4905 results for "*oma"

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• Orthotopic murine Group 3 medulloblastoma in C57Bl/6 mice treated with sham or craniospinal irradiation

  Mice with medulloblastoma (Group 3) were treated with sham (isofluorane and imaging xray) or CSI as described by Abbas et al (2022). Total RNA was isolated with RNeasy Plus Mini Kit (Qiagen), library preparation (SureSelect, Agilent), rRNA depletion (Ribo-Zero Plus, Illumina) and sequencing were carried out by GenomicsWA or Australian Genome Research Facility. Libraries were sequenced on NovaSeq 6000 S1 flow cells as paired-end 150bp reads (Illumina).

  Dataset EGAD00001008510

• ChIPseq Sequencing data for epigenetic subgroups of meningioma

  Bam files for 16 meningioma tumor samples; ChIPseq performed on Illumina HiSeq 2000

  Dataset EGAD00001005021

• Activation of Wnt/β-catenin signalling by mutually exclusive FBXW11 and CTNNB1 hotspot mutations drives salivary gland basal cell adenoma - RNA

  Wnt signalling must be 'just right' to promote tumour growth. Basal cell adenoma (BCA) and basal cell adenocarcinoma (BCAC) of the salivary gland are rare tumours that can be difficult to distinguish from each other and other salivary gland tumour subtypes. Due to their rarity, the genomic profiles of BCA and BCAC have not been explored. Using whole-exome and transcriptome sequencing of BCA and BCAC cohorts, we identify a novel recurrent FBXW11 missense mutation (p.F517S) in BCA, that was mutually exclusive with the previously reported CTNNB1 p.I35T gain-of-functon (GoF) mutation. These driver events collectively accounted for 94% of BCAs. In vitro, mutant FBXW11 had a dominant negative affect, characterised by defective binding to β-catenin and the accumulation of β-catenin in cells. This was consistent with the nuclear expression of β-catenin observed in BCA cases harbouring the FBXW11 p.F517S mutation and activation of the Wnt/β-catenin pathway and defines a novel mechanism of Wnt pathway control. The genomic profiles of BCAC were distinct from BCA, with hotspot DICER1 and HRAS mutations and putative driver mutations affecting PI3K/AKT and NF-κB signalling pathway genes. A single BCAC, which may represent a malignant transformation of BCA, harboured the recurrent FBXW11 mutation. These findings have important implications for the diagnosis and treatment of BCA and BCAC, which, despite histopathologic overlap, may be unrelated entities.

  Dataset EGAD00001015366

• Genome and transcriptome sequence data from a neuroblastoma tumor patient

  Genome and transcriptome sequence data from a neuroblastoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015294

• Exploring the driver events of eccrine poromas and porocarcinomas: A retrospective, cross-institutional study of 90 cases

  Eccrine poroma (EP) and porocarcinoma (EPC) are rare benign and malignant adnexal neoplasms of the terminal sweat gland duct, respectively. Both can arise de novo, however, EPCs can also arise from a pre-existing EP. To-date, genetic investigation of these tumors has involved studies with small sample sizes and/or limited analyses. To comprehensively compare the driver events and mutational landscape of these tumors, we performed a retrospective multi-institutional whole-exome sequencing and RNA sequencing study on the largest cohort of EPs and EPCs to-date (n=90). We uncovered novel events and delineated different pathways of tumorigenesis underlying these tumors, with EPs driven largely by fusion genes, and EPCs driven largely by somatic mutations, with rare YAP1 and frequent PAK gene novel fusions.

  Dataset EGAD00001015378

• Genome and transcriptome sequence data from a ependymoma tumor patient

  Genome and transcriptome sequence data from a ependymoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015287

• Genome and transcriptome sequence data from a neuroblastoma tumor patient

  Genome and transcriptome sequence data from a neuroblastoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015296

• Paired RNA-Seq of Tumor Organoids from glioblastoma, 2 patients, treated with different small molecule inhibitors

  Tumor Organoids from glioblastoma, 2 patients, treated with different small molecule inhibitors. Paired RNA-Seq was done on NovaSeq 6000 with the Illumina TruSeq stranded mRNA Kit. The small inhibitors GW2580, BLZ945 and PLX3397 were used. DMSO was used as control.

  Dataset EGAD00001011274

• Genome and transcriptome sequence data from a glioblastoma tumor patient

  Genome and transcriptome sequence data from a glioblastoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015300

• Breast implant-associated anaplastic large cell lymphoma shallow whole genome sequencing for copy number analysis and Whole exome sequencing data.

  Shallow whole genome sequencing of 29 BIA-ALCL patients for copy number analysis and 24 Alk-negative ALCL samples as control cohort. 7 Whole exome sequencing BIA-ALCL samples.

  Dataset EGAD00001006433