16624 results for "sec+and+unspecified+malignant+neoplasm"

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• Malignant mesothelioma EWAS on European prospective study

  Study EGAS00001006432

• Human normal brain bulk RNA-seq

  We profiled 43 normal human adult brain and 11 normal human fetal brain specimens by bulk RNA-seq. The raw fastqs are provided.

  Dataset EGAD00001005130

• Whole genome sequencing of the healthy breast

  Whole genome sequencing of 29 donors of healthy mammary tissue. BAM files of stromal and epithelial DNA are included.

  Dataset EGAD00001006402

• Targeted capture sequencing for LySeqST

  Targeted capture sequencing of 445 lymphoma samples and 13 normal samples for LySeqST: A targeted sequencing assay for robust genomic classification of diffuse large B-cell lymphoma.

  Dataset EGAD50000002290

• Repertoire sequencies from three different protocols

  This dataset contains sequencing data from Bulk RNAseq, PCR-based RepSeq and SMRT sequencing to compare immunoglobulin repertoire profiling strategies using matched human B-cell samples

  Dataset EGAD50000002217

• H3K27me3 Cut&Tag on beta cells

  H3K27me3 Cut&Tag datasets in human pancreatic islets and the EndoC-bH1 cell line

  Dataset EGAD50000000463

• RNA-seq

  Bulk RNA-seq data of 8 RNA samples were generated. Libraries were prepared using the Stranded mRNA Library Prep, Ligation Kit (Illumina) following manufacturer’s recommendations and sequenced on a NextSeq 2000 (2x50 bp, Illumina).

  Dataset EGAD00001010308

• JMML targeted sequencing (2013)

  Juvenile myelomonocytic leukemia (JMML) is a rare myelodysplastic myeloproliferative neoplasm of early childhood initiated by germline or somatic RAS-activating mutations (Chang, Dvorak et al. 2014). Clinical evolution is heterogeneous, with acute myeloid leukemia (AML) transformation in 1/3 of cases and frequent relapses after hematopoietic-stem-cell transplantation (HSCT), although some patients experience spontaneous remission (Locatelli, Nollke et al. 2005; Matsuda, Shimada et al. 2007; Takagi, Piao et al. 2013; Locatelli and Niemeyer 2015). The initiating lesion incompletely predicts outcome, suggesting the involvement of additional mutations. Genetic profiling of a large JMML cohort (n=118), including whole-exome sequencing (WES) in 30 cases, uncovered additional genetic abnormalities in 56 cases (47%). Somatic events were rare (0.38/case/Mb) and restricted to sporadic (47/78; 60%) or NF1-associated (8/8; 100%) JMML. Multiple concomitant genetic hits were identified targeting the RAS pathway in 13/78 (17%), RAC2D63V, which activates the PI3K/PDK1/AKT and the mTORC2 pathways, and a novel pathway for JMML, the polycomb repressive complex 2 (PRC2), in 26/78 (33%) of the sporadic JMML cases. Interestingly, PRC2 imbalance was recently shown to synergize with RAS activation (De Raedt, Beert et al. 2014). JMML outcome was associated to the mutational profile, suggesting a dose-dependent effect for RAS-pathway activation, distinguishing very aggressive JMML rapidly progressing to AML.

  Study EGAS00001001324

• Changes in alternative splicing and associated neo-antigens due to therapy

  Recent studies have identified alternative splicing (AS) as a novel source of neoantigens for immunotherapy. Surprisingly little is known about the AS milieu in recurrent glioblastoma (GBM), despite this being the venue for most clinical trials. We profiled 29 primary-recurrent paired human GBM specimens via RNA sequencing and re-analyzed RNA-sequencing data from non-malignant human brain tissues. From these data, we reconstructed the landscape of AS in GBM through recurrence and contrasted that to isoforms observed in non-malignant brain. The AS events we identified were cross-referenced with single-cell GBM atlases to determine cell-type specific splicing patterns. From this we identified novel splicing events in cell-surface proteins that are suitable targets for engineered T-cell therapies. We found recurrent-specific isoforms of mitogen-activated kinase pathway genes which are expressed exclusively by GBM stem-like cells that enhance invasiveness. These studies shed light on the effect of therapy on AS and identify novel targets for emerging immunotherapies.

  Study EGAS00001004524

• A single-cell multi-omic atlas of nodal B-cell non-Hodgkin lymphomas

  CITE-Seq (cellular indexing of transcriptomes and epitopes) of 51 lymph node (LN) samples from including mantle cell lymphoma (MCL, n = 8), follicular lymphoma (FL, n = 12), germinal center (GCB, n = 5) or activated B-cell (non-GCB/ABC, n = 7) diffuse large B-cell lymphoma (DLBCL), and marginal zone lymphomas (MZL, n = 11), in addition to non-malignant reactive lymph nodes (rLN, n = 8). Of the malignant LN samples, 20 were collected at the time of initial diagnosis and 23 were from patients who had previously undergone one or more lines of systemic treatment. Relapse samples were collected at least 3 months after cessation of systemic treatment. This dataset also includes 5 prime RNA sequencing and immune receptor sequencing (10X Genomics) for 11 of these samples (2 rLN, 2 MCL, 3 FL, 2 DLBCL (GCB) and 2 MZL).

  Dataset EGAD50000000497