Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA133097 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-Wide Analysis of Somatic Copy Number Alterations (CGH, SNP) and Gene Expression (RNA-seq) in Metastatic Melanoma
| PRJNA133103 | ENA
Project description:Genome-wide copy number variation in human metastatic melanoma cell lines
| PRJNA132185 | 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. 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:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy.
2013-07-07 | GSE39280 | GEO
Project description:Metastatic urothelial carcinoma (UC) of the bladder is associated with multiple somatic copy number alterations (SCNAs). We evaluated SCNAs to identify predictors of poor survival in patients with metastatic UC treated with platinum chemotherapy.
2013-07-07 | GSE39281 | GEO
Project description:All cancers are diseases of the genome. A combination of somatic point mutations, focal amplifications and deletions, and chromosome level aberrations conspire to disrupt gene expression and the interplay between signaling pathways that control normal growth and tissue homeostasis. Here we investigate somatic copy number abberations in metastatic melanomas. A metastatic melanoma was assayed on Affymetrix SNP arrays to detect copy number abberations. 7 cutaneous melanomas as well as their matched control ( peripheral blood lymphocytes (PBL) or Epstein-Barr virus transformed lymphoblastoid cell lines ) and 2 control melanocytes were assayed on Illumina SNP arrays. 7 metastatic melanomas were hybridized on Agilent CGH arrays using donor matched control as reference.
2011-04-07 | E-GEOD-22928 | biostudies-arrayexpress
Project description:Background: Metastases result in 90% of all cancer deaths. Prostate cancer primary tumors evolve to become metastatic through selective alterations, such as amplification and deletion of genomic DNA. Methods: Genomic DNA copy number alterations were used to develop a gene signature that measured the metastatic potential of a prostate cancer primary tumor. We studied the genomic landscape of these alterations in 294 primary tumors and 49 metastases from 5 independent cohorts. Receiver-operating characteristic cross-validation and Kaplan-Meier survival analysis were performed to assess the accuracy of our predictive model. The signature was measured in a panel of 337 cancer cell lines from 29 different tissue origins. Results: We identified 399 copy number alterations around genes that were over-represented in metastases and predictive of whether a primary tumor will metastasize. Cross-validation analysis resulted in a predictive accuracy of 80.5% and log rank analysis of the metastatic potential score was significantly related to the endpoint of metastasis-free survival (p=0.014). The metastatic signature was observed in cell lines originating from lung, breast, colon, thyroid, rectum, pancreas and melanoma. The signature was comprised in part of genes of known or putative metastatic role — 8 solute carrier genes, 6 Cadherin family genes and 5 potassium channel genes — that function in metabolism, cell-to-cell adhesion and escape from anoikis/apoptosis. Conclusions: Somatic Copy number alterations are an independent predictor of metastatic potential. The data indicate a prognostic utility for using primary tumor genomics to assist in clinical decision making and developing therapeutics for prostate and likely other cancers. genomic DNA from 29 prostate cancer tumors with matched normals run on Affymetrix 6.0 SNP arrays.
2013-12-01 | E-GEOD-27105 | biostudies-arrayexpress
Project description:In this experiment, FFPE samples of 41 primary cutaneous melanoma, 2 metastatic melanoma and 6 normal skin were used for DNA extraction and genotyping by Affymetrix OncoScan FFPE Assay, in order to define chromosomal alterations in copy number and loss of heterozygosity. Genomic damage was then correlated with clinical features of melanoma.
2015-11-01 | E-MTAB-3481 | biostudies-arrayexpress
Project description:Uveal melanoma (UM) is a rare form of melanoma with a genetics and immunology that is different from skin melanoma. Previous studies have identified genetic driver events of early stage disease when the tumor is confined to the eye. In this study, we have characterized genomic events in UM metastases using whole-genome and RNA sequencing from thirty-two and twenty-eight patients, respectively, and profiled individual tumor infiltrating lymphocytes in a number of the metastases. We find that 91% of the patients have metastases carrying inactivating events in the tumor suppressor BAP1 and this coincided with somatic alterations in GNAQ, GNA11, CYSLTR2, PLCB4, SF3B1 and/or CDKN2A. Mutational signature analysis revealed a rare subset of tumors with prominent signs of UV damage, associated with outlier mutational burden. We study copy number variations (CNV) and find overrepresented events, some of which were not altered in matched primary eye tumors. A focused siRNA screen identified functionally significant genes of some of the segments recurrently gained. We reintroduced a functional copy of BAP1 into a patient-derived BAP1 deficient tumor cell line and found broad transcriptomic changes of genes associated with subtype distinction and prognosis in primary UM. Lastly, our analysis of the immune microenvironments of metastases revealed a presence of tumor-reactive T cells. However, a large fraction expressed the immune checkpoint receptors such as TIM-3, TIGIT and LAG3. These results provide an updated view of genomic events represented in metastatic UM and immune interactions in advanced lesions.
2020-03-18 | PXD017743 | Pride