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• Colorectal adenomas and carcinomas NKI-AvL TGO series Gut2009

  Colorectal cancer (CRC) develops from normal epithelium, through a benign precursor lesion called adenoma, by accumulation of genetic alterations affecting oncogenes and tumour suppressor genes. These CRC-related genomic alterations often result in specific RNA-expression patterns. RNA isolated from fresh frozen specimen of 32 adenomas and 29 CRCs was obtained from the previously published study (Carvalho et al. 2009) and RNA-sequencing was performed with the aim to examine RNA expression changes in colorectal adenoma-to-carcinoma progression.

  Study EGAS00001002758

• Genomic profiling of matched well differentiated and de-differentiated liposarcoma.

  Well-differentiated (WD) and de-differentiated (DD) liposarcoma, subtypes of adipocytic sarcomas, are pathologically and clinically dissimilar, but are poorly distinguishable at the molecular level. These tumors harbor neochromosomes formed from amplifications and rearrangements of chr12q. Nineteen selected patients with matched WD and DD tumors underwent extensive exomic and transcriptomic profiling to distinguish genomic features between the two subtypes. Shared point mutations suggest a common tumor origin and de-differentiated tumors have higher burdens of deletions.

  Study EGAS00001002807

• A_compendium_of_mutational_signatures_due_to_environmental_exposures

  Analysis of mutational signatures caused by exposure to known mutagens in human induced pluripotent stem (iPS) cells. A reference human iPS cell-line will be exposed to 100 chemicals known or proposed to be mutagenic. Following exposure to mutagen, cells will undergo a period of recovery before sub clones are generated and sequenced. The progenitor “parental” IPS cell-line will be used to generate reference sequence data, in order to determine the mutational signatures acquired as a result of exposure to different mutagens.

  Study EGAS00001002060

• Endothelium-derived stromal cells contribute to bone marrow niche formation

  Comprehensive transcriptional characterization of bone marrow stromal cells by RNA sequencing was performed to determine the molecular properties/signatures of endothelium during niche formation.Here, we identify a rare subset of cells in the human fetal BM that co-express endothelial and stromal markers, including low-affinity nerve growth factor receptor (LNGFR/CD271). They display transcriptional reprogramming consistent with endothelial-to-mesenchymal transition (EndoMT), reflected in their potential to generate stromal cells with in vivo BM niche forming capacity.

  Study EGAS00001004946

• Convergent evolution drives therapy resistance in DNA repair-deficient mCRPC

  These are FASTQ files obtained from RNA-sequencing and DNA-sequencing of tumor biopsies obtained from metastatic castration-resistant prostate tumors. Patients were treated with multiple lines of therapy with samples obtained at the time of rapid autopsy following the CASCADE protocol. Multiple biopsies were obtained from each patient under guidance of pathology. DNA were analyzed by high-depth whole genome, exome, and targeted sequencing. RNA were analyzed using a Nugen amplification protocol as described in Quigley Cell 2018.

  Study EGAS00001007147

• Transcriptome profiling of three giant cell tumour of bone cell lines

  Transcriptome profiling of three established giant cell tumour of bone (GCTB) cell lines on the BGISEQ-500 platform (PE100). Cell lines consist of neoplastic "stromal" cells harboring a heterozygous H3F3A p.G34W mutation. Data was used in a study (Venneker et al., Histone deacetylase inhibitors as a therapeutic strategy to eliminate neoplastic “stromal” cells from giant cell tumors of bone, 2022) to determine H3F3A-WT/MT expression ratios, to identify pathogenic variants, and to examine the expression levels of epigenetic modifiers and regulators.

  Study EGAS00001006441

• RNAseq - Discovery of resistance mechanisms to the BRAF inhibitor vemurafenib in metastatic BRAF mutant melanoma

  We propose to biopsy 20 consented BRAF mutant melanoma patients at Addenbrooke's Hospital pre-treatment with vemurafenib and also upon the development of resistant disease, with the aim of using exome sequence and SNP6 data to identify novel sequence variants and copy number alterations that can be used to validate observed resistance mechanisms in our cell line models and also to use these models to inform as to likely candidate small molecule inhibitors to overcome resistance and that could be tested in the clinical trial setting.

  Dataset EGAD00001001050

• Discovery of resistance mechanisms to the BRAF inhibitor vemurafenib in metastatic BRAF mutant melanoma

  We propose to biopsy 20 consented BRAF mutant melanoma patients at Addenbrooke's Hospital pre-treatment with vemurafenib and also upon the development of resistant disease, with the aim of using exome sequence and SNP6 data to identify novel sequence variants and copy number alterations that can be used to validate observed resistance mechanisms in our cell line models and also to use these models to inform as to likely candidate small molecule inhibitors to overcome resistance and that could be tested in the clinical trial setting.

  Dataset EGAD00001001046

• DNA whole-exome sequencing data from patients with metastatic basal cell carcinoma

  Whole-exome sequencing data in fastq format of matched tumour and germline DNA from 8 patients with metastatic basal cell carcinoma. Samples are labeled as Primary, Local or Metastasis: Primary: Sample was obtained from primary tumour. Local: Sample was obtained from local recurrence of primary tumour. Metastasis: Sample was obtained from a metastatic site. Germline: Sample was obtained from normal adjacent tissue. DNA was isolated from FFPE tissue sections of the tumor biopsies using the AllPrep DNA/RNA FFPE Kit (Qiagen) and quality controls conducted using the Qubit fluorometer (Thermo Fisher Scientific). Library preparation was performed using the Agilent SureSelect Human All Exon v7 XTHS2 probes and sequenced on a NovaSeq 6000 S2 2x100bp

  Dataset EGAD00001008675

• WES

  Genomic DNA was extracted from PBMCs and whole blood using the Chemagic Prime DNA Blood 4k kit. DNA quality and integrity were assessed by Qubit and Tapestation, and only samples with sufficient quantity, DIN > 6, and confirmed sex were used. Whole-exome libraries were prepared with the SureSelect XT Human All Exon V8 kit (Agilent), covering all human protein-coding regions. DNA was fragmented, adapter-ligated, captured, and amplified following the manufacturer’s protocol. Libraries were quantified, pooled (95 samples), and sequenced on an Illumina NovaSeq 6000 using S4 flow cells, generating up to 12 billion paired-end reads per run.

  Dataset EGAD50000002037