4736 results for "*oma"

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• Sequencing data for oesophageal and related samples - Ng, Contino et al (WGS)

  Data supporting "Interplay of processes shapes structural variations undergoing selection in oesophageal adenocarcinoma" Ng, Contino et al. WGS (BAM files) 383 oesophageal adenocarcinoma samples 383 normal samples

  Dataset EGAD00001007808

• RNAseq on 20 samples of multiple myeloma patients and 3 normal plasma cells

  RNAseq on 20 samples of multiple myeloma patients and 3 normal plasma cells. RNAseq was performed using 200 ng of total RNA by GATC Biotech. Directional libraries were performed after mRNA selection by polyA selection using UTP method. RNA-seq libraries were sequenced on HiSeq2500 Illumina machine using 100bp paired-end reads. Reads alignment was performed using the STAR aligner (version 2.4.0f1) and human genome hg19 as reference.

  Dataset EGAD00001007813

• van Hijfte snRNA glioblastoma dataset

  van Hijfte snRNA glioblastoma dataset

  Dataset EGAD00001009871

• Functional dissection of inherited non-coding variation influencing multiple myeloma risk

  This dataset contains ATAC sequencing of plasma cells from multiple myeloma (MM) patients. The data was used to investigate genotype-specific chromatin accessibility quantitative trait locus (caQTL) using caQTLseg (https://github.com/abhisheknrl/caQTLseg). This dataset contains 161 bam files.

  Dataset EGAD00001007814

• Small-molecule inhibitors in melanoma - Kenski / Kong - WES (2019-04-11)

  Small-molecule inhibitors targeting the most commonly activated pathway in melanoma, MAPK pathway (either alone or in combination) are already given to melanoma patients for few years, and initially reduce tumour burden dramatically, eventually melanomas become resistant and tumours progress while on treatment. Resistance to this treatment occurs by acquisition of additional mutations or other alterations that affect the mitogen-activated protein kinase (MAPK) pathway by either direct or indirect signalling. Many resistance mechanisms somehow lead to reactivation of extracellular signal-regulated kinase (ERK), thereby restoring signalling of the oncogenic BRAF/MEK/ERK pathway. In addition, PI3K pathway activation contributes to resistance to BRAF inhibition. Less frequent but equally important to the phenomenon of targeted drug resistance is the observation that B15-20% of BRAF mutant melanoma patients fail to respond to BRAF inhibition already early on treatment, owing to intrinsic resistance. These patients have little therapeutic options, unless immunotherapy can be given. To better understand the resistance mechanisms in MAPK inhibitor-treated melanoma patients and melanoma biology, our lab generated a big panel of MAPK inhibitor resistant melanoma cell lines by continuous drug exposure. The understanding of the genetic landscape and gene expression as well as cross resistance to other treatment regimens, and other aspects of melanoma biology such as phenotype switch, will allow us to better exploit new therapeutic strategies for melanoma patients. . This dataset contains all the data available for this study on 2019-04-11.

  Dataset EGAD00001004952

• Enhanced reduced representation bisulfite sequencing (eRRBS) on 45 multiple myeloma samples and 3 normal plasma cell

  Enhanced reduced representation bisulfite sequencing (eRRBS) on 45 multiple myeloma samples and 3 normal plasma cell. Enhanced reduced representation bisulfite sequencing (eRRBS) on 45 multiple myeloma samples and 3 normal plasma cell. Libraries were sequenced on a HiSeqTM4000 Illumina machine using 75bp paired-end reads

  Dataset EGAD00001007822

• 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 EGAD00001008942

• Whole genome sequencing (bam files) of 5 samples of myxofibrosarcoma and 5 matched pairs

  Myxofibrosarcoma (MFS) is a rare subtype of sarcomas in the elderly, whose genetic basis is poorly understood. To elucidate it, the whole genome sequence was performed.

  Dataset EGAD00001007825

• G-SAM: Transcriptional Evolution of Glioblastomas Treated With Standard of Care

  Collection of mostly matching primary and recurrent glioblastoma RNA-seq sample pairs, also matching with an earlier DNA sequencing study

  Dataset EGAD00001007860

• RNAseq of 25 sarcoma samples

  100 bp paired-end fastq RNAseq files for 25 sarcoma samples. RNAseq data from exon capture library prep.

  Dataset EGAD00001010839

• SF6420

  Oligodendroglioma (WHO gr. 2)

  Dataset EGAD00001008306

• A practical guide for mutational signature analysis in hematological malignancies

  Analysis of mutational signatures is becoming routine in cancer genomics, with implications for pathogenesis, classification, prognosis, and even treatment decisions. However, the field lacks a consensus on analysis and result interpretation. Using whole-genome sequencing of multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, we compare the performance of public signature analysis tools. We describe caveats and pitfalls of de novo signature extraction and fitting approaches, reporting on common inaccuracies: erroneous signature assignment, identification of localized hyper-mutational processes, overcalling of signatures. We provide reproducible solutions to solve these issues and use orthogonal approaches to validate our results. We show how a comprehensive mutational signature analysis may provide relevant biological insights, reporting evidence of c-AID activity among unmutated CLL cases or the absence of BRCA1/BRCA2-mediated homologous recombination deficiency in a MM cohort. Finally, we propose a general analysis framework to ensure production of accurate and reproducible mutational signature data.

  Dataset EGAD00001005028

• Medulloblastoma cfDNA low-coverage WGS

  Whole genome sequencing of cell free DNA from CSF across timepoints from medulloblastoma clinical trial patients.

  Dataset EGAD00001008277

• Genomic profiling of subcutaneous patient derived xenograft models of solid childhood cancer

  The pediatric cancer cohort in this study included 70 PDX models from 65 different individuals. This cohort included a total of 16 different pediatric solid tumor subtypes, including fourteen Wilms tumors, thirteen hepatoblastomas, thirteen osteosarcomas, ten germ cell tumors, four neuroblastomas, three clear cell sarcomas, two adrenal cortical carcinomas, two leydig cell tumors, two medulloblastomas, one embryonal rhabdomyosarcoma (ERMS), one Ewing sarcoma, one pleomorphic sarcoma, one adenocarcinoma, one glioblastoma, one mesothelioma and one ovarian tumor. Notably, we have five samples with multiple PDX models from same patient, including two cases with duplicates (564 and 564-Dup, 1796 and 1796-Dup), one case with two different metastasis (560-SM, 560-LM), one case with two blocks from same tumor (1939 and 1939-Dup), and one case with different primary tumor from same patient (2264 and 1932). We have a total of 353 sequencing data, including 82 RNA sequencing data (RNA-seq), 138 whole-exome sequencing (WES) and 135 low-pass whole-genome sequencing (WGS). For RNA-seq data, we have 61 PDXs and 21 PTs; for WES, we have 67 PDXs, 30 PTs and 40 matched normal germlines; for WGS, we have 64 PDXs, 30 PTs and 40 matched normal germlines. Of which, 19 PT-PDX paired RNA-seq, 28 paired PT-PDX paired WES and WGS were included.

  Dataset EGAD00001009863

• Ewings sarcoma sequencing data

  This dataset contains samples from 5 patients with ewings sarcoma. 5 samples have whole exome tumor data. 1 sample has tumor RNAseq data. 4 samples have matched normal dna sequence data

  Dataset EGAD00001008282

• TK-EPN862 - Patient-derived xenograft model of Posterior Fossa A Ependymoma - RNAseq

  In Vivo Loss of Tumorigenicity in a Patient-Derived Orthotopic Xenograft Mouse Model of Ependymoma. Whitehouse et al. 2023 Frontiers in Oncology. We describe the establishment of a patient-derived orthotopic xenograft (PDOX) model of posterior fossa A (PFA) EPN, derived from a metastatic cranial lesion. Patient and PDOX tumors were analyzed using RNA sequencing. RNAseq data (paired end) provided here correspond to Primary tumour, two metastatic lesions (one spinal, one cranial), and a patient-derived xenograft derived from the patient.

  Dataset EGAD00001009870

• Genome and transcriptome sequence data from a metastatic lymphoepithelial carcinoma of the parotid gland patient

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

  Dataset EGAD00001010993

• Follicular T cell lymphoma

  Paired-end RNA-seq of follicular T cell lymphoma for the discovery of fusion transcripts

  Dataset EGAD00001006379

• NEC

  This multi-centre, non-randomized, open-label, phase II trial (NCT03016338), assessed niraparib monotherapy (cohort 1, C1), or niraparib and dostarlimab (cohort 2, C2) in patients with recurrent serous or endometrioid endometrial carcinoma. The primary endpoint was clinical benefit rate (CBR). Secondary outcomes were safety and objective response rate (ORR). Translational research was an exploratory outcome. Potential biomarkers were evaluated in archival tissue by immunohistochemistry and next generation sequencing panel. Feasibility of liquid biopsy by ctDNA was assessed.

  Dataset EGAD00001010056

• Whole genome, RNA-seq and single-cell Multiome profile of multiple myeloma

  We analyzed multiple myeloma samples from two patients included in the observational prospective cohort MYRACLE before talquetamab treatment and after relapse. Five other myelomas from the same cohort were included for comparison. Normal plasma cells were also retrieved. All samples were analyzed by whole genome sequencing and single-nucleus Multiome, except one that could only be analyzed by bulk RNA sequencing.

  Dataset EGAD00001010057

• VRK3 depletion in Pontine Diffuse Midline Glioma DMG-K27 altered cells

  In order to investigate possible mechanisms underlying the phenotype of cell fitness decline observed following decrease of VRK3 in pontine DMG-K27 altered cells 7, we examined differences in global gene expression. RNA-seq was performed 44h and 60h post-transduction with two distinct shRNAs targeting VRK3 to be able to evaluate the early impact of VRK3 knock-down (KD) in four independent in vitro models of DMG

  Dataset EGAD00001010097

• SF7233

  Astrocytoma (WHO gr. 2)

  Dataset EGAD00001008305

• Osteosarcoma sequencing data

  This dataset contains samples from 13 patients with osteosarcoma. 13 samples have whole exome tumor data. 12 samples have tumor RNAseq data. 3 samples have matched normal dna sequence data

  Dataset EGAD00001008117

• Platelets contain a repertoire of DNA fragments that map over the human nuclear genome, including tumour-derived DNA in patients with active malignancy.

  This dataset consists of WGS from six patients with a recent diagnosis of gastrointestinal adenocarcinoma. DNA-Seq libraries were prepared from platelet DNA (pDNA) and plasma cfDNA obtained from the same peripheral blood sample. pDNA was size selected into 2 groups (small, s-pDNA: less than 600 bp and long, b-pDNA: greater than 600 bp). The short fragments were further cleaned to remove <100 bp fragments and large platelet fragments were fragmented via sonication. Libraries were then prepared using the NEBNext Ultra II DNA Sample Preparation Kit for Illumina according to the manufacturer’s protocol and sequenced on an Illumina NextSeq 500 (300 cycle PE) at low-pass (0.1X) for all samples, and 10X for the cfDNA and s-pDNA, using four lanes in each sample.

  Dataset EGAD00001009856

• Genomic Analysis of a Metastatic Fusion-negative Embryonal Rhabdomyosarcoma

  Autopsy-derived, later snap-frozen tissue fragments from a 5-year-old female with recurrent metastatic fusion-negative embryonal rhabdomyosarcoma (RMS) primary tumor of the left thigh were analyzed. No quality matched tissue was available. Prior panel analysis identified 2 prominent genetic changes: NRAS Q61K, PIK3CA H1047R, CDKN2A/B loss, and ERBB3 overexpression.

  Dataset EGAD00001009973