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1 of myoid and melanocytic markers (HMB-45 /or Melan-A).
2 expressing the melanoma-associated Ag MART-1/Melan A.
3 noma cells, which expressed S100, HMB45, and melan A.
4 el focally for melanocytic markers HMB45 and Melan A.
5 elated proteins 1 and 2, Pmel 17, and MART-1/Melan-A.
6 35, but negative for cytokeratin, HMB-45 and Melan-A.
7 nt for NY-ESO-1 and proteasome-dependent for Melan-A.
8 -ester-dependent murine melanocyte cell line melan-a.
9 died the in vitro cross-priming potential of Melan-A 16-40 LP bearing the HLA-A2-restricted epitope 2
10 er with DC maturating agents, especially the Melan-A 16-40(A27L) LP, for the treatment of HLA-A2(+) m
11 AGE-C2(336-344)) or the standard proteasome (Melan-A(26-35), tyrosinase(369-377), gp100(209-217)).
12 enhanced ability to recognize the HLA A*0201-Melan A(27-35) (HLA A*0201-AAGIGILTV) antigen expressed
17 ning 5 tumors (45%) were diagnosable by both melan-A and H-E staining, likely as a result of simply c
22 with loss of differentiation markers such as melan-A and tyrosinase, enhanced aldehyde dehydrogenase
24 rtant melanoma diagnostic antibodies HMB-45, melan-A, and MITF (D5) recognize gene products of the me
26 fferentiation proteins Pmel-17/gp100, MART-1/Melan-A, and tyrosinase, expressed via recombinant vacci
27 of the immunodominant T cell-defined MART-1/Melan-A antigen and downregulation of the TAP-1 gene in
29 ognized by T cells 1 (MART-1), also known as Melan-A, by ELISPOT assay following local rV-B7.1 vaccin
30 were significantly different between B16 and melan-a cells and whose expression was altered by RA tre
31 titutively activated M-Ras mutant in control melan-a cells as monitored by an AP-1-luciferase reporte
32 or gamma in immortalized murine melanocytes (melan-a cells) enables these cells to form tumors in SCI
33 inducing cellular transformation in control melan-a cells, while over-expression of dominant negativ
36 een as overexpressed in MGSA/GRO transformed melan-a clones was the newly described M-Ras or R-Ras3 g
37 ins are also elevated in MGSA/GRO-expressing melan-a clones, leading to an overall increase in the am
39 nohistochemically (S-100, HMB-45, PNL-2, and Melan-A) confirmed diagnosis of malignant melanoma of th
41 n conclusion, autologous induction of MART-1/Melan A CTL by whole Ag processing and presentation is r
42 of B16 melanoma cells and untreated B16 vs. melan-a data set show that RA "normalized" the expressio
44 The pigmented murine melanocyte cell line melan-a expressed msg1, as did pigmented primary culture
47 by simultaneously providing both the MART-1/Melan-A gene (by retroviral transfer) and the TAP-1 gene
49 he 203 genes was more closely related to the melan-a gene set than any other RA treatment time point.
51 cific for the melanocyte-associated antigens Melan-A, gp100, tyrosinase, and TRP-2 in the blood of HL
54 1/Melan A-specific CTL confirmed that MART-1/Melan A immunodominance is strongly restricted to the AA
56 7-35), of the melanoma (self) antigen MART-1/melan A is frequently observed in tumor-infiltrating lym
60 genetically engineered to express the MART-1/Melan-A (MART-1) tumor-associated Ag, express MART-1 mRN
61 h IFA, CpG, and the native/EAA or analog/ELA Melan-A(MART-1)(26-35) peptide, binding with low or high
64 (s), which down-regulates melanocyte lineage Melan-A/MART-1 Ag expression by melanoma cells with conc
65 together, these data support the use of this Melan-A/MART-1 DR4-restricted melanoma epitope in future
69 americ epitopes from the melanoma-associated Melan-A/MART-1 protein presented by the class I MHC HLA-
71 ally coexisted with a high frequency of anti-Melan-A/MART-1(27-35) reactive CD8(+) T cells in freshly
72 and also lysed, T2.DR4 cells pulsed with the Melan-A/MART-1(51-73) peptide and DR4(+) melanoma target
73 , CD4(+) T cell immunoreactivity against the Melan-A/MART-1(51-73) peptide typically coexisted with a
75 DC transfected with RNA encoding the MART (Melan-A/MART-1) melanoma Ag were then used to stimulate
77 e containing multiple Ags, including MAGE-3, Melan-A/MART-1, gp100, tyrosinase, melanocortin receptor
78 expressed by melanocytes (ie, Silver/Pmel17, Melan-A/MART-1, LAMP2, Rab 27, transferrin, c-kit, adapt
79 moval of factor-containing supernatants from Melan-A/MART-1-expressing cells results in up-regulation
81 rvations may have important implications for Melan-A/MART-1-specific CTL-mediated immunotherapy of me
83 ession and, in Me18105 cells, recognition by Melan-A/MART-1-specific, HLA-A2-restricted cytotoxic T l
84 derives from the melanocyte/melanoma protein Melan A/MART1 and is a target epitope of CD8+ T cells, c
86 h the cell body and dendrites of transfected melan-a melanocytes emphasizes the role of the mu gene i
87 er1 and Bmal1) expression in cultured murine Melan-a melanocytes synchronized by medium changes, and
88 mined the gene expression profiles of murine melan-a melanocytes treated with ASP or alphaMSH over a
92 rating T lymphocytes (TIL), including MART-1/Melan-A melanoma antigen-specific CD8 T cells, predomina
94 xylin-eosin and immunohistochemical markers (melan-A, microphthalmia-associated transcription factor,
97 ults with A103 showed a 20-22-kDa doublet In Melan-A mRNA positive melanoma cell lines and no reactiv
100 staining of tumor cell cytoplasm in 16 of 17 Melan-A mRNA-positive cases and no reactivity with the t
104 resence of circulating T cells responding to Melan-A or NY-ESO-1 had strong independent prognostic im
105 s possessing T cells responding to NY-ESO-1, Melan-A, or both was 21 months, compared with 6 months f
106 cells responding to peptides from NY-ESO-1, Melan-A, or MAGE-3 and the M category according to the A
107 n interferon gamma-producing T cells against Melan-A (P =.015) after vaccination, but not against an
109 ected with plasmid DNA encoding human MART-1/Melan-A, pMel-17/gp100, tyrosinase, MAGE-1, or MAGE-3 by
113 pitopes and variants derived from the MART-1/Melan-A protein are widely used as clinical vaccines.
114 e epitopes of the melanoma-associated MART-1/Melan-A protein, both presented by the class I MHC prote
115 the properties of the Melan-A gene product, Melan-A recombinant protein was produced in Escherichia
117 ), melanoma antigen recognized by T cells 1 (Melan-A), S100, and Ki67 using VR and a double panmelano
119 ity of the in vivo model by showing that the melan-A-specific (MART-1-specific) TCR DMF5 induces reje
120 ion between the magnitude of the increase in Melan-A-specific cells and clinical response (P =.046).
121 work describes the emergence of high-avidity Melan-A-specific clonotypes as a surrogate marker of tre
125 d the composition and functions of the large Melan-A-specific T-cell repertoire in the peripheral blo
128 ngent epitope/allele requirements for MART-1/Melan A/TCR interactions were not associated with limita
129 whose expression was significantly higher in melan-a than in B16 cells and 2054 genes whose expressio
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