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Whole genome expression of matched primary-metastases medulloblastomas

ABSTRACT: Affymetrix Human Gene 2.0 ST Array profiling of 9 pairs of matched primary-metastases medulloblastoma samples. Total RNA was extracted from primary and metastases medulloblastoma samples and hybridized to Affymetrix Human Gene 2.0 ST Arrays (24-Array Plates) according to the manufacturer's instructions.

ORGANISM(S): Homo sapiens

SUBMITTER: Wang Xin

PROVIDER: S-ECPF-GEOD-63668 | biostudies-other |

REPOSITORIES: biostudies-other

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Whole genome expression of matched primary-metastases medulloblastomas

Project description:Affymetrix Human Gene 2.0 ST Array profiling of 9 pairs of matched primary-metastases medulloblastoma samples.

2015-04-01 | GSE63668 | GEO

Whole genome expression of matched primary-metastases medulloblastomas

Project description:Affymetrix Human Gene 2.0 ST Array profiling of 9 pairs of matched primary-metastases medulloblastoma samples. Total RNA was extracted from primary and metastases medulloblastoma samples and hybridized to Affymetrix Human Gene 2.0 ST Arrays (24-Array Plates) according to the manufacturer's instructions.

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Whole genome expression and DNA methylation analysis of matched primary-metastases medulloblastomas

Project description:This SuperSeries is composed of the SubSeries listed below.

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Whole genome expression and DNA methylation analysis of matched primary-metastases medulloblastomas

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DNA methylation of matched primary-metastases medulloblastomas

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DNA methylation of matched primary-metastases medulloblastomas

Project description:DNA methylation was generated from 11 pairs of matched primary-metastases medulloblastoma samples using the Illumina Infinium HumanMethylation450 BeadChip array Total DNA was extracted from primary and metastases medulloblastoma samples, bisulfite converted and hybridized to Illumina Infinium HumanMethylation450 BeadChip according to the manufacturer's instructions.

2015-04-01 | E-GEOD-63669 | biostudies-arrayexpress

Project description:To better understand and characterize chromosomal structural variation during breast cancer progression, we enumerated chromosomal rearrangements for 11 patients by performing low-coverage whole-genome sequencing of 11 primary breast tumors and their 13 matched distant metastases. The tumor genomes harbored a median of 85 (range 18-404) rearrangements per tumor, with a median of 82 (26-310) in primaries compared to 87 (18-404) in distant metastases. Concordance between paired tumors from the same patient was high with a median of 89% of rearrangements shared (range 61-100%), whereas little overlap was found when comparing all possible pairings of tumors from different patients (median 3%). The tumors exhibited diverse genomic patterns of rearrangements: some carried events distributed throughout the genome while others had events mostly within densely clustered chromothripsis-like foci at a few chromosomal locations. Irrespectively, the patterns were highly conserved between the primary tumor and metastases from the same patient. Rearrangements occurred more frequently in genic areas than expected by chance and among the genes affected there was significant enrichment for cancer-associated genes including disruption of TP53, RB1, PTEN, and ESR1, likely contributing to tumor development. Our findings are most consistent with chromosomal rearrangements being early events in breast cancer progression that remain stable during the development from primary tumor to distant metastasis.

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Genome-wide aberrant methylation in primary metastatic UM and their matched metastases.

Project description:Uveal melanoma (UM) is an aggressive intra-ocular cancer with a strong tendency to metastasize. Metastatic UM is associated with mutations in BAP1 and SF3B1, however only little is known about the epigenetic modifications that arise in metastatic UM. In this study we aim to unravel epigenetic changes contributing to UM metastasis using a new genome-wide methylation analysis technique that covers over 50% of all CpG's. We identified aberrant methylation contributing to BAP1 and SF3B1-mediated UM metastasis. The methylation data was integrated with expression data and surveyed in matched UM metastases from the liver, skin and bone. UM metastases showed no commonly shared novel epigenetic modifications, implying that epigenetic changes contributing to metastatic spreading and colonization in distant tissues occur early in the development of UM and epigenetic changes that occur after metastasis are mainly patient-specific. Our findings reveal a plethora of epigenetic modifications in metastatic UM and its metastases, which could subsequently result in aberrant repression or activation of many tumor-related genes. This observation points towards additional layers of complexity at the level of gene expression regulation, which may explain the low mutational burden of UM.

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Whole genome sequencing of matched primary and metastatic acral melanomas.

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