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• Genome and transcriptome sequence data from a ewing sarcoma tumor patient

  Genome and transcriptome sequence data from a ewing sarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015315

• Genome and transcriptome sequence data from a rhabdomyosarcoma, alveolar tumor patient

  Genome and transcriptome sequence data from a rhabdomyosarcoma, alveolar patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015318

• Genome and transcriptome sequence data from a anaplastic astrocytoma tumor patient

  Genome and transcriptome sequence data from a anaplastic astrocytoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015319

• Genome and transcriptome sequence data from a embryonal rhabdomyosarcoma tumor patient

  Genome and transcriptome sequence data from a embryonal rhabdomyosarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015324

• Genome and transcriptome sequence data from a alveolar rhabdomyosarcoma tumor patient

  Genome and transcriptome sequence data from a alveolar rhabdomyosarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015329

• Genome and transcriptome sequence data from a embryonal rhabdomyosarcoma tumor patient

  Genome and transcriptome sequence data from a embryonal rhabdomyosarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015330

• Genome and transcriptome sequence data from a pIlomyxoid astrocytoma tumor patient

  Genome and transcriptome sequence data from a pIlomyxoid astrocytoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015333

• Genome and transcriptome sequence data from a wilms tumor tumor patient

  Genome and transcriptome sequence data from a wilms tumor patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015334

• Genome and transcriptome sequence data from a rhabdomyosarcoma, alveolar tumor patient

  Genome and transcriptome sequence data from a rhabdomyosarcoma, alveolar patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015335

• Genome and transcriptome sequence data from a infantile fibrosarcoma tumor patient

  Genome and transcriptome sequence data from a infantile fibrosarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015263

• Genome and transcriptome sequence data from a CNS sarcoma tumor patient

  Genome and transcriptome sequence data from a CNS sarcoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015268

• Genome and transcriptome sequence data from a ocular melanoma tumor patient

  Genome and transcriptome sequence data from a ocular Melanoma patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015269

• Genome and transcriptome sequence data from a aggressive fibromatosis tumor patient

  Genome and transcriptome sequence data from a aggressive fibromatosis patient, generated as part of the BC Cancer Agency's Pediatric Personalized Onco-Genomics study

  Dataset EGAD00001015279

• Efficacy of two different FGFR-inhibitors in a patient with extrahepatic cholangiocarcinoma harboring an FGFR2 mutation

  Cholangiocarcinomas (CCAs) is a type of cancer with few effective systemic therapies. Elucidation of the molecular landscape of the disease from genomic studies based on next generation sequencing (NGS) has contributed to the introduction of new targeted therapies. One of these treatments consists of a class of small molecules that target members of the FGFR family of receptor tyrosine kinases. These drugs are effective and have been approved for cholangiocarcinomas with fusions or rearrangements of FGFR genes. In contrast, the role of these inhibitors in cholangiocarcinomas with mutations in FGFR genes is less well defined. We report here a patient with a cholangiocarcinoma bearing a FGFR2 p.Ser252Trp mutation. The patient was treated with two different FGFR inhibitors, as the first caused ocular toxicity. She obtained clinical benefit from both. This case illustrates the efficacy of FGFR inhibitors on cholangiocarcinoma with specific point mutations. This is the first case to report the clinical benefit of these drugs in FGFR2 p.Ser252Trp mutation. Clinical benefit can be sustained, as seen in our patient. Our case also shows that FGFR inhibitors-induced adverse effects, such as ocular toxicities, may not recur after re-challenge with an alternative drug of the same class.

  Dataset EGAD50000000021

• Selenium Chemoprevention: Benefits and Harms

  Selenium is a trace element that may have anti-carcinogenetic effect, but heterogenous treatment effects have been observed. This genome-wide association study investigates if genetic variation modifies the effect of selenium chemoprevention in the Selenium and Celecoxib Trial, a randomized, double-blind, placebo-controlled trial conducted at the University of Arizona Cancer Center. The objective of the clinical trial was to determine whether daily intake of 200 µg/d of selenium as a supplement could reduce the risk for developing metachronous colorectal adenomas. The study participants were recruited between 2001 and 2011. Genome-wide association study was performed for 1,323 study participants who provided blood sample at the time of study entry.

  Study phs002283

• Single Cell Genome Variation Induced by Mutational Processes in Cancer - HGSOC Trios Study

  Mutational signatures derived from whole genome sequencing have potential prognostic significance. Identification of high grade serous ovarian cancer patients with deficiency in homologous recombination repair pathways could identify a subset of patients that would benefit from homologous recombination deficiency-specific treatments independent of identification of a pathological BRCA1/2 gene mutation. Clinical protocols rely on a pathologist's assessment of formalin-fixed paraffin-embedded (FFPE) tissues, and thus FFPE tissue samples are readily available. However, the bulk of mutational signature analyses have been performed on fresh frozen tissues. In this study, we aimed to assess the reliability of whole genome sequencing, variant calling, and mutational signature analysis from FFPE tissue samples.

  Study phs003036

• Preclinical Modeling of Leiomyosarcoma Identifies Susceptibility to Transcriptional CDK Inhibitors through Antagonism of E2F-Driven Oncogenic Gene Expression

  Leiomyosarcoma (LMS) is a smooth muscle-derived mesenchymal cancer commonly found to have recurrent loss of tumor suppressor genes and a poorly defined oncogenic program. Empiric cytotoxic chemotherapy is the standard systemic treatment for LMS, and while more targeted and effective therapies are urgently needed, insights into therapeutic vulnerabilities in LMS have been limited by available preclinical models. We generated a panel of LMS patient-derived xenograft (PDX) models and evaluated fidelity to their tumors of origin using RNA sequencing and ultra-low passage whole-genome sequencing (ULP-WGS). Data available at dbGaP include RNA sequencing and ULP-WGS of primary tumors and early and late passages of PDX. 

  Study phs002587

• Molecular Genetics of Heroin Dependence in China

  Our principal goal was to determine the chromosomal locations of genetic variations associated with increased vulnerability to heroin dependence. This goal was attained by identifying specific DNA markers that are genetically linked to heroin dependence. We collected blood and diagnostic information (using a structured diagnostic interview) from 1230 people (sib-pairs) having DSM-IV defined heroin dependence as well as from their parents and other affected and unaffected siblings, when possible. Genotype and clinical data was archived using database software. We conducted a multipoint linkage analysis using the guidelines of Lander and Kruglyak to assert statistical significance, and followed up on regions of interest with a dense set of markers to evaluate candidate genes.

  Study phs001213

• Multiethnic Cohort Adiposity Phenotype Study (MEC-APS)

  A total of 1,861 healthy men and postmenopausal women aged 60-77 years with body mass indexes (BMIs) of 17.1-46.2 kg/m2 were enrolled into the study. Stratified sampling was conducted based on sex, race/ethnicity, and six BMI categories (18.5-21.9, 22-24.9, 25-26.9, 27-29.9, 30-34.9, and 35-40 kg/m2) to balance the sample size across the wide range of BMI and optimize adjustment for total adiposity in populations with different BMI distributions. Study participants underwent body composition assessment, in person interview, blood collection, and completed a self-administered questionnaire. A genome-wide association study of obesity phenotypes was conducted among five racial/ethnic groups of the Multiethnic Cohort Study.

  Study phs001689

• Paired Acute Myeloid Leukemia (AML) Epigenetics Study on Epialleles and Clonality

  We describe methclone, a novel method to identify epigenetic loci that harbor large changes in the clonality of their epialleles (epigenetic alleles). Methclone efficiently analyzes genome-wide DNA methylation sequencing data. We quantify the changes using a composition entropy difference calculation and also introduce a new measure of global clonality shift, loci with epiallele shift per million loci covered, which enables comparisons between different samples to gauge overall epiallelic dynamics. Finally, we demonstrate the utility of methclone in capturing functional epiallele shifts in leukemia patients from diagnosis to relapse. Methclone is open-source and freely available at https://code.google.com/p/methclone. Reprinted with permission from BMC Publishing (Genome Biology).

  Study phs000793

• Mega-GWAS ALS I

  Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder clinically characterized by rapidly progressive paralysis and death due to respiratory failure, typically within two to three years of symptom onset. The number of ALS cases across the globe will increase to nearly 400,000 in 2040, predominantly due to aging of the population. Unraveling the genetics underlying ALS provides insights into the cellular mechanism leading to motor neuron death and provides targets for therapeutic intervention. We performed a genome-wide association study involving a meta-analysis of 20,806 ALS cases and 59,804 controls. The current study release makes available genotype data of the 15,480 subjects assayed in the Laboratory of Neurogenetics for this effort.

  Study phs000101

• Whole Exome Sequencing Analysis of Carfilzomib-Related Cardiotoxicity in Multiple Myeloma Patients

  This study investigated the contribution of germline genetic variants in protein-coding genes in carfilzomib-related cardiovascular adverse events among patients with multiple myeloma using whole-exome sequencing (WES) analysis. We analyzed 247 patients with multiple myeloma who had been treated with carfilzomib at the Moffitt Cancer Center. We identified a missense mutation in the TMSB10/TRABD2A locus that appeared to be associated with a higher risk for cardiovascular adverse events in these patients. In this submission, we will provide all the genotype data along with the phenotype data of whether or not a patient developed cardiovascular adverse events after carfilzomib treatment and all the covariates used in this analysis.

  Study phs003308

• Diabetes Multi-Omic Investigation of Drug Response (DIAMOND)

  The Diabetes Multi-omic Investigation of Drug Response (DIAMOND) cohort is a population-based cohort of individuals with type-2 diabetes (T2D) who receive their care through a large health system serving southeast Michigan and metropolitan Detroit. The cohort represents the diversity of the population from which it was created. Because of their health plan membership, participants have a rich dataset of longitudinal clinical health information related to their care. The intent of the DIAMOND study is to use genomic profiling, drug exposure information, and electronic health record (EHR) derived outcome data to identify genetic predictors of treatment response. Genome-wide genotyping was performed using the AxiomTM Precision Medicine Research Array (ThermoFisher Scientific Inc.).

  Study phs003350

• HiDEF-seq single-molecule sequencing of single-strand mismatches and damage

  Our study sought to resolve, with single-molecule fidelity, the mismatches and damage events that precede DNA mutations. Using a novel single-molecule, long-read sequencing method (HiDEF-seq) we detect base substitutions when present in either one or both DNA strands. We also detect cytosine deamination, a common type of DNA damage, with single-molecule fidelity. This study profiled 134 samples from diverse tissues, including from individuals with cancer predisposition syndromes. These samples revealed single-strand mismatch and damage signatures. Since double-strand DNA mutations are only the endpoint of the mutation process, our approach enables new studies of how mutations arise in a variety of contexts, especially in cancer and aging.

  Study EGAS50000000318

• Fragmentomics profiling and quantification of plasma Epstein-Barr virus DNA enhance prediction of future nasopharyngeal carcinoma.

  This study evaluated the clinical utility of fragmentomics analysis of plasma Epstein-Barr virus (EBV) DNA in nasopharyngeal carcinoma (NPC) screening. The first-round EBV-positive blood samples from a two-round large-scale prospective NPC screening cohort were analyzed. The EBV DNA of subjects who developed NPC in the second round displayed a distinctive mononucleosomal size pattern, an NPC-associated end motif profile, and aberrations in methylation deduced by fragmentomics-based methylation analysis (FRAGMA). Subjects with these aberrant fragmentomics features and higher EBV DNA quantity showed a dramatically increased risk of NPC development, demonstrating the potential of plasma DNA fragmentomics in predicting future cancer risk.

  Study EGAS50000000395