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• Kalirin-RAC controls nucleokinetic migration in ADRN-type neuroblastoma

  The migrational propensity of neuroblastoma is affected by cell identity, but the mechanisms behind the divergence remain unknown. Using RNAi and time-lapse imaging, we show that ADRN-type NB cells exhibit RAC1- and kalirin-dependent nucleokinetic (NUC) migration that relies on several integral components of neuronal migration. Inhibition of NUC migration by RAC1 and kalirin-GEF1 inhibitors occurs without hampering cell proliferation and ADRN identity. Using three clinically-relevant expression dichotomies, we reveal that most of up-regulated mRNAs in RAC1- and kalirin-GEF1-suppressed ADRN-type NB cells are associated with low-risk characteristics. The computational analysis shows that, in a context of overall gene set poverty, the upregulomes in RAC1- and kalirin-GEF1-suppressed ADRN-type cells are a batch of AU-rich elements (ARE)-containing mRNAs, which suggests a link between NUC migration and mRNA stability. GSEA-based search for vulnerabilities reveals prospective weak points in RAC1- and kalirin-GEF1-suppressed ADRN-type NB cells, including activities of H3K27- and DNA methyltransferases. Altogether, these data support the introduction of NUC inhibitors into cancer treatment research.

  Study EGAS00001005023

• Targeted Linked-Read DNA-seq Analysis of Castration-Resistant Prostate Cancers

  Androgen receptor (AR) inhibition is standard of care for advanced prostate cancer (PC). However, its efficacy is limited by progression to castration-resistant PC (CRPC), usually due to AR re-activation via mechanisms that include AR amplification and structural rearrangement. These two classes of AR alterations often co-occur in CRPC tumors, but it is unclear whether this reflects intercellular or intracellular heterogeneity of AR. It is important to resolve the mechanisms of AR genomic rearrangements to develop new therapies and predictive biomarkers for PC. We developed a targeted linked-read DNA sequencing assay to interrogate alterations in AR and a panel of genes known to be amplified or mutated in CRPC. Linked-read DNA-sequencing libraries were generated using the 10X Genomics Chromium platform and subjected to hybridization enrichment using a custom-designed Agilent SureSelect bait panel. Post-capture DNA-seq libraries were pooled and sequenced on an Illumina HiSeq 2500 using 2x150 bp settings. This targeted linked-read DNA-seq assay was used to interrogate a set of 6 benchmarking samples harboring known AR gene rearrangements and other alterations in AR, as well a panel of 6 patient-derived xenograft CRPC tumors and 23 clinical CRPC tumors. In this cohort, we identified a subset of samples that developed complex, multiply-rearranged AR gene structures in conjunction with very high AR copy number. The data that will be made available through dbGaP are raw FASTQ files.

  Study phs003343

• DNA sequencing for gastric cancer ascites

  Whole-exome sequencing (WES) was performed on a total of 34 PC specimens, with 15 cases having matched gDNAs extracted from blood.

  Dataset EGAD00001004364

• RNA sequencing for gastric cancer ascites

  Whole transcriptome sequencing (RNA-seq) was performed on 39 PC specimens. Among them, 21 specimens also had WES data.

  Dataset EGAD00001004365

• Single-cell RNA sequencing for metastatic gastric adenocarcinoma

  Single-cell RNA sequencing was performed on a total of 20 PC specimens.

  Dataset EGAD00001006172

• Extensive patient-to-patient single nuclei transcriptome heterogeneity in pheochromocytomas and paragangliomas

  Pheochromocytomas (PC) and paragangliomas (PG) are rare neuroendocrine tumors of varied genetic makeup, associated with high cardiovascular morbidity and a variable risk of malignancy. We focused on PCPG tumors with germline SDHB and RET mutations, representing distinct prognostic groups with worse or better prognoses, respectively. We applied single-nuclei RNA sequencing (snRNA-seq) on tissue samples from 11 patients.

  Study EGAS00001006230

• The Mutational Landscape of CTCL and Sezary Syndrome

  Sezary syndrome is a leukemic and aggressive form of cutaneous T-cell lymphoma (CTCL) resulting from the malignant transformation of skin-homing central memory CD4+ T cells. To identify new genetic alterations involved in Sezary syndrome and CTCL transformation we performed whole-exome sequencing of tumor-normal sample pairs from 26 Sezary syndrome and 16 CTCL patients. These analyses revealed a distinctive pattern of somatic copy number alterations in Sezary syndrome including highly prevalent recurrent chromosomal deletions involving the TP53, RB1, PTEN, DNMT3A, and CDKN1B tumor suppressor genes. Mutation analysis identified a broad spectrum of somatic mutations involving key genes involved in epigenetic regulation (TET2, CREBBP, MLL3, BRD9, SMARCA4 and CHD3) and signaling, including mutations in MAPK1, BRAF, CARD11 and PRKG1 driving increased MAPK, NFKB and NFAT activity upon T-cell receptor stimulation. Collectively, our findings provide new insights into the genetics of Sezary syndrome and CTCL and support the development of personalized therapies targeting key oncogenically activated signaling pathways for the treatment of these diseases.

  Study phs000994

• Whole exome sequencing of endometriod ovarian cancer tumours

  Whole Exome sequencing data of tumour samples for 112 patients with endometrioid ovarian carcinoma in FASTQ format. Data was derived as summarized below: Library Preparation: Libraries were prepared from each DNA sample using the Illumina TruSeq Exome Library Prep kit (#FC-150-1002) according to the provided protocol using modifications for working with FFPE sourced material. Libraries were quantified using the Qubit 2.0 Fluorometer and the Qubit DNA HS assay (#Q32854) and the size distribution of fragments was assessed using the Agilent Bioanalyser with the DNA HS Kit (#5067-4626). Library QC: Exome-captured sequencing library pools were quantified using the Qubit 2.0 Fluorometer and the Qubit DNA HS assay (#Q32854) and the size distribution of fragments was assessed using the Agilent Bioanalyser with the DNA HS Kit (#5067-4626). Fragment size and quantity measurements were used to calculate molarity for each library pool. Sequencing: Sequencing was performed using the NextSeq 500/550 High-Output v2 (150 cycle) Kit (# FC-404-2002) on the NextSeq 550 platform (Illumina Inc, #SY-415-1002).

  Dataset EGAD00001006389

• QuantSeq 3'-mRNAseq of pathogen-stimulated PBMCs

  5 donors, 4 stimuli, 2 time points

  Study EGAS50000000007

• Exome sequencing of 142 gastric cancer and matched normal from Japanese cohorts (UT)

  As a contribution to the International Cancer Genome Consortium, exome sequencing of 142 Japanese gastric cancer with various histological subtypes have been conducted. This study aims to identify unique and common driver genes and molecular subtypes in Japanese gastric cancer. Please refer ICGC website for detail: http://icgc.org/icgc/cgp/69/420/1012357

  Study EGAS00001002891