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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 ry showed tumor cells to stain for HMB45 and Melan A.
4 ox 10, vimentin proteins, and MITF-regulated melan A.
5 noma cells, which expressed S100, HMB45, and melan A.
6 ox 10, vimentin proteins, and MITF-regulated melan A.
7 el focally for melanocytic markers HMB45 and Melan A.
8 elated proteins 1 and 2, Pmel 17, and MART-1/Melan-A.
9 35, but negative for cytokeratin, HMB-45 and Melan-A.
10 nt for NY-ESO-1 and proteasome-dependent for Melan-A.
11 -ester-dependent murine melanocyte cell line melan-a.
12 died the in vitro cross-priming potential of Melan-A 16-40 LP bearing the HLA-A2-restricted epitope 2
13 er with DC maturating agents, especially the Melan-A 16-40(A27L) LP, for the treatment of HLA-A2(+) m
14 AGE-C2(336-344)) or the standard proteasome (Melan-A(26-35), tyrosinase(369-377), gp100(209-217)).
15 enhanced ability to recognize the HLA A*0201-Melan A(27-35) (HLA A*0201-AAGIGILTV) antigen expressed
16 t negative M-Ras in MGSA/GROalpha-expressing melan-a-6 cells blocked transformation.
17 restricted epitopes from melanoma Ags MART-1/Melan A and glycoprotein 100.
18 n expression was suppressed by siRNA in both Melan-a and B16-F10 cells.
19 Tissue sections were also double labeled for Melan-A and CD34.
20 ning 5 tumors (45%) were diagnosable by both melan-A and H-E staining, likely as a result of simply c
21      In conjunctival MLs, the use of VR with Melan-A and HMB45 provides substantial sensitivity for a
22                                     We found Melan-A and HMB45 to best characterize MLs.
23 indings support the therapeutic relevance of Melan-A and NY-ESO-1 as targets for immunotherapy.
24              However, colocalization of both Melan-A and S100 protein with CD34 was demonstrated.
25  Although the stains for melanocytic markers melan-A and SOX10 facilitate assessment of melanocytic i
26                              The addition of melan-A and SOX10 immunohistochemical stains did not dow
27                              The addition of melan-A and SOX10 immunohistochemical stains resulted in
28 with loss of differentiation markers such as melan-A and tyrosinase, enhanced aldehyde dehydrogenase
29 h hematoxylin-eosin (H-E), melanoma antigen (melan-A), and again with H-E.
30 markers associated with ACC, including SF-1, Melan A, and inhibin alpha.
31 ls of B-catenin-regulated genes VIM, MITF-M, melan A, and TYRP1 (a tyrosinase family member critical
32 of beta-catenin-regulated genes VIM, MITF-M, melan A, and TYRP1 (a tyrosinase family member critical
33 rtant melanoma diagnostic antibodies HMB-45, melan-A, and MITF (D5) recognize gene products of the me
34  recombinant NY-ESO-1, MAGE-1, MAGE-3, SSX2, Melan-A, and tyrosinase proteins.
35 fferentiation proteins Pmel-17/gp100, MART-1/Melan-A, and tyrosinase, expressed via recombinant vacci
36  of the immunodominant T cell-defined MART-1/Melan-A antigen and downregulation of the TAP-1 gene in
37  EAAGIGILTV, LLLGIGILVL, and NLSALGIFST from Melan A, BST2, and IMP2, respectively.
38 1, and the melanoma differentiation antigen, Melan-A by human DC subsets.
39 ognized by T cells 1 (MART-1), also known as Melan-A, by ELISPOT assay following local rV-B7.1 vaccin
40 were significantly different between B16 and melan-a cells and whose expression was altered by RA tre
41 titutively activated M-Ras mutant in control melan-a cells as monitored by an AP-1-luciferase reporte
42 or gamma in immortalized murine melanocytes (melan-a cells) enables these cells to form tumors in SCI
43  inducing cellular transformation in control melan-a cells, while over-expression of dominant negativ
44 n in both numbers and length of dendrites of melan-a cells.
45                          MGSA/GRO-expressing melan-a clones exhibited enhanced AP-1 activity.
46 een as overexpressed in MGSA/GRO transformed melan-a clones was the newly described M-Ras or R-Ras3 g
47 ins are also elevated in MGSA/GRO-expressing melan-a clones, leading to an overall increase in the am
48 -luciferase activity in MGSA/GRO-transformed melan-a clones.
49 nohistochemically (S-100, HMB-45, PNL-2, and Melan-A) confirmed diagnosis of malignant melanoma of th
50                       In this system, MART-1/Melan A could not efficiently immunize in association wi
51 n conclusion, autologous induction of MART-1/Melan A CTL by whole Ag processing and presentation is r
52  of B16 melanoma cells and untreated B16 vs. melan-a data set show that RA "normalized" the expressio
53  and DMF5 in complex with both of the MART-1/Melan-A epitopes.
54    The pigmented murine melanocyte cell line melan-a expressed msg1, as did pigmented primary culture
55 the expression of 203 (87%) genes toward the melan-a expression level.
56 ents were HLA-A2-positive and had documented Melan-A expression.
57  by simultaneously providing both the MART-1/Melan-A gene (by retroviral transfer) and the TAP-1 gene
58           To determine the properties of the Melan-A gene product, Melan-A recombinant protein was pr
59 he 203 genes was more closely related to the melan-a gene set than any other RA treatment time point.
60 he 5' untranslated (UT) region of the MART-1/Melan-A gene was cloned and sequenced.
61 cific for the melanocyte-associated antigens Melan-A, gp100, tyrosinase, and TRP-2 in the blood of HL
62           T cells responding to NY-ESO-1 and Melan-A (hazard ratios, 0.29 and 0.18, respectively) rem
63                                   The MART-1/Melan-A human melanoma tumor antigen can be recognized b
64 1/Melan A-specific CTL confirmed that MART-1/Melan A immunodominance is strongly restricted to the AA
65 ortion was only 22% for NY-ESO-1 and 23% for Melan-A in those who died within 6 months.
66 increases in melanocyte markers (tyrosinase; Melan-A) in NSV lesions in the 50 mg ritlecitinib groups
67 7-35), of the melanoma (self) antigen MART-1/melan A is frequently observed in tumor-infiltrating lym
68                                              Melan-A labeled all melanocytes (100% sensitivity; panme
69                             Using the MART-1/Melan-A (MART-1) antigen system as a prototype human tum
70  of genetic immunization to the human MART-1/Melan-A (MART-1) melanoma antigen.
71 genetically engineered to express the MART-1/Melan-A (MART-1) tumor-associated Ag, express MART-1 mRN
72 h IFA, CpG, and the native/EAA or analog/ELA Melan-A(MART-1)(26-35) peptide, binding with low or high
73 of a new melanocyte differentiation antigen, Melan-A(MART-1).
74 ) T cells to the melanoma-associated antigen Melan A/MART-1.
75 (s), which down-regulates melanocyte lineage Melan-A/MART-1 Ag expression by melanoma cells with conc
76 together, these data support the use of this Melan-A/MART-1 DR4-restricted melanoma epitope in future
77                      This down-modulation of Melan-A/MART-1 expression, which we refer to as "Ag sile
78                                    The human Melan-A/MART-1 gene encodes an HLA-A2-restricted peptide
79 lanoma target cells naturally expressing the Melan-A/MART-1 gene product.
80 americ epitopes from the melanoma-associated Melan-A/MART-1 protein presented by the class I MHC HLA-
81                      In this study using the Melan-A/MART-1(27-35) peptide as a model for self but me
82 ally coexisted with a high frequency of anti-Melan-A/MART-1(27-35) reactive CD8(+) T cells in freshly
83 and also lysed, T2.DR4 cells pulsed with the Melan-A/MART-1(51-73) peptide and DR4(+) melanoma target
84 , CD4(+) T cell immunoreactivity against the Melan-A/MART-1(51-73) peptide typically coexisted with a
85                                          The Melan-A/MART-1(51-73) peptide was able to induce the in
86   DC transfected with RNA encoding the MART (Melan-A/MART-1) melanoma Ag were then used to stimulate
87 tional stimulus to TAA expression, including Melan-A/MART-1, gp100, and MAGE-A1.
88 e containing multiple Ags, including MAGE-3, Melan-A/MART-1, gp100, tyrosinase, melanocortin receptor
89 expressed by melanocytes (ie, Silver/Pmel17, Melan-A/MART-1, LAMP2, Rab 27, transferrin, c-kit, adapt
90 moval of factor-containing supernatants from Melan-A/MART-1-expressing cells results in up-regulation
91            In contrast to EBV, influenza, or Melan-A/MART-1-specific CD8(+) T cells, NY-ESO-1-specifi
92 rvations may have important implications for Melan-A/MART-1-specific CTL-mediated immunotherapy of me
93 ells with concomitant loss of recognition by Melan-A/MART-1-specific T cells.
94 ession and, in Me18105 cells, recognition by Melan-A/MART-1-specific, HLA-A2-restricted cytotoxic T l
95 derives from the melanocyte/melanoma protein Melan A/MART1 and is a target epitope of CD8+ T cells, c
96             Immortal mouse melanocyte lines (melan-a, melan-b, and melan-c) provide opportune models
97 guanine and cyclobutane pyrimidine dimers in Melan-A melanocytes and HaCaT keratinocytes.
98 h the cell body and dendrites of transfected melan-a melanocytes emphasizes the role of the mu gene i
99 er1 and Bmal1) expression in cultured murine Melan-a melanocytes synchronized by medium changes, and
100 mined the gene expression profiles of murine melan-a melanocytes treated with ASP or alphaMSH over a
101 ntial bioactive compounds using immortalized melan-a melanocytes.
102 e mutants as well as the wild-type Rab27b in melan-a melanocytes.
103 or antisense constructs were introduced into melan-a melanocytes.
104 rating T lymphocytes (TIL), including MART-1/Melan-A melanoma antigen-specific CD8 T cells, predomina
105 s from the melanoma tumor-associated protein Melan-A/Melanoma Ag recognized by T cells-1.
106 xylin-eosin and immunohistochemical markers (melan-A, microphthalmia-associated transcription factor,
107 file (no RA treatment) between non-malignant melan-a mouse melanocytes and B16 melanoma cells.
108 melanoma cell lines were screened for MART-1/Melan-A mRNA expression.
109 ults with A103 showed a 20-22-kDa doublet In Melan-A mRNA positive melanoma cell lines and no reactiv
110 itive cases and no reactivity with the three Melan-A mRNA-negative cases.
111 e melanoma cell lines and no reactivity with Melan-A mRNA-negative cell lines.
112 staining of tumor cell cytoplasm in 16 of 17 Melan-A mRNA-positive cases and no reactivity with the t
113  recognized several other protein species in Melan-A mRNA-positive cell lines.
114 specific and uniform cytoplasmic staining in Melan-A mRNA-positive cell lines.
115                  Following exposure of black melan-a murine melanocytes to purified recombinant ASP i
116  cyclobutane pyrimidine dimers in melanocyte Melan-a or keratinocyte HaCat cells in vitro.
117 resence of circulating T cells responding to Melan-A or NY-ESO-1 had strong independent prognostic im
118 s possessing T cells responding to NY-ESO-1, Melan-A, or both was 21 months, compared with 6 months f
119  cells responding to peptides from NY-ESO-1, Melan-A, or MAGE-3 and the M category according to the A
120 n interferon gamma-producing T cells against Melan-A (P =.015) after vaccination, but not against an
121        A phase II study of immunization with Melan-A peptide-pulsed PBMC + rhIL-12 was conducted in 2
122 ected with plasmid DNA encoding human MART-1/Melan-A, pMel-17/gp100, tyrosinase, MAGE-1, or MAGE-3 by
123 luding loricrin, filaggrin, lipocalin-2, and Melan-A positive cells.
124                Four cases (12%) showed a few melan-A-positive cells in the dermis, which was insuffic
125 oprotein also inhibits melanin production by melan-A primary melanocytes in vitro.
126                            The 233-bp MART-1/Melan-A promoter does not appear to have cytokine (IL-2,
127 pitopes and variants derived from the MART-1/Melan-A protein are widely used as clinical vaccines.
128 e epitopes of the melanoma-associated MART-1/Melan-A protein, both presented by the class I MHC prote
129  the properties of the Melan-A gene product, Melan-A recombinant protein was produced in Escherichia
130                                              Melan-A responses were found in 42% and 47% of patients
131 ), melanoma antigen recognized by T cells 1 (Melan-A), S100, and Ki67 using VR and a double panmelano
132                    Clonal analysis of MART-1/Melan A-specific CTL confirmed that MART-1/Melan A immun
133 ity of the in vivo model by showing that the melan-A-specific (MART-1-specific) TCR DMF5 induces reje
134 ion between the magnitude of the increase in Melan-A-specific cells and clinical response (P =.046).
135 work describes the emergence of high-avidity Melan-A-specific clonotypes as a surrogate marker of tre
136 yzed in detail the recognition of PS-SCLs by Melan-A-specific CTL clones.
137 esulting in tumor cell sensitivity to MART-1/Melan-A-specific cytotoxic T lymphocytes.
138                                     Although Melan-A-specific T cells were detectable at levels compa
139 d the composition and functions of the large Melan-A-specific T-cell repertoire in the peripheral blo
140                 We observed amplification of Melan-A-specific Vss subfamilies undetectable before the
141                                              Melan-A-stained slides showing definitive invasion were
142 ngent epitope/allele requirements for MART-1/Melan A/TCR interactions were not associated with limita
143 tumor antigen (Ag) as confirmed using HLA-A2:Melan-A tetramers.
144 whose expression was significantly higher in melan-a than in B16 cells and 2054 genes whose expressio
145  whose expression was significantly lower in melan-a than in B16 cells.
146            CTL specific for the melanoma Ags melan-A, tyrosinase, and MAGE3 were cloned from the peri

 
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