8221 results for "canc*"

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• Genome and transcriptome sequence data from an unspecified tissue chordoma patient

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

  Dataset EGAD00001008013

• CPC-GENE primary prostate benign and tumour tissue Hi-C sequencing reads

  This dataset contains the raw sequencing data, in FASTQ format, for Hi-C assays from 17 primary prostate tissue samples. The sequencing data is paired-end, 150 bp sequencing data from an Illumina NovaSeq 6000 machine, and contains 5 benign tissue samples and 12 primary tumour samples from the Canadian Prostate Cancer Genome Network (CPC-GENE) project. Tumour samples have IDs starting with the "CPCG" prefix, and benign tissue samples have IDs starting with the "BP" suffix.

  Dataset EGAD00001008024

• Whole genome sequencing of a breast cancer cohort with known functional homologous recombination status

  41 breast cancer patients with known functional homologous recombination status (matched normal and tumor genomes, n=82)

  Dataset EGAD00001008027

• Exome and RNA sequencing of pancreatic cancer biopsies and PDX models

  Pancreatic cancer biopsies and matching normal controls from 10 patients were exome sequenced. The same biopsies and PDX models derived from these were also subject to RNA sequencing.

  Dataset EGAD00001008113

• Somatic mutation rates scale with lifespan across mammals

  The rates and patterns of somatic mutation in normal tissues are largely unknown outside of humans. Comparative analyses can shed light on the diversity of mutagenesis across species and on long-standing hypotheses regarding the evolution of somatic mutation rates and their role in cancer and ageing. Here, we used whole-genome sequencing of 208 intestinal crypts from 56 individuals to study the landscape of somatic mutation across 16 mammalian species. We found somatic mutagenesis to be dominated by seemingly endogenous mutational processes in all species, including 5-methylcytosine deamination and oxidative damage. With some differences, mutational signatures in other species resembled those described in humans, although the relative contribution of each signature varied across species. Remarkably, the somatic mutation rate per year varied greatly across species and exhibited a strong inverse relationship with species lifespan, with no other life-history trait studied displaying a comparable association. Despite widely different life histories among the species surveyed, including ~30-fold variation in lifespan and ~40,000-fold variation in body mass, the somatic mutation burden at the end of lifespan varied only by a factor of ~3. These data unveil common mutational processes across mammals and suggest that somatic mutation rates are evolutionarily constrained and may be a determinant of lifespan.

  Dataset EGAD00001008032

• Enrichment of homologous recombination repair alteration in prostate cancer brain metastases

  Whole exome sequencing from 51 patients with brain metastases from prostate cancer

  Dataset EGAD00001008033

• Development and Validation of a Prognostic and Predictive 32-Gene Signature for Gastric Cancer

  We applied this signature to a 567-patient GC cohort to establish genomic-based molecular subtypes and then used a support vector machine to build a molecular subtype-based risk-scoring model. Both source code and supplementary datasets for risk score prediction are available at https://github.com/hwanglab/Yonsei_gastric_cancer_32genes.

  Dataset EGAD00001008091

• Mutational landscape of normal epithelial cells in Lynch Syndrome patients

  Lynch Syndrome (LS) is an autosomal dominant disease conferring a high risk of colorectal cancer due to germline heterozygous mutations in a DNA mismatch repair (MMR) gene. Although cancers in LS patients show elevated somatic mutation burdens, information on mutation rates in normal tissues and understanding of the trajectory from normal to cancer cell is limited. Here we whole-genome sequenced 152 crypts from normal and neoplastic epithelial tissues from LS patients. In normal tissues the repertoire of mutational processes and mutation rates were similar to those found in wild type individuals. A morphologically normal colonic crypt with an increased mutation burden and mutational signatures consistent with MMR deficiency was identified, which may represent a very early stage of LS pathogenesis. Phylogenetic tress of tumour crypts indicated that the most recent ancestor cell of each tumour was already MMR deficient and had experienced multiple clonal evolution cycles. This study demonstrates the genomic stability of epithelial cells with heterozygous germline MMR gene mutations and highlights important differences in the pathogenesis of LS from other colorectal cancer predisposition syndromes.

  Dataset EGAD00001008092

• May 2021 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency as part of the International Human Epigenome Consortium.

  May 2021 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies (Canadian Epigenetics, Environment and Health Research Consortium), Genome Sciences Center, B.C. Cancer Agency, Vancouver, Canada as part of the International Human Epigenome Consortium.

  Dataset EGAD00001008100

• August 2021 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies, Genome Sciences Center, B.C. Cancer Agency as part of the International Human Epigenome Consortium.

  August 2021 data update (fastq) for reference epigenomes generated at Centre for Epigenome Mapping Technologies (Canadian Epigenetics, Environment and Health Research Consortium), Genome Sciences Center, B.C. Cancer Agency, Vancouver, Canada as part of the International Human Epigenome Consortium.

  Dataset EGAD00001008101