously in Syrian Golden hamsters, we confirmed these results in vivo: tumor growth was markedly delayed in animals treated with 100 mg/kg 5-aminolevulinic acid intravenously and irradiated with coherent light at 635 nm as compared to animals irradiated at 630 nm [15].

Biological context of Melanoma, Amelanotic

• We measured changes in transepithelial electrical resistance (TEER) of a tight epithelial MDCK-C7 monolayer in response to highly invasive amelanotic melanoma cells (A7-clone) in combination with different platinum complexes (cis-, oxali- and carboplatin) [16].
• The transfection of Ty cDNA, rather than nuclear DNA-binding master regulatory gene, can induce, within both Ty-deficient amelanotic melanoma cells and also within fibroblasts, melanin polymer formation [17].
• A detailed study of the kinetics and mechanism for the inhibition of purified thioredoxin reductases from human metastatic melanotic and amelanotic melanomas by the nitrosoureas showed significantly different inhibitor constants [18].

Anatomical context of Melanoma, Amelanotic

• We explored the nature of the association of the cathepsin B-like activity with the plasma membrane using fractions from the spontaneously metastatic B16 amelanotic melanoma [19].
• Adhesion of murine B16 amelanotic melanoma cells (B16a) to murine microvascular endothelial cells (CD3) was enhanced, in a dose- and time-dependent manner, by pretreating CD3 cells with 12(S)-hydroperoxyeicosatetraenoic acid [i.e., 12(S)-HETE], a 12-lipoxygenase metabolite of arachidonic acid [20].
• In tyrosinase-positive amelanotic melanoma cells, inactive tyrosinase accumulates in the endoplasmic reticulum [21].
• In contrast, tyrosinase activity in an amelanotic melanoma cell line (MM96L) was rapidly inhibited without consumption of cystamine/cysteamine, in association with the generation of free thiol in the culture medium, and could be enhanced by the cystine transport inhibitor, glutamate [22].
• These results suggest that at least some amelanotic melanoma cells may contain significant levels of catalytically inactive tyrosinase molecules and that the level of pigmentation in mammalian melanocytes may be regulated by a tyrosinase activation process [23].

Gene context of Melanoma, Amelanotic

• Both c-Kit (expressed in superficial spreading disease) and VEGF (expressed in amelanotic melanoma) may have significant therapeutic implications as molecular targets, which warrants further investigation [24].
• However, ABCB 5alpha/beta expression was undetectable in two amelanotic melanomas (M14 and LOX-IMVI) [25].
• In addition, there are some kinds of human amelanotic melanomas, such as MEL2A, in which expression of tyrosinase is repressed or lacking though tyrosinase-related protein (TRP)-1 and TRP-2 are well expressed [26].
• A protocol was developed to distinguish between initial tumor-cell (B16 amelanotic melanoma; B16a) adhesion to and spreading on fibronectin [27].
• We have cloned the tryptophan hydroxylase cDNA from hamster pituitary and demonstrated its expression in the skin, melanotic and amelanotic melanomas, spleen, heart, and the eye [28].

Analytical, diagnostic and therapeutic context of Melanoma, Amelanotic

• We studied 15 cases of amelanotic melanoma by using light microscopy (in conjunction with Fontana staining and S-100 immunostaining) and electron microscopy [29].
• Thus, in the patient seen with a nonpigmented choroidal mass that may represent either a choroidal hemangioma, amelanotic melanoma, or metastatic tumor, plasma CEA levels may be useful in the differential diagnosis [30].
• Subcellular distribution of cathepsin L, the major protein released by transformed or ras transfected fibroblasts, was examined in murine liver, murine B16 amelanotic melanoma and human A2058 melanoma after sequential differential and Percoll density gradient centrifugation [31].
• Combination chemotherapy with cisplatin and nifedipine: synergistic antitumor effects against a cisplatin-resistant subline of the B16 amelanotic melanoma [32].
• Thus, HMB-45 and S-100 protein immunohistochemistry confirmed the diagnosis of amelanotic melanoma [33].

References