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• Mucoepidermoid Carcinoma

  Whole exome sequencing data for 18 mucoepidermoid carcinoma samples. The samples were used for Illumina TruSeq library construction and captured using Agilent V4 exome panel. The PE fastq files are provided.

  Dataset EGAD00001003958

• Additional WGS files for Genomic Landscape ALL paper

  Additional WGS files for Genomic Landscape ALL paper titled "The genomic landscape of pediatric acute lymphoblastic leukemia"

  Dataset EGAD00001010270

• Targeted sequencing using SPET for Mesothelioma.

  Targeted sequencing using SPET for Mesothelioma.

  Dataset EGAD00001001916

• Mucoepidermoid carcinoma- normals

  Whole exome sequencing data for 18 mucoepidermoid carcinoma samples. The samples were used for Illumina TruSeq library construction and captured using Agilent V4 exome panel. The PE fastq files are provided.

  Dataset EGAD00001004946

• MT amplicon sequencing reads of 217 Egyptian individuals

  This data set contains for 217 Egyptian individuals the amplicon sequencing reads mapping to chrM. These were subsequently used for haplogroup assignment.

  Dataset EGAD00001006040

• Mosaic Chromosomal Aneuploidies Detection in Clinical Samples

  Mosaic chromosomal aneuploidy occurs when only a subset of cells carries an abnormal number of chromosomes. Mosaic aneuploidy has been reported in multiple types of diseases. Here we have developed a new sequencing-based approach to identify, characterize and quantify mosaic aneuploidy events in human tissue samples. This ongoing study has begun with results from sequencing data from two clinical patients, one with autism spectrum disorder (ASD) and the other with hemihyperplasia (OMIM 235000). We captured ~100,000 common SNPs from the samples to identify the nature of the mosaic aneuploidy events in each of the samples.

  Study phs001557

• Detection of Somatic Mutations In Vitro Aging Cells

  Deep sequencing was performed to analyze the prevalence of somatic mutations during in vitro cell aging. Primary dermal fibroblasts from healthy subjects of young and advanced age, from Hutchinson-Gilford progeria syndrome, and from Xeroderma Pigmentosum complementation group A (XPA) and C (XPC), were first restricted in number and then expanded in vitro. DNA was obtained from cells pre- and post-expansion and sequenced at high depth, over a cumulative 290 kb target region, including the exons of 44 aging-related genes. Allele frequencies of 58 somatic mutations differed between the pre- and post-cell culture expansion passages.

  Study phs001867

• Novel APC Promoter and Exon 1B Deletion and Allelic Silencing in Three Mutation-Negative Classic Familial Adenomatous Polyposis Families

  The ~80% of individuals with classic familial adenomatous polyposis (FAP) have detectable mutations in the coding sequence of the adenomatous polyposis coli (APC) gene. To investigate the 20% of families without detectable causative mutations, we used exome sequencing and second-generation sequencing of the APC locus including non-coding regions. We identified a novel ~11kb deletion 44kb upstream of APC that was present only in affected individuals of three kindreds. SNP analysis showed that this ~11kb deletion was accompanied by silencing of one of the APC alleles in blood-derived RNA of affected individuals.

  Study phs000904

• Mutation signatures in melanocytic nevi reveal characteristics of defective DNA repair

  Nevi are common benign melanocytic neoplasms that can be found on any skin location and share many of the genomic hallmarks of melanoma. In our recent report involving whole-exome sequencing of acquired nevi (Stark et al., 2018), ultra-violet radiation (UVR) related somatic mutation signatures (“signature 7”) (Alexandrov et al., 2013) were frequently observed in all lesions that were located on sun-exposed sites. In the study presented herein, we sought to investigate whether an independent Spanish cohort (Valencia, Spain) of minimally sun exposed nevi had genomic features consistent with our previous findings.

  Study EGAS00001004274

• Fetal hemoglobin in sickle cell disease patients from Tanzania

  Levels of fetal hemoglobin have been associated with differences in severity and outcome of sickle cell disease (SCD). While some genetic associations have been reported between SNPs and HbF level, little of the variance in the trait is explained, and most studies have focused on African American, rather than African samples. We have carried out a GWAS in a collection of SCD patients from Dar es Salaam, Tanzania. This sample represents a diverse, metropolitan collection of individuals from East Africa. Omni 2.5M genotypes and HbF levels (measured after 5 years of age) are available.

  Study EGAS00001000990