Melanoma study
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB38525 | ENA |
REPOSITORIES: ENA
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Project description:Single-cell copy number analysis in melanoma
| PRJNA635693 | ENA
Project description:Melanoma cell lines were genotyped to evaluate copy number differences between nodular melanoma (NM) and superficial spreading melanoma (SSM). Cell lines were also evaluated for copy number alterations in the SKP2/p27 axis. Affymetrix SNP arrays were performed according to manufacturer's instructions using DNA extracted from 18 melanoma cell lines and 4 melanocyte controls.
2010-10-21 | GSE22305 | GEO
Project description:Melanoma cell lines were genotyped to evaluate copy number differences between nodular melanoma (NM) and superficial spreading melanoma (SSM). Cell lines were also evaluated for copy number alterations in the SKP2/p27 axis. Affymetrix SNP arrays were performed according to manufacturer's instructions using DNA extracted from 18 melanoma cell lines and 4 melanocyte controls. Affymetrix SNP6.0 Array data for melanoma cell lines Copy number analysis of Affymetrix SNP 6.0 arrays was performed on 18 melanoma cell lines including 2 primary superficial spreading melanoma, 2 primary nodular melanoma, 2 metastatic nodular melanoma, and 12 metastatic cell lines. Four melanocyte control lines were also evaluated including 2 immortalized melanocyte cell lines (Hermes 1 and 2B) and 2 normal melanocyte lines cultured from neonatal foreskin (HEM-N and HEM-LP) that were used to construct the baseline for copy number analysis.
2010-10-21 | E-GEOD-22305 | biostudies-arrayexpress
Project description:We performed shallow single-cell copy number analysis across 1,475 cells from a melanoma COLO829 line, to resolve overall tumor complexity and clonality. We identified at least four major sub-clones by discriminant analysis of principal components (DAPC). Re-analysis of previous spectral karyotyping data recapitulated these sub-clone hallmark features and explains why previous experiments generated conflicting results. Overall, our results demonstrate how single cell sequencing can uncover significant hidden insights in a melanoma sample.
2020-05-29 | GSE151409 | GEO
Project description:Metastatic melanoma is an aggressive treatment-refractory malignancy. Recently, c-Kit mutations were discovered in certain mucosal melanomas. A clinical trial was initiated with the c-Kit inhibitor imatinib mesylate. The first treated patient experienced dramatic clinical improvement within days, followed by major responses by PET/CT four weeks later at all sites of metastatic disease. Several established mucosal melanoma cell lines exhibited imatinib sensitivity in a fashion correlating with c-Kit mutational status. Although c-Kit mutations are uncommon in cutaneous melanoma, they may arise in geographically distinct subsets for whom use of c-Kit targeted kinase inhibition should be considered in a rational therapeutic approach. Keywords: Whole genome copy number analysis Copy number analysis using high-density SNP arrays to investigate genetic gains and losses involved in the genesis of mucosal and cutaneous melanoma. GSE8164_raw_copy_number_calls.xls contains raw copy number calls generated by dChip (build 5/2007) for GIST, K008, K029, M34, MEL1, MEL40, M6, and 5 Affymetrix controls (copy number identity 2 i.e. normal), which are available on the HapMAP site.
2008-12-23 | E-GEOD-8164 | biostudies-arrayexpress
Project description:Comparison between the copy number of differentially methylated sites between lymph node metastasis from melanoma patients with good prognosis and melanoma brain metastasis. All samples are taken from different patients, and were established as cell lines in the John Wayne Cancer Institute.
2013-09-19 | GSE44019 | GEO
Project description:This study explored the role of targeting protein for Xklp2 (TPX2), located with 20q11.2, in melanoma pathogenesis, based on initial findings that it was commonly gained and overexpressed. TPX2 copy number was evaluated in melanoma cell lines compared to control DNA.
2012-08-27 | GSE38946 | GEO
Project description:Melanoma is the least common form of skin cancer, but accounts for the most deaths. Dermatopathologists face difficult diganostic determinations with a subset of ambiguous melanoma cases. Copy number variation in melanoma can serve as an additional biomarker to distinguish melanoma from benign melanocytic lesions.
2016-04-22 | GSE68476 | GEO
Project description:The two most common melanoma histopathologic subtypes, superficial spreading (SSM) and nodular melanoma (NM), are believed to represent sequential phases of linear progression from radial to vertical growth. Studies suggest, however, that SSM and NM are biologically distinct. We utilized an integrative genomic approach to examine the possibility that SSM and NM are the result of independent pathways characterized by unique molecular alterations. Cell lines including SSM, NM, metastatic melanoma, and melanocyte controls were evaluated for copy number changes and differential mRNA expression using single nucleotide polymorphism array (SNP 6.0, Affymetrix) and gene array (U133A 2.0, Affymetrix). Data sets were integrated to identify copy number alterations that correlated with gene expression, and array results were validated using immunohistochemistry on human tissue microarrays (TMAs) and an external data set. The functional effect of genomic deletion was assessed by lentiviral overexpression. Integrative genomics revealed 8 genes in which NM/SSM-specific copy number alterations were correlated with NM/SSM differential gene expression (P<0.05, Spearman’s rank). Pathways analysis of differentially expressed genes (N=114) showed enrichment for metabolic-related processes. SSM-specific genomic deletions (DIS3, MTAP, G3BP2, SEC23IP, USO1) were verified in an expanded panel of cell lines, and forced overexpression of MTAP in SSM resulted in reduced cell growth. Metabolism-related gene ALDH7A1 was verified as overexpressed in NM using human TMAs.The identification of recurrent genomic deletions in SSM not present in NM challenges the linear model of melanoma progression and supports the unique molecular classification of SSM and NM. Gene expression profiling using Affymetrix U133A 2.0 arrays was performed on 18 melanoma cell lines including 2 primary superficial spreading melanoma, 2 primary nodular melanoma, 2 metastatic nodular melanoma, and 12 metastatic cell lines. Four melanocyte control lines were also evaluated including 2 immortalized melanocyte cell lines (Hermes 1 and 2B) and 2 normal melanocyte lines cultured from neonatal foreskin (HEM-N and HEM-LP).
2010-12-01 | E-GEOD-22301 | biostudies-arrayexpress
Project description:Epigenetic regulation of tumor suppressor genes (TSGs) has been shown to play a central role in melanomagenesis. Integrating gene expression and methylation array analysis we identified novel candidate TSGs frequently methylated in melanoma. We validated the methylation status of the most promising TSGs using the highly sensitive, specific and comprehensive Sequenom Epityper assay in a large panel of melanoma cell lines and resected melanomas, and compared the findings with that from cultured melanocytes. We found transcript levels of UCHL1, COL1A2, THBS1 and TNFRSF10D were inversely correlated with promoter methylation. The effect of this methylation on expression was confirmed at the protein level. Identification of these candidate TSGs and how their silencing is related to melanoma development will increase our understanding of the etiology of this cancer and may provide tools for its early diagnosis. Analysed samples consisted of 11 melanoma cell lines and 1 neonatal foreskin melanocyte pool as a reference. Melanoma cell lines overlap with members of the DNA copy number analysis series GSE9003 and expression profiling series GSE7127 . The matching copy number data GEO samples IDs are noted in characteristics: Matching CN Sample ID and characteristics: Matching expn Sample ID columns respectively.
2011-10-24 | E-GEOD-28356 | biostudies-arrayexpress