7201 results for "canc*"

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• Genome and transcriptome sequence data from a uveal melanoma patient

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

  Dataset EGAD00001002566

• Normal sample for patient SA591

  Whole genome sequencing of normal sample for triple negative breast cancer patient SA591

  Dataset EGAD00001009241

• Genome and transcriptome sequence data from a serous endometrial cancer patient

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

  Dataset EGAD00001002631

• Genome and transcriptome sequence data from a metastatic pancreatic cancer patient

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

  Dataset EGAD00001002636

• Raw RNA-seq data for clinical efficacy and biomarker analysis of neoadjuvant atezolizumab in operable urothelial carcinoma in the ABACUS trial

  ABACUS is a single arm phase 2 study that investigated 2 cycles of atezolizumab (1200mg Q3) prior to cystectomy in 95 patients with muscle invasive transitional cell cancer (T2-4N0M0). Pathological complete response (pCR) occurring in ≥20% of patients was the primary endpoint. Biomarker analysis on sequential tissue was a co-primary endpoint. This dataset includes the raw RNA-seq data.

  Dataset EGAD00001006205

• WES melanoma biopsies (UV1-hTERT-mm)

  The dataset contains phenotypes of 14 melanoma biopsies sequenced in connection with the study UV1-hTERT-mm, where the thereapeutic cancer vaccine UV1 is combined with ipilimumab in treatment of melanoma patients.

  Dataset EGAD00001007648

• Genome and transcriptome sequence data from a colon cancer patient

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

  Dataset EGAD00001005826

• Genome and transcriptome sequence data from a chondrosarcoma patient

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

  Dataset EGAD00001005848

• Genome and transcriptome sequence data from a metastatic squamous cell carcinoma of the lung patient

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

  Dataset EGAD00001005850

• Genome and transcriptome sequence data from a malignant epithelial mesothelioma (THR) patient

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

  Dataset EGAD00001005877

• 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

• ScRNA-seq of 6 human FL

  Follicular lymphoma (FL) is an indolent cancer of mature B-cells but carries increased risk of transformation to a more aggressive histology over time. We present here comprehensive profiling both tumor and immune compartments in 6 diagnostic FL biopsies by single-cell RNA sequencing. This confirmed results from 155 FL tumors characterized by mass cytometry (CyTOF) which revealed two distinct evolutionary trajectories with disparate risk of transformation and alternate biologies.

  Dataset EGAD00001007691

• Elevated somatic mutation burdens in normal human cells due to defective DNA polymerases

  Mutation accumulation over time in normal somatic cells contributes to cancer development and is proposed as a cause of ageing. DNA polymerases POLE and POLD1 replicate DNA with high fidelity during normal cell divisions. However, in some cancers defective proofreading due to acquired mutations in the exonuclease domains of POLE or POLD1 causes markedly elevated somatic mutation burdens with distinctive mutational signatures. POLE and POLD1 exonuclease domain mutations also cause familial cancer predisposition when inherited through the germline. Here, we sequenced normal tissue DNA from individuals with germline POLE or POLD1 exonuclease domain mutations. Increased mutation burdens with characteristic mutational signatures were found to varying extents in all normal adult somatic cell types examined, during early embryogenesis and in sperm. Mutation burdens were further markedly elevated in neoplasms from these individuals. Thus human physiology is able to tolerate ubiquitously elevated mutation burdens. Indeed, with the exception of early onset cancer, individuals with germline POLE and POLD1 exonuclease domain mutations are not reported to show abnormal phenotypic features, including those of premature ageing. The results, therefore, do not support a simple model in which all features of ageing are attributable to widespread cell malfunction directly resulting from somatic mutation burdens accrued during life.

  Dataset EGAD00001006212

• WGBS for T-Cell and B-Cell, control and tumor

  WGBS data for 75 paired fastq, spread over 31 samples (4 healthy T-cell, 7 healthy B-cell, 20 B-cell CLL tumors) of the CancerEpiSys-PRECiSe project.

  Dataset EGAD00001005970

• Tumor/Normal WXS and RNASeq from patients dosed with neoTCR T-cell therapy

  Sixteen patients with refractory solid cancers received up to three distinct neoTCR-transgenic cell products, each expressing a patient-specific neoTCR, in a cell dose-escalation, first-in-human phase 1 clinical trial (NCT03970382). Included are the tumor and normal WXS and tumor RNAseq for dosed patients.

  Dataset EGAD00001009830

• February 2020 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.

  February 2020 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 EGAD00001006220

• A developmental cell atlas of the human thyroid gland - WGS

  The thyroid gland produces hormones essential for health from embryogenesis to adulthood. Thyroid disorders, including congenital hypothyroidism and thyroid carcinoma, are prevalent and pose significant health challenges. Congenital hypothyroidism often results from thyroid dysgenesis or impaired hormone synthesis, is particularly prevalent in trisomy 21 (T21), while thyroid carcinoma is the most frequent endocrine malignancy, affecting both paediatric and adult populations. Understanding the molecular basis of these conditions requires deeper insights into fetal thyroid development. We generated a spatiotemporal atlas of the human thyroid during early pregnancy, revealing key cell types, including hormone-producing thyrocytes. Thyroid follicular cells are heterogeneous, with two functional cell states (fTFC1, fTFC2) that persist into adulthood, with fTFC2 characterised by elevated PAX8 expression. We demonstrated that T21 thyroids displayed dysgenesis with disrupted follicular morphology, and altered extracellular matrix interactions, and that the fTFC2 signature was enriched in paediatric papillary thyroid cancer compared to adults. These findings uncover thyrocyte heterogeneity across the lifespan, advancing understanding of thyroid development and disease.

  Dataset EGAD00001015447

• Illumina_RNA_T-XEN_Validation_Cohort

  RNAseq on Illumina HiSeq2000/2500 of Patient-derived xenograft derived from colorectal cancer sample of a validation cohort of 60 PDX

  Dataset EGAD00001002883

• Distribution of ctDNA levels in plasma of early-stage non-small cell lung cancer patients measured using personalised ctDNA analysis

  Blood-based assays have shown increasing ability to detect circulating tumour DNA (ctDNA) in patients with early-stage cancer. However, detection of ctDNA in patients with non-small cell lung cancer (NSCLC) has continued to prove challenging. We performed retrospective analysis to quantify ctDNA levels in a cohort of 100 patients with early-stage NSCLC prior to treatment with curative intent. Where tumour tissue was available for whole exome sequencing, mutations identified were used to define patient-specific sequencing assays. For those 90 patients, plasma cell-free DNA was sequenced to high depth across capture panels targeting a median of 328 mutations specific to each patient. Data was analysed using Integration of Variant Reads (INVAR), detecting ctDNA in 66.7% of patients, including 52.7% (29 of 55) patients with stage I disease and >88% detection for patients with stage II and III disease (16/18 and 15/17). ctDNA was detected in plasma at fractional concentrations as low as 9.1x10-6, and in patients with tumour volumes as low as 0.23 cm3. A 36-gene sequencing panel (InVisionFirst-LungTM) was used to analyse plasma DNA in 27 samples including the 10 cases without tumour exome data, and detected ctDNA in 59% of samples tested (16 of 27). Across the entire cohort, detection rates were higher in squamous cell carcinoma patients compared to adenocarcinoma patients (81% vs. 59%). Detection of ctDNA prior to treatment was associated with significantly shorter time free from relapse, across all patients and in patient subgroups, with Hazard Ratios ranging from 2.25 to >11. Our analysis indicates that for patients with stage I NSCLC, the median ctDNA fraction in plasma is approx. 12 parts per million (0.0012%). This indicates the limits of detection that would be required for ctDNA-based liquid biopsies to detect ctDNA in the majority of patients with early-stage NSCLC.

  Dataset EGAD00001006230

• 133 CRC RNA-seq fastq

  This dataset contain 133 pairs of colorectal tumor and adjacent normal tissue. For each sample paired RNA-seq fastq were generated using an Illuma Myseq-2000. Those colorectal cancer comprise 101 MSI and 32 MSS tumors.

  Dataset EGAD00001006667

• Genome and transcriptome sequence data from a cholangiocarcinoma patient

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

  Dataset EGAD00001005838

• Genome and transcriptome sequence data from a uveal melanoma patient

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

  Dataset EGAD00001010956

• Somatic mutation in edited cholangiocyte organoids

  Primary human cells cultured in organoid format have great promise as potential regenerative cellular therapies. However, their immunogenicity and mutagenic profile remain unresolved, impeding effective long-term translation to the clinic. In this study we report, for the first time, the generation of human leukocyte antigen (HLA)-I and HLA-II knock-out human expandable primary cholangiocyte organoids (PCOs) using CRISPR-Cas9 as a potential ‘universal’ low-immunogenic therapy for bile duct disorders. HLA-edited PCOs (ePCOs) displayed the same phenotypic and functional characteristics as parental unedited PCOs. Despite minimal off-target edits, duplex sequencing approaches demonstrated that ePCOs and PCOs acquire mutations in culture at similar rates, but without evident selection for cancer-driver mutations. ePCOs induced reduced T cell-mediated immunity and donor-dependent NK cell cytotoxicity in vitro and evaded cytotoxic responses with increased graft survival in humanized mice in vivo. Our findings have important implications for assessment of safety and immunogenicity of primary cell-derived organoid cellular therapies.

  Dataset EGAD00001015455

• Combination Immune Checkpoint Inhibition in Australian Rare Cancers_WES

  Combination immune checkpoint inhibition (ICI) with anti-CTLA-4 and anti-PD-1 blockade has demonstrated significant clinical activity across tumour types. Rare cancer patients have limited treatment options due to the scarcity of studies of novel treatment options, so they are often offered chemotherapies untested in their disease. ONJ2016-001/CA209-538 is a prospective, multicentre clinical trial of combination ICI (ipilimumab and nivolumab) in patients with advanced rare cancers, including biliary tract, adrenocortical, rare gynaecological and neuroendocrine cancers (https://clinicaltrials.gov/ct2/show/NCT02923934). The primary endpoint is clinical benefit rate (complete response + partial response + stable disease >3 months) by RECIST 1.1. This study involves generation and analysis of pre-treatment formalin fixed paraffin embedded (FFPE) tumour DNA sequencing data, paired with germline DNA sequencing data, to potentially identify genomic biomarkers that may associate with clinical benefit or other clinical efficacy / toxicity metrics.

  Dataset EGAD00001015465

• Hyperpolarized 13C MRI in breast cancer

  Transcriptomics for samples obtained from six patients (MBR01, MBR03, MBR05, MBR07, MBR10, MBR11)

  Dataset EGAD00001005760