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• Whole genome analysis of mutation hotspots in gastric cancer

  Tissue-specific driver mutations in non-coding genomic regions remain undefined for most cancer types. In this study, we unbiasedly analysed 212 gastric cancer whole genomes to identify recurrently mutated non-coding regions in gastric cancer. Applying comprehensive statistical approa- ches to accurately model background mutational processes, we observe significant enrich- ment of non-coding indels (insertions/deletions) in three gastric lineage-specific genes. We further identify 34 mutation hotspots, of which 11 overlap CTCF binding sites (CBSs).

  Study EGAS00001002872

• Whole genome sequencing of multiple myeloma identifies novel structural and non-coding mutations.

  The coding region of the myeloma genome is well understood with key mutations having been identified. However, the non-coding regions of the myeloma genome are yet to be analyzed. Here we have performed whole genome sequencing of myeloma patient samples to identify structural abnormalities including chromothripsis and chromoplexy, as well as gene dysregulation through super-enhancer juxtaposition with key oncogenes. We have also identified non-coding region hotspots of mutation, especially in promoter regions, that affect gene expression.

  Study EGAS00001003164

• The distinct DNA methylome of acute lymphoblastic leukemia

  Here, using whole genome bisulfite sequencing (WGBS) data of over one hundred patients from multiple subtypes of acute lymphoblastic leukemia (ALL), controls samples and ALL cell lines, we show that in contrast to the prevailing paradigm, ALL samples exhibit CpG island hypermethylation but little to no global loss of methylation. The subtype-specific CpG island hypermethylation levels in T cell ALL span a broad range of methylation levels rather than previous binary classifications and are influenced by multiple factors, including TET2 expression.

  Study EGAS00001005203

• Sequencing of an adolescent patient with germline RET mutant alveolar rhabdomyosarcoma

  An adolescent patient presented with an alveolar rhabdomyosarcoma made more unique by the presence of a germline RET mutation ordinarily associated with and a known driver of multiple endocrine neoplasia type 2A (MEN2A) cancer. To better understand the role of this germline RET mutation in the genetics and phenotypic response of this unique alveolar rhabdomyosarcoma, we performed DNA and RNA sequencing of the patients in addition to functional studies on patient-derived cultures and genetically similar similar cell models.

  Study EGAS00001004359

• Genomic characterization of co-existing biliary tract intraepithelial neoplasia and carcinoma lesions reveals distinct evolutionary paths of gallbladder cancer

  Gallbladder carcinoma is the most common cancer of the biliary tract with dismal survival largely due to delayed diagnosis. Biliary tract intraepithelial neoplasia (BilIN) is the common benign tumor that is suspected to be precancerous lesions. However, the genetic and evolutionary relationships between BilIN and carcinoma remain unclear. Here we performed whole-exome sequencing of coexisting low-grade BilIN (adenoma), high-grade BilIN, and carcinoma lesions, and normal tissues from the same patients.

  Study EGAS00001005402

• Genotyping by OncoArray and Global Screening Array for colorectal cancer risk prediction

  The study was conducted to build a Polygenic risk scores (PRS) based on a reported set of 140 single nucleotide polymorphisms that were identified to be associated with a higher risk of colorectal cancer (CRC). Genotyping by OncoArray and Global Screening Array was performed using DNA extracted from blood samples collected at baseline of 187 participants who develop CRC and 176 randomly selected controls without diagnosis of CRC identified within 14 years of follow-up.

  Study EGAS00001005411

• Single cell RNA sequencing of normal endometrial derived organoids uncovers novel cell type markers for prognostication

  Endometrial carcinoma, the most common gynecologic cancer, develops from endometrial epithelium which is composed of secretory and ciliated cells. Pathologic classification is unreliable and there is a need for prognostic tools. We used single cell sequencing to study organoid model systems derived from normal endometrial endometrium to discover novel markers specific for endometrial ciliated or secretory cells. We performed single cell sequencing on endometrial and ovarian tumors and found both secretory-like and ciliated-like tumor cells.

  Study EGAS00001004466

• Identifying the role of ID3 in DNA repair and maintenance of genome integrity

  The inhibitor of DNA-binding 3 (ID3) is a transcriptional repressor protein that limits the binding of basic helix­loop-helix (bHLH) transcription factors to DNA. Preliminary results from our lab confirm that cellular depletion of ID3 is associated with an impaired DNA damage response. we hypothesize that ID3 has the potential to epigenetically affect DNA repair. This is based on our observation that upon cellular ID3 knockdown, a reduction of chromatin-bound H4K16ac and H3K36me3.

  Study EGAS00001004478

• Molecular analysis of FIT interval colorectal cancers

  To optimize a fecal immunochemical test-based screening program, the rate of missed colorectal cancers (CRCs), so-called FIT-interval CRCs, should be minimized. A specific molecular make-up of those CRCs could be an explanation for those interval CRCs. Knowledge of the molecular make-up of these missed lesions could facilitate more accurate detection of all precursor lesions. In this study we aimed to compare the molecular make-up of FIT-interval CRCs and screen-detected CRCs (SD-CRCs).

  Study EGAS00001004683

• DGCR8 and the six hit, three-step model of schwannomatosis

  In our manuscript, we report the second case of a patient with peripheral schwannomatosis and thyroid alterations cause by the germline pathogenic variant E518K in DGCR8 and analyzed a total of 13 schwannomas from patients in the two kindreds identified up to date. Our analyses revealed how path to tumorigenesis prompted by DGCR8 requires the loss of the wild type allele of Chrm22q and in more than two thirds of the tumors a complete inactivation of NF2.

  Study EGAS00001005665