Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA98267 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. The aim of this study was to identify potential downstream targets of key oncogenes and TSGs in melanoma (including p14ARF, p16INK4A, BRAF etc). Publications relevant to this series include:; Johansson et al. Pigment Cell Res 2007. Experiment Overall Design: 63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. These cell lines were sequenced for key tumour suppressor genes (TSGs) and oncogenes known to be involved in melanoma development. The microarray data was then analysed together with a particular genotype status (see relevant publications) to identify genes that potentially act downstream of these oncogenes and TSGs to contribute to melanoma development. See publications for analysis methods.
2008-06-15 | E-GEOD-7127 | biostudies-arrayexpress
Project description:35 Melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 microarrays were analysed for genes differentially expressed between cell lines carrying wild-type p14ARF and those with mutant 14ARF. All of these cell lines contained wild-type p53 (so that the effects of p14ARF mutations could be analysed without contamination from p53). Experiment Overall Design: The aim of this study was to identify downstream effectors of p14ARF in melanoma. Relevant paper: Packer et al. (2007) Int J Cancer.
2008-06-15 | E-GEOD-7152 | biostudies-arrayexpress
Project description:Genotype data from early passage UACC melanoma cell lines
| PRJNA387590 | ENA
Project description:Expression profiles of 17 melanoma cell lines were analysed to identify genes differentially expressed between cell lines harbouring wild-type or mutant p16INK4A. Relevant paper: Pavey et al. (2007). Note: all of these cell lines contained wild-type p14ARF, so that the transcriptional effects of p16INk4A could be determined without interference from p14ARF. Experiment Overall Design: The aim of this study was to identify genes which are transcriptional targets of p16INK4A in melanoma.
2008-06-15 | E-GEOD-7153 | biostudies-arrayexpress
Project description:35 Melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 microarrays were analysed for genes differentially expressed between cell lines carrying wild-type p14ARF and those with mutant 14ARF. All of these cell lines contained wild-type p53 (so that the effects of p14ARF mutations could be analysed without contamination from p53). Keywords: Affymetrix Hu133_Plus microarrays
2007-03-31 | GSE7152 | GEO
Project description:Expression profiles of 17 melanoma cell lines were analysed to identify genes differentially expressed between cell lines harbouring wild-type or mutant p16INK4A. Relevant paper: Pavey et al. (2007). Note: all of these cell lines contained wild-type p14ARF, so that the transcriptional effects of p16INk4A could be determined without interference from p14ARF. Keywords: Affymetrix Hu133_Plus microarrays
2007-10-01 | GSE7153 | GEO
Project description:Immunotherapy has achieved tremendous success in melanoma. However, only around 50 % of advanced melanoma patients benefit from immunotherapy with immunogenicity of melanomas playing a key role. CDKN2A encoding the two tumor-suppressor proteins p14ARF and p16INK4a belongs to the most frequently inactivated gene loci in advanced melanoma where decreased T cell infiltration is accompanied. While the role of p16INK4a has been aberrantly investigated, knowledge about the function of p14ARF in melanoma therapy is scarce. In this study, we elucidate the impact of reduced p14ARF expression on melanoma immunogenicity. Knockdown of p14ARF in melanoma cell lines diminished the recognition and killing by melanoma differentiation antigen (MDA)-specific T cells. Resistance was caused by a reduction of the peptide surface density of presented MDAs. While antigen presentation via HLA-I molecules was enhanced upon p14ARF downregulation in general, absolute and relative expression of cognate peptides was decreased. Limiting WNT5A signaling reverted this phenotype suggesting an involvement of non-canonical Wnt signaling. Taken together, our data indicate a new mechanism limiting MDA-specific T cell responses by decreasing both absolute and relative MDA-peptide presentation in melanoma.
2023-12-13 | GSE249763 | GEO
Project description:Microarray analysis of primary melanoma patient cells, melanoma cell lines, and HL cell lines
| PRJNA192682 | ENA
Project description:63 melanoma cell lines hybridized to Affymetrix Hu133_Plus 2 oligo arrays. The aim of this study was to identify potential downstream targets of key oncogenes and TSGs in melanoma (including p14ARF, p16INK4A, BRAF etc). Publications relevant to this series include: Johansson et al. Pigment Cell Res 2007. Keywords: melanoma
2007-03-31 | GSE7127 | GEO