8253 results for "canc*"

in 13.28 milliseconds.

• Exome sequencing of 142 gastric cancer and matched normal from Japanese cohorts (UT)

  As a contribution to the International Cancer Genome Consortium, exome sequencing of 142 Japanese gastric cancer with various histological subtypes have been conducted. This study aims to identify unique and common driver genes and molecular subtypes in Japanese gastric cancer. Please refer ICGC website for detail: http://icgc.org/icgc/cgp/69/420/1012357

  Dataset EGAD00001004041

• Exome sequencing of 102 gastric cancer and matched normal from Japanese cohorts (YCU)

  As a contribution to the International Cancer Genome Consortium, exome sequencing of 102 Japanese gastric cancer with various histological subtypes have been conducted. This study aims to identify unique and common driver genes and molecular subtypes in Japanese gastric cancer. Please refer ICGC website for detail: http://icgc.org/icgc/cgp/69/420/1012357

  Dataset EGAD00001004042

• Exome sequencing files for "A single mutant clone populates the pancreatic ductal system to generate coexisting neoplastic lesions"

  Files from whole exome sequencing of eight tumors from eight pancreatic cancer patients along with matched PanIN precursor lesion(s) and a matched normal tissue.

  Dataset EGAD00001004044

• Reference Epigenomes and Regulatory Landscape of CLL

  Analysis of the reference epigenomes and regulatory landscape of CLL as a whole and its major clinico-biological subtypes (with mutated and unmutated IGHV) in the light of the normal B-cell differentiation. We have extensively characterized the reference epigenomes of seven primary chronic lymphocytic leukemia samples (CLLs) with mutated (n=5) and unmutated IGHV (n=2) as well as several mature B-cell subpopulations (naive B cells from blood and tonsil, germinal center B cells, memory B cells and plasma cells from tonsil) using genome-wide maps of six histone marks (H3K4me3, H3K4me1, H3K27ac, H3K36me3, H3K9me3 and H3K27me3), DNA accessibility (ATAC-seq), DNA methylation (whole-genome bisulfite sequencing) and gene expression (RNA-seq). Furthermore, we have mapped the regulatory chromatin landscape of 100 additional CLL cases using chIP-seq of H3K27ac and ATAC-seq and linked these data to additional layers of information (whole-genome and/or whole-exome sequencing (WGS/WES), RNA-seq and DNA methylation microarrays) studied in the context of the International Cancer Genome Consortium (ICGC).

  Dataset EGAD00001004046

• Genomic analysis of Japanese gastric cancer

  fastq of 345 Japanese gastric cancer

  Dataset EGAD00001004051

• Single-cell transcriptome sequencing of regulatory and conventional T cells in breast cancer patients and healthy individuals.

  Identification of tumor-specific effects on gene expression profile of regulatory T cells and conventional T cells in humans, investigation of the clonal origin of regulatory T cells and impact analysis of tumor-specific conversion of conventional T cells into induced regulatory T cells on the peripheral regulatory T cell repertoire in humans.

  Dataset EGAD00001004069

• Low-coverage Whole Genome Sequencing, Colorectal adenomas, NKI-AvL TGO series Stool-Proteomics

  For this tissue dataset, we applied low-pass whole genome sequencing to 98 non-advanced and advanced adenomas. As small number of lesions was sequenced multiple times, this dataset consists of 103 fastq files. These adenomas were classified as lesions with low-risk or high-risk of progression, according to the presence of specific DNA copy number changes (Carvalho et al, CancerPrevRes, 2018).

  Dataset EGAD00001004075

• Low-coverage Whole Genome Sequencing, Colorectal advanced adenomas, NKI-AvL TGO COCOS series

  For this tissue dataset, we applied low-pass whole genome sequencing to 96 advanced adenomas. Advanced adenomas were classified as lesions with low-risk or high-risk of progression, according to the presence of specific DNA copy number changes (Carvalho et al, CancerPrevRes, 2018).

  Dataset EGAD00001004078

• Comprehensive cancer predisposition gene testing in an adult multiple primary tumor series shows a broad range of deleterious variants and atypical tumor phenotypes

  Multiple primary tumors (MPT) affect a substantial proportion of cancer survivors and may result from various causes including inherited predisposition. Currently, germline genetic testing of MPT cases for cancer predisposition gene (CPG) variants is mostly targeted by tumor type. We ascertained pre-assessed MPT cases from genetics centers (defined as ≥2 primaries by age 60 years or ≥3 by 70) and performed whole genome sequencing (WGS) on 460 individuals from 440 families. Despite previous negative genetic assessment/molecular investigations, pathogenic variants in moderate and high-risk CPGs were detected in 67/440 (15.2%) of probands. WGS detected variants that would not be (or were not) detected by targeted resequencing strategies including structural variants at low frequency (6/440 (1.4%) of probands). In most individuals with a germline variant assessed as pathogenic or likely pathogenic (P/LP), at least one of their tumor types was characteristic of variants in the relevant CPG. However, in 29 probands (42.2% of those with a P/LP variant) the tumor phenotype appeared discordant. The frequency of individuals with truncating or splice site CPG variants and at least one discordant tumor type was significantly higher than a control population (χ2=43.642 P=<0.0001). 2/67 (3%) of probands with P/LP variants had evidence of multiple inherited neoplasia allele syndrome (MINAS) with deleterious variants in two CPGs. Summing together variant detection rates from a similarly ascertained previous MPT case series, the present results suggest that first-line comprehensive CPG analysis in a clinical genetics referral-based MPT cohort would detect a deleterious variant in about a third of cases.

  Dataset EGAD00001004088

• Udated data for October 2017 data release 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.

  October 2017 data update (bam/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 EGAD00001003906