7253 results for "canc*"

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• Normal sample for patient SA294

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA294

  Dataset EGAD00001009565

• WES of HCC

  WES of HCC by HiSeq 2000,total 71 samples including Hepatocellular carcinoma cell lines and nornal sample(Peripheral Blood or the adjacent tissues of cancer)

  Dataset EGAD00001001249

• Normal sample for patient SA284

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA284

  Dataset EGAD00001009562

• Normal sample for patient SA271

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA271

  Dataset EGAD00001009559

• Normal sample for patient SA278

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA278

  Dataset EGAD00001009561

• Genome and transcriptome sequence data from a metastatic melanoma patient

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

  Dataset EGAD00001005851

• Normal sample for patient SA296

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA296

  Dataset EGAD00001009566

• Genome and transcriptome sequence data from a cecum adenocarcinoma patient

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

  Dataset EGAD00001005895

• 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

• Genome and transcriptome sequence data from a pancreatic ductal adenocarcinoma patient

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

  Dataset EGAD00001005904