Disease relevance of Melanoma, Experimental

• We report here that the accumulation of cyclic AMP induced by MSH or forskolin shows a strong positive correlation with the ability of B16 melanoma clones to form pulmonary tumour colonies when injected intravenously (i.v.) into syngeneic mice ('experimental metastasis') [1].
• PTEA and PTPA treatment increased survival times in BDF1 mice bearing the P388 lymphoma, L1210 leukemia, B16 melanoma, and Lewis lung tumors [2].
• The antitumor activity of 2-[bis-(2-chloroethyl)-amino]ethanesulfonic acid (also referred to here as "taurine mustard" or "taumustine") was evaluated in the murine P388 and L1210 lymphocytic leukemias and in the pigmented and nonpigmented B16 melanoma systems [3].
• Ecteinascidins (Ets), isolated from the Caribbean tunicate Ecteinascidia turbinata, protect mice in vivo against P388 lymphoma, B16 melanoma, M5076 ovarian sarcoma, Lewis lung carcinoma, and the LX-1 human lung and MX-1 human mammary carcinoma xenografts [4].
• In vitro modification of B16 melanoma cell surface uPA activity has been shown to alter the invasive and metastatic potential of these murine melanoma cells in vivo [5].

High impact information on Melanoma, Experimental

• We show that the NORM-2 antibody recognizes an integral 83 kd glycoprotein that is mobile in the plane of the plasma membrane of B16 melanoma cells [6].
• Melanocyte-stimulating hormone promotes activation of pre-existing tyrosinase molecules in Cloudman S91 melanoma cells [7].
• Heparan sulfate degradation: relation to tumor invasive and metastatic properties of mouse B16 melanoma sublines [8].
• Oral administration of alpha-difluoromethyl ornithine suppressed B16 melanoma development in mice 85 percent whereas interferon given subcutaneously inhibited tumor growth only 24 percent [9].
• The activity of the lysosomal proteinase cathepsin B is significantly elevated in a variant of the B16 melanoma with high metastatic potential [10].

Chemical compound and disease context of Melanoma, Experimental

• alpha-Difluoromethyl ornithine and mouse type 1 interferon, when administered simultaneously, were highly toxic to B16 melanoma cells in culture [9].
• However, mice immunized intraperitoneally with dead BCG are not protected against tumor formation when B16 melanoma cells are injected subcutaneously [11].
• The interaction of doxorubicin and N-trifluoroacetyladriamycin-14-valerate (AD32) with B16 melanoma cell variants that exhibit distinct metastatic properties was explored [12].
• In the present study, both poorly and highly metastatic clones derived from the C57BL/6 mouse B16 melanoma were used with cyclophosphamide in an attempt to elicit host antibody responses against cell surface markers expressed on highly metastatic tumor variants [13].
• The inhibitory effects were dependent on retinoid concentration and increased from 55 and 30% at 10(-9) M retinoic acid to 85 and 82% at 10(-5) M retinoic acid for S91 and B16 melanoma cells, respectively [14].

Biological context of Melanoma, Experimental

• Treatment of H-2-deficient nonmetastatic B16 melanoma cells with physiological doses of interferon gamma (IFN-gamma) reduced cellular growth in vitro but induced a shift to the lung-colonizing phenotype as assessed after intravenous injection of the treated cells [15].
• Sphingosine 1-phosphate (Sph-1-P), the initial product of Sph degradation by Sph kinase, was shown to be a strong inhibitor of cell motility and phagokinesis of B16 melanoma and other types of cells at 10-100 nM concentration [16].
• Interferon gamma induces lung colonization by intravenously inoculated B16 melanoma cells in parallel with enhanced expression of class I major histocompatibility complex antigens [15].
• N'-[2-chloroethyl]-N[2-(methylsulfonyl) ethyl]-N'-nitrosourea (cystemustine),a chloroethylnitrosourea antineoplastic drug, provokes cellular proliferation inhibition and redifferentiation, but there was no cell death in B16 melanoma tumors [17].
• Liposomal N,N,N-trimethylsphingosine (TMS) as an inhibitor of B16 melanoma cell growth and metastasis with reduced toxicity and enhanced drug efficacy compared to free TMS: cell membrane signaling as a target in cancer therapy III [18].

Anatomical context of Melanoma, Experimental

• Such mice had a higher incidence of tumor development, induced either with MCA or by inoculation of B16 melanoma cells, compared with mice with IFN-gamma-competent gammadelta T cells [19].
• Co-injection of BCG-elicited peritoneal cells with B16 melanoma cells into nude or sublethally irradiated (650 rad) mice inhibits tumor formation in > 85% of the mice, indicating that additional participation of host bone marrow- or thymus-derived leukocytes is not required to eradicate the tumor implant [11].
• Combination immunotherapy of B16 melanoma using anti-cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and granulocyte/macrophage colony-stimulating factor (GM-CSF)-producing vaccines induces rejection of subcutaneous and metastatic tumors accompanied by autoimmune depigmentation [20].
• The extracellular matrix deposited in culture by the mouse endodermal cell line (PF HR9) was used as an experimental model to study the interactions between basement membranes and several tumorigenic and nontumorigenic cell lines, including the metastatic B16 melanoma cell sublines [21].
• Effect of cell wall skeleton and monophosphoryl lipid A adjuvant on the immunogenicity of a murine B16 melanoma vaccine [22].

Gene context of Melanoma, Experimental

• Dominant negative LEF-1 decreased Nr-CAM expression and antibodies to Nr-CAM inhibited the motility of B16 melanoma cells [23].
• Interestingly, CD80-negative tumor cell lines such as MC38 colon carcinoma and B16 melanoma express CD80 at dim levels during in vivo growth in syngeneic mice [24].
• Expression of CXC chemokine receptor-4 enhances the pulmonary metastatic potential of murine B16 melanoma cells [25].
• T cell-mediated, IFN-gamma-facilitated rejection of murine B16 melanomas [26].
• The inhibition of early N-glycan processing targets TRP-2 to degradation in B16 melanoma cells [27].

Analytical, diagnostic and therapeutic context of Melanoma, Experimental

• The results demonstrate that vaccination with TRP2 peptide-loaded bone marrow-derived dendritic cells (DCs) results in activation of high avidity TRP2-specific CTLs, displaying lytic activity against both B16 melanoma cells and normal melanocytes in vitro [28].
• Dietary influence of tyrosine and phenylalanine on the response of B16 melanoma to carbidopa-levodopa methyl ester chemotherapy [29].
• Growth response of B16 melanoma to in vivo treatment with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU) at the initial stage after tumor transplantation [30].
• Treatment of established intracranial B16 melanoma tumors with subcutaneous injection of irradiated GM-CSF-secreting B16 cells significantly delayed death, as compared to injection of irradiated nontransduced B16 cells or no treatment [31].
• Adoptive immunotherapy of metastatic B16 melanoma with allogeneic immune cells sensitized to minor histocompatibility antigens [32].

References