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• Reference epigenome ADMSC02 input ChIP-Seq data generated from KEP study

  ADMSC02 input ChIP-Seq paired end data

  Dataset EGAD00001007367

• Reference epigenome ADMSC03 h3k27ac ChIP-Seq data generated from KEP study

  ADMSC03 h3k27ac ChIP-Seq paired end data

  Dataset EGAD00001007368

• Reference epigenome ADMSC03 h3k36me3 ChIP-Seq data generated from KEP study

  ADMSC03 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007369

• Reference epigenome ADMSC03 h3k4me1 ChIP-Seq data generated from KEP study

  ADMSC03 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007370

• Reference epigenome ADMSC03 h3k4me3 ChIP-Seq data generated from KEP study

  ADMSC03 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007371

• Reference epigenome ADMSC03 h3k9me3 ChIP-Seq data generated from KEP study

  ADMSC03 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007372

• Reference epigenome ADMSC03 input ChIP-Seq data generated from KEP study

  ADMSC03 input ChIP-Seq paired end data

  Dataset EGAD00001007373

• Reference epigenome ADMSC05 h3k27Ac ChIP-Seq data generated from KEP study

  ADMSC05 h3k27Ac ChIP-Seq paired end data

  Dataset EGAD00001007374

• Reference epigenome ADMSC05 h3k36me3 ChIP-Seq data generated from KEP study

  ADMSC05 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007376

• Reference epigenome ADMSC05 h3k4me1 ChIP-Seq data generated from KEP study

  ADMSC05 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007377

• Reference epigenome ADMSC05 h3k4me3 ChIP-Seq data generated from KEP study

  ADMSC05 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007378

• Reference epigenome ADMSC05 h3k9me3 ChIP-Seq data generated from KEP study

  ADMSC05 h3k9me3 ChIP-Seq paired end data

  Dataset EGAD00001007379

• Reference epigenome ADMSC05 input ChIP-Seq data generated from KEP study

  ADMSC05 input ChIP-Seq paired end data

  Dataset EGAD00001007380

• Reference epigenome ADMSC06 h3k27Ac ChIP-Seq data generated from KEP study

  ADMSC06 h3k27Ac ChIP-Seq paired end data

  Dataset EGAD00001007381

• Reference epigenome ADMSC06 h3k27me3 ChIP-Seq data generated from KEP study

  ADMSC06 h3k27me3 ChIP-Seq paired end data

  Dataset EGAD00001007382

• Reference epigenome ADMSC06 h3k36me3 ChIP-Seq data generated from KEP study

  ADMSC06 h3k36me3 ChIP-Seq paired end data

  Dataset EGAD00001007383

• Reference epigenome ADMSC06 h3k4me1 ChIP-Seq data generated from KEP study

  ADMSC06 h3k4me1 ChIP-Seq paired end data

  Dataset EGAD00001007384

• Reference epigenome ADMSC06 h3k4me3 ChIP-Seq data generated from KEP study

  ADMSC06 h3k4me3 ChIP-Seq paired end data

  Dataset EGAD00001007385

• Metadata annotation table

  Clinical data from IMblaze370: Clinical data include disease, treatment arm, MSI status, KRAS oncogenic mutation status, sex, and overall survival (1=dead, 0=alive)

  Dataset EGAD00001008551

• Sample sheet

  Sample sheet linking anonymized sample IDs and anonymized patient IDs.

  Dataset EGAD00001011108

• Whole exome sequencing of an invasive diffuse intrinsic pontine glioma sampled from different sites

  The lateral ventricle subventricular zone (SVZ) is a frequent site of high-grade glioma (HGG) spread and tumor invasion of the SVZ is a predictor of a worse clinical prognosis. A range of HGG types invade the stem cell niche of the SVZ, including both adult glioblastoma and pediatric high-grade gliomas such as diffuse intrinsic pontine glioma (DIPG). The cellular and molecular mechanisms mediating this frequent invasion of the SVZ are poorly understood. Here we demonstrate that neural precursor cell (NPC):glioma cell communication underpins the propensity of glioma to colonize the SVZ. SVZ NPCs secrete chemoattractant signals toward which glioma cells home. Biochemical and proteomic analyses of factors secreted by SVZ NPCs revealed a discrete list of candidate proteins. Necessity and sufficiency testing implicated the neurite outgrowth-promoting factor pleiotrophin, along with three required binding partners (secreted protein acidic and rich in cysteine (SPARC), SPARC-like protein 1, and heat shock protein 90B), as key mediators of this chemoattractant effect. Pleiotrophin protein expression is strongly enriched in the SVZ, and knockdown of pleiotrophin expression starkly reduced glioma invasion of the SVZ in the adult murine brain. Pleiotrophin, in complex with the three binding partners, activated the Rho/ROCK pathway in DIPG cells, and inhibition of ROCK resulted in decreased DIPG invasion toward SVZ neural precursor cell-secreted factors. These findings demonstrate a pathogenic role for neural precursor cell – glioma interactions and potential therapeutic targets to limit glioma invasion.

  Study EGAS00001002326

• Genomic stratification and liquid biopsy in a rare adrenocortical carcinoma (ACC) case, with dual lung metastases

  Adrenocortical carcinoma is a rare malignancy with a poor prognosis and few treatment options. Molecular characterization of this cancer remains limited. We present a case of an adrenocortical carcinoma (ACC) in a 37-yr-old female, with dual lung metastases identified 1 yr following commencement of adjuvant mitotane therapy. As standard therapeutic regimens are often unsuccessful in ACC, we undertook a comprehensive genomic study into this case to identify treatment options and monitor disease progress. We performed targeted and whole-genome sequencing of germline, primary tumor, and both metastatic tumors from this patient and monitored recurrence over 2 yr using liquid biopsy for ctDNA and steroid hormone measurements. Sequencing revealed the primary and metastatic tumors were hyperhaploid, with extensive loss of heterozygosity but few structural rearrangements. Loss-of-function mutations were identified in MSH2, TP53, RB1, and PTEN, resulting in tumors with mismatch repair signatures and microsatellite instability. At the cellular level, tumors were populated by mitochondria-rich oncocytes. Longitudinal ctDNA mutation and hormone profiles were unable to detect micrometastatic disease, consistent with clinical indicators of disease remission. The molecular signatures in our ACC case suggested immunotherapy in the event of disease progression; however, the patient remains free of cancer. The extensive molecular analysis presented here could be applied to other rare and/or poorly stratified cancers, to identify novel or repurpose existing therapeutic options, thereby broadly improving diagnoses, treatments, and prognoses.

  Study EGAS00001003497

• SF11940

  SF11940 snATAC Sequencing.Anaplastic Astrocytoma, IDH-mutant. Tumor location: Left Frontal. Age: 29. Sex: Male .

  Dataset EGAD00001006311

• SF10207

  SF10207 snATAC Seq. Oligodendroglioma, Anaplastic (WHO gr. 3). Tumor Location:Frontal. Age:43. Sex: Male

  Dataset EGAD00001006319

• 4C-seq data of a primary AML with t(3;8)

  The viewpoints used in the 4C-seq data were either the EVI1 promoter or the MYC super-enhancer

  Dataset EGAD00001006818