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1 ization to the human MART-1/Melan-A (MART-1) melanoma antigen.
2  RA by downregulating expression of PRAME, a melanoma antigen.
3 ization with a post-translationally modified melanoma antigen.
4 ng gp100 and CTL clones specific for a gp100 melanoma antigen.
5 27, which gave rise to an HLA-DR4-restricted melanoma antigen.
6 stricted peptides derived from either HIV or melanoma antigens.
7 r Ags, including melanoma-associated Ag 1, B melanoma antigen 1, and Wilm tumor Ag 1.
8 screen, we identified an interaction between melanoma antigen-11 (MAGE-11) cancer-testis antigen and
9                                 A variety of melanoma antigen A (MAGE-A) genes are commonly detected
10  The menstrual cycle-dependent expression of melanoma antigen-A11 (MAGE-11) in the mid-secretory huma
11  (N/C) interaction enables direct binding to melanoma antigen-A11 (MAGE-11), an AR coregulator that i
12                    X-linked primate-specific melanoma antigen-A11 (MAGE-A11) is a human androgen rece
13                                              Melanoma antigen-A11 (MAGE-A11) is a low-abundance, prim
14 rimate-specific steroid receptor coregulator melanoma antigen-A11 (MAGE-A11).
15  AR WXXLF motif (433)WHTLF(437) required for melanoma antigen-A11 and p300 to stimulate transcription
16  We conclude that the coregulator effects of melanoma antigen-A11 on the AR NH(2)- and carboxyl-termi
17 ys that depend on the coregulator effects of melanoma antigen-A11.
18   Here we identify the cancer/testes antigen melanoma antigen-A4 (MAGE-A4) as a tumour cell-specific
19 , oncogenesis (TGFbeta1, cathepsin L, IGFR1, melanoma antigen) and apoptosis (Bcl-2, Bid, Bad, p53) a
20        The GM2 ganglioside is a well-defined melanoma antigen, and anti-GM2 antibodies have been asso
21         Whereas many of the identified human melanoma antigens are normal tissue differentiation prot
22  When analyzing T-cell recognition of shared melanoma antigens before and after adoptive cell therapy
23  expressed the CT antigen CT7 (also known as melanoma antigen C1 [MAGE-C1]) and 70% expressed MAGE-A3
24 s or enhances T cell function in response to melanoma antigens, depending on the dose of drug in the
25 ein-1 and -2 (TRP-1 and TRP-2), gp100, human melanoma antigen-encoding genes 1 and 3 (MAGE-1 and MAGE
26 lanoma-specific CTL precursors that can kill melanoma antigen-expressing targets.
27 with exogenous peptides or transduction with melanoma antigen-expressing viruses.
28                                    Necdin, a melanoma antigen family protein, promotes neuronal and m
29 GABAA) receptor gene family, a member of the melanoma antigen gene (MAGE) family, and several members
30                        MageB2 belongs to the melanoma antigen gene (MAGE-I) family of tumor-specific
31    In all of the CSAGE positive samples, the melanoma antigen gene family was also expressed.
32 eport, we identified the X chromosome-linked melanoma antigen gene product MAGE-11 as an AR coregulat
33                                              Melanoma antigen gene protein 11 (MAGE-11) is an AR core
34  interactions is supported by the effects of melanoma antigen gene protein-11, an AR coregulator that
35                In humans and other primates, melanoma antigen gene protein-A11 (MAGE-11) is an AR sel
36  with coregulatory proteins that include the melanoma antigen gene protein-A11 (MAGE-11).
37 ognized by T cells-1 (MART-1), and universal melanoma antigen gene-A (uMAG-A).
38  (antigen recognized by T cells-1), MAGE-A3 (melanoma antigen gene-A3 family), GalNAc-T (beta1-->4-N-
39 ox homeotic gene transcription factor 3; and melanoma antigen gene-A3 family, and the changes of CTCs
40 endritic cells (DCs) engineered to express a melanoma antigen generates antigen-specific, MHC-restric
41  of dendritic cells (DCs) expressing a model melanoma antigen generates antigen-specific, MHC-restric
42 both the target antigen Tyrp1 and a distinct melanoma antigen gp100 in an Fc receptor-dependent mecha
43 s recognize an epitope derived from the self/melanoma antigen gp100.
44 ioma cell lines (GL26 and GL261) express the melanoma antigens gp100 and tyrosinase-related protein 2
45 ssional antigen-presenting cells loaded with melanoma antigens gp100 and tyrosinase.
46  enhances DNA vaccination against a distinct melanoma antigen, gp100(pmel17/silver locus), improving
47 c cells loaded with peptide derived from the melanoma antigen, gp100, failed to mediate regression of
48 e (amino acids 209-217) derived from a human melanoma antigen, gp100.
49        Characterization of immunogenic human melanoma antigens has been a major focus of tumor immuno
50  cells specific for idealized or established melanoma antigens in mice.
51     NRAGE (neurotrophin receptor-interacting melanoma antigen) interacted with a component of the E-c
52 llectively, this study links three important melanoma antigens into a common transcriptional pathway
53       Cytotoxic T lymphocyte priming towards melanoma antigens is also obtained with cells from metas
54 ass I molecules, we hypothesized that mature melanoma antigen-loaded DCs engineered to process antige
55                                          The melanoma antigen (MAGE) family consists of more than 60
56                                              Melanoma antigen (MAGE) genes are conserved in all eukar
57 D27(+)CD8(+) T cells against the four shared melanoma antigens: MAGE-3, gp100, tyrosinase, and MART-1
58 ity T-cell receptors (TCRalpha/beta) for the melanoma antigen MART-1/HLA-A*0201 [recognized by F5 cyt
59  DMF5, a T-cell receptor that recognizes the melanoma antigen MART-127-35 (DMF5(TLR5L) T cells), disp
60 th mature DCs transfected with RNAs encoding melanoma antigens MART1, MAGE-3, gp100, and tyrosinase.
61  were pulsed with peptides derived from four melanoma antigens [(MelAgs) MelanA/MART-1, tyrosinase, M
62 s were stained with hematoxylin-eosin (H-E), melanoma antigen (melan-A), and again with H-E.
63  by using cells raised against the candidate melanoma antigen mutant B-Raf or its phosphorylated coun
64 tion between the class II epitope-containing melanoma antigen New York esophageal 1 and MHC class II.
65 activated B cells to stimulate T cells using melanoma antigens or melanoma cell lysates.
66 sion and led to endogenous responses against melanoma antigens other than NY-ESO-1.
67 d tyrosinase-related protein-2 (TRP-2), is a melanoma antigen overexpressed in most chemo-/radiothera
68 te antigen (HLA) class I antigen-restricted, melanoma antigen-reactive T-cell receptors; however, sub
69 e, we describe the identification of a novel melanoma antigen recognized by an human histocompatibili
70 s the melanoma-associated antigens gp100 and melanoma antigen recognized by T cells (MART-1).
71 d frequency of gp100 and T cells specific to melanoma antigen recognized by T cells 1 (MART-1), also
72 se (TYR), TYR-related protein 2 (TRP-2), and melanoma antigen recognized by T cells 1 (MART-1); all t
73 abeled with human melanoma black 45 (HMB45), melanoma antigen recognized by T cells 1 (Melan-A), S100
74 ression of four melanoma-associated markers: melanoma antigen recognized by T cells 1; beta1 --> 4-N-
75  by MM-RT-PCR, using the markers tyrosinase, melanoma antigen recognized by T cells-1 (MART-1), and u
76 l structure of a phosphopeptide derived from melanoma antigen recognized by T cells-1 (pMART-1), sele
77  33%, 5%, and 13% (negative) for tyrosinase, melanoma antigen recognized by T cells-1, tyrosinase-rel
78        This protein has been identified as a melanoma antigen recognized by tumor reactive CTLs deriv
79   Autologous dendritic cells pulsed with the melanoma antigen recognized T cells 1 self-peptide were
80 ss in the structural identification of human melanoma antigens recognized by autologous cytotoxic T c
81                Several epitopes in the human melanoma antigens recognized by HLA-A2-restricted CTLs h
82 , DCT (tyrosinase-related protein 2), MART1 (melanoma antigens recognized by T-cells) gp100 (Pmel17/s
83 are able to prime an immune response against melanoma antigens shared between K1735 and B16.
84  lymphocytes (TIL), including MART-1/Melan-A melanoma antigen-specific CD8 T cells, predominantly exp
85 inflammatory responses and the production of melanoma antigen-specific CD8(+) T cells.
86 tudinal phenotypic analysis was performed on melanoma antigen-specific CD8+ T cells during their tran
87  of Akt, resistance to cell death induced by melanoma antigen-specific cytotoxic T cells, and phospha
88 re not recognized by HLA class I-restricted, melanoma antigen-specific cytotoxic T lymphocytes even f
89 or LAQ824 and the adoptive transfer of gp100 melanoma antigen-specific pmel-1 T cells.
90 ogous gene-modified lymphocytes expressing a melanoma antigen-specific TCR at the National Cancer Ins
91 and not by CTL specific for more traditional melanoma antigens such as TRP2 or gp100.
92 ector T cells specific for either EBNA1 or a melanoma antigen, suggesting that these CD4(+) Treg cell
93           Recent studies have identified new melanoma antigens that are recognised by CD4(+) T cells.
94 to be due to an immune response generated to melanoma antigens that cross-react with normal skin.
95  then trans-fected with RNA encoding defined melanoma antigens, these DCs were superior inducers of a
96 ass I MHC (HLA-A2)-restricted epitope of the melanoma antigen tyrosinase was isolated from a CD4(+) t
97 artic acid to an isoaspartic acid within the melanoma antigen tyrosinase-related protein (TRP)-2 pept
98 rophylactic prime-boost vaccination with the melanoma antigen tyrosinase-related protein 2, which als
99 ice bearing a TCR transgene specific for the melanoma antigen tyrosinase-related protein-2 (TRP-2, Dc
100 isteria monocytogenes vaccine expressing the melanoma antigen tyrosinase-related protein-2 to protect
101 nsfer of genes encoding TCRs recognizing the melanoma antigen tyrosinase.
102 ma patients were immunized against the gp100 melanoma antigen using autologous peptide-pulsed, CD40L/
103           Interestingly, T cells specific to melanoma antigens were generated.
104 otein of 113 kDa, originally identified as a melanoma antigen, whose expression is associated with tu

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