3735 results for "*oma"

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• Genome and transcriptome sequence data from an endometrioid ovary carcinoma patient

  Genome and transcriptome sequence data from an endometrioid ovary carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005859

• Genome and transcriptome sequence data from a transformed diffuse large B cell lymphoma patient

  Genome and transcriptome sequence data from a transformed diffuse large B cell lymphoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005869

• Genome and transcriptome sequence data from a chordoma patient

  Genome and transcriptome sequence data from a chordoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005871

• Genome and transcriptome sequence data from a breast carcinoma patient

  Genome and transcriptome sequence data from a breast carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005888

• Genome and transcriptome sequence data from a thyroid hurthle cell carcinoma patient

  Genome and transcriptome sequence data from a thyroid hurthle cell carcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005891

• Genome and transcriptome sequence data from a metastatic gallbladder adenocarcinoma patient

  Genome and transcriptome sequence data from a metastatic gallbladder adenocarcinoma patient, generated as part of the BC Cancer Agency's Personalized OncoGenomics (POG) study

  Dataset EGAD00001005903

• Spatial and temporal transcriptomics of medulloblastoma with chromothripsis identifies multiple genetic clones that resist to treatment and lead to relapse

  From all paediatric brain tumours, medulloblastomas with chromothripsis, a form of genome instability leading to massive genome rearrangements, are particularly aggressive. To dissect the complex biology underlying the aggressiveness of chromothriptic medulloblastomas, we applied spatial transcriptomics to i) chromothriptic and non-chromothriptic medulloblastomas from the same molecular subgroup (n=13) and ii) patient-derived xenografts from chromothriptic medulloblastoma, from the minimal residual disease stage to regrown tumours (n=11). Chromothriptic medulloblastomas showed higher spatial intra-tumour heterogeneity, proliferation and stemness, but lower immune infiltration and differentiation, as compared with non-chromothriptic medulloblastomas. Spatial mapping of genetic clones identified phenotypic features such as degree of differentiation, proliferation and immune infiltration enriched in specific clones. Cells from multiple genetic clones resisted treatment and gave rise to relapse in patient-derived xenografts of chromothriptic medulloblastoma. We identified a potential role of tumour microtubes in treatment resistance in chromothriptic medulloblastoma.

  Study EGAS00001007128

• Raw data for "Spatial and temporal transcriptomics of medulloblastoma with chromothripsis identifies multiple genetic clones that resist to treatment and lead to relapse"

  FASTQ files from Illumina sequencing of 10x Visium experiments.

  Dataset EGAD00001010260

• Single-cell multi-omic profiling of glioblastoma-associated myeloid cells

  Study EGAS00001004871

• WES of Colorectal cancer organoid-stroma biobank cohort

  In colorectal cancers (CRC) the tumor microenvironment plays a key role for prognosis and therapy efficacy. Patient-derived tumor organoids (PDTOs) show enormous potential for preclinical testing, however, in purely epithelial cultures features including the ‘consensus molecular subtypes’ (CMS) are largely eradicated. To better reflect cell heterogeneity, we established the CRC organoid-stroma biobank of matched PDTOs and cancer-associated fibroblasts (CAFs) from 30 patients. Context-specific phenotyping showed that xenotransplantation or co-culture with CAFs restores the individual transcriptomic status and instructs subtype-specific stromal gene expression. Furthermore, co-culture exposed CMS4-specific resistance to Gefitinib and SN-38 and revealed prognostic gene expression signatures. Chemogenomic library screening identified patient- and therapy-dependent mechanisms of stromal resistance including MET as common target. Our results demonstrate that CRC phenotypes are encrypted in the cancer epithelium in a plastic fashion that strongly depends on the context. Consequently, CAFs are essential for faithful representation of molecular subtypes and therapy responses ex vivo.

  Study EGAS00001007301