Dd2ed193-2af3-43ee-b51a-8415809635aa - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001009712 | EGA |
REPOSITORIES: EGA
Similar Datasets
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Project description:Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that in many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis. We analyzed 16 tissue samples from four patients. For each patient we analyzed the DNA of a primary colon tumor sample, a normal colon tissue sample, a metastatic liver tumor sample and a normal liver tissue sample. The normal colon and normal liver samples serve as a control for the primary and metastatic tumor samples.
2011-10-11 | E-GEOD-32711 | biostudies-arrayexpress
Project description:We noticed that a recently identified poor prognosis stem/serrated molecular subtype of colorectal cancer (CRC) is characterized by up-regulation of transcripts known to be also expressed by stromal cells. To better define the origin of such transcripts, we analyzed RNAseq and microarray datasets from CRC mouse xenografts, where human cancer cells are supported by murine stroma. The analysis revealed that mRNA levels of stem/serrated subtype genes are mostly due to stromal expression, even when the stromal fraction is below 5%. Indeed, a classifier based on genes exclusively expressed by cancer-associated fibroblasts was significantly associated, in multiple datasets, to poor prognosis of CRC and to radioresistance of rectal cancer. Molecular Characterization of 72 primary rectal cancer formalin-fixed, paraffin-embedded (FFPE) specimens including 58 pretreatment specimens, 14 surgical specimens.
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Project description:To compare the gene expression profile in primary human colorectal cancer samples and samples passaged in mice for two generations
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Project description:We present a meta-dataset comprising of a total of 1566 samples including both primary tumors and tumor-free colorectal tissues from 15 independent GEO datasets. To minimise inter-platform variation, only datasets generated from the GPL570 platform (Affymetrix Human Genome U133 Plus 2.0 Array) were processed to develop the meta-dataset. Using multiple open source R packages implemented in our previously developed bioinformatics pipeline, each dataset has been preprocessed with RMA normalisation, merged, and batch effect-corrected via Combat method. With increased sample size, the present meta-dataset serves an excellent 'discovery cohort' for discovering differentially expressed in diseased phenotype.
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Project description:Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that in many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.
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