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• DAC for EGAS00001006660

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  Dac EGAC00001003402

• ProHealth: Kaiser Permanente Genome-wide Association Study of Prostate Cancer

  A genome-wide association study (GWAS) of prostate cancer (PCa) was conducted in Kaiser Permanente (KP) Northern California health plan members (7,783 cases, 38,595 controls; 80.3% non-Hispanic white, 4.9% African-American, 7.0% East Asian, and 7.8% Latino) [PMID: 26034056]. The data for these members were drawn from three KP cohort studies: Research Program in Genes, Environment and Health (RPGEH) ProHealth, and California Men's Health Study (CMHS) (described further under Study History). Four custom arrays were designed for genotyping, one for each of the four major race-ethnicity groups in the RPGEH cohort: African Americans, East Asians, Latinos, and Non-Hispanic Whites. The number of SNPs and SNP content varied by array, with SNP content designed to maximize the genome-wide coverage of low frequency and more common variants specific to the different race-ethnicity groups, including newly identified SNPs from sequencing projects, and SNPs with established associations with disease phenotypes and risk factors [PMIDs: 21565264, 21903159]. Within the total study cohort, n=34,736 completed a consent which permitted deposition of data to NIH. Genotyping followed the same general procedure described in [PMIDs: 26092718, plus additional quality control (QC) steps for the additional men, in order to control for potential batch and kit effects, described in [PMID: 26034056. Briefly, we first repeated the filters described in [PMID: 26092718] for all four arrays (EUR, LAT, EAS, AFR). Then, on an array-wise basis, we removed SNPs with MAF<0.01, with a call rate<95%, or with Hardy-Weinberg Equilibrium (HWE) p-value in homogeneous groups<1x10ˆ-5. Furthermore, on the EUR array, to adjust for potential kit effect, we conducted a GWAS of kit, and removed those kit associated SNPs with p<1x10ˆ-6; we also re-genotyped each of the new samples (those not genotyped with the original GERA data) with some of the original GERA data, and removed SNPs with >13/1,268 (1%) mismatches. For the AFR array, to adjust potential plate batch issues, we conducted a GWAS of whether an individual was in the original GERA data vs. in the newly genotyped data and removed those batch-associated SNPs with p<0.05 (we used a stronger threshold than that used for the EUR array because there were fewer individuals on the AFR array); we also re-genotyped each of the new samples with the original GERA data and removed SNPs with >2/78 (2.6%). After the QC described above, imputation was performed as described in [PMID: 26034056]. Imputation was performed on an array-wise basis, pre-phasing with SHAPE-IT v2.5 [PMID: 22138821], and imputing from the 1000 Genomes Project October 2014 release as a cosmopolitan reference panel with IMPUTE2 [PMID: 22384356]. In addition to the GWAS described above, a nested exome-wide association study (EWAS) of PCa was also conducted (7,489 cases, 7,323 controls; 78% non-Hispanic white, 9% African-American, 3% East Asian, 6% Latino, 4% Other). A custom EWAS array primarily focused on rare variants was designed for genotyping that complemented the GWAS arrays [PMID: 26034056]. The EWAS array content included missense and loss-of-function mutations, and rare exonic mutations from The Cancer Genome Atlas (TCGA) and dbGaP prostate cancer tumor exomes [PMID: 26544944; PMID: 26544944]. Much of the EWAS array design content overlapped with the probesets on the UK Biobank Affymetrix Axiom array [PMID: 30305743]. Genotyping and QC steps taken to filter out samples exhibiting low quality and variants with low call rates are described in Emami et al., 2020 [biorXiv]. The resulting EWAS array genotypes are provided here.

  Study phs001221

• Detection of rare mutations, copy number variation, and DNA methylation in the same template DNA molecules

  The analysis of cell-free DNA (cfDNA) from plasma offers great promise for the earlier detection of cancer. At present, changes in DNA sequence, methylation, or copy number are the most sensitive ways to detect the presence of cancer. To further increase the sensitivity of such assays with limited amounts of sample, it would be useful to be able to evaluate the same template molecules for all these changes. Here we report an approach, called MethylSaferSeqS, that achieves this goal, and can be applied to any standard library preparation method suitable for massively parallel sequencing. The innovative step was to copy both strands of each DNA-barcoded molecule with a primer that allows the subsequent separation of the original strands (retaining their 5-methylcytosine residues) from the copied strands (in which the 5-methylcytosine residues are replaced with unmodified cytosine residues). The epigenetic and genetic alterations present in the DNA molecules can then be obtained from the original and copied strands, respectively. We applied this approach to plasma from 265 individuals, including 198 with cancers of the pancreas, ovary, lung and colon, and found the expected patterns of mutations, copy number alterations, and methylation. Furthermore, we could determine which original template DNA molecules were methylated and/or mutated. MethylSaferSeqS should be useful for addressing a variety of questions relating genetics and epigenetics in the future.

  Study EGAS00001006839

• Genetics of Chemotherapy Induced Peripheral Neuropathy in N08C1 and N08CB

  Chemotherapy-induced peripheral neuropathy (CIPN) is a common and potentially dose-limiting toxicity of chemotherapy treatment. CIPN severity varies widely between cancer patients, and previous studies had found evidence of genes and single nucleotide variants (SNV) being associated with CIPN. The goal of this study was to further identify genetic markers and pathways associated with CIPN severity using whole exome sequencing (WES) and whole genome sequencing (WGS) of participants in two clinical studies which collected longitudinal patient-reported outcome (PRO) measures of CIPN. NCCTG/Alliance study N08C1 was a prospective cohort study of the natural history of paclitaxel-associated acute pain syndrome (P-APS) and CIPN. NCCTG/Alliance trial N08CB was a randomized, placebo-controlled trial of calcium and magnesium for prevention of oxaliplatin-induced sensory neuropathy in which the treatment had no significant effect on either acute pain or sensory neuropathy. Both N08C1 and N08CB collected patient assessments of CIPN symptoms before each cycle of chemotherapy using the EORTC QLQ-CIPN20 instrument. For this study, CIPN cases were selected from each of N08C1 and N08CB as those patients with the most severe CIPN symptoms (assessed longitudinally). CIPN controls were selected as those with the least severe symptoms. WGS was obtained for N08C1 samples (WES had been obtained and analyzed previously), and WES was obtained for N08CB samples.

  Study phs001480

• High Density SNP Association Analysis of Lung Cancer

  This research builds upon an extensive resource of a case-control study that has been ongoing at the UT MD Anderson Cancer Center since 1991. To identify risk variants for lung cancer, we conducted a genome-wide association study. Cases are newly diagnosed, histologically-confirmed patients presenting at MD Anderson Cancer and who had not previously received treatment other than surgery. Controls are healthy individuals seen for routine care at Kelsey-Seybold Clinics, the largest physician group-practice plan in the Houston Metropolitan area. This lung GWAS led to the identification of a susceptibility locus for lung cancer at 15q25.1. We used data from 315,450 tagging SNPs in 1,154 current and former (ever) smoking cases of European ancestry and 1,137 frequency-matched, ever-smoking controls from Houston, Texas in the discovery followed by the replication of the ten SNPs most significantly associated with lung cancer in an additional 711 cases and 632 controls from Texas and 2,013 cases and 3,062 controls from the UK. Two SNPs, rs1051730 and rs8034191, were significantly associated with risk of lung cancer with combined analysis yielded odds ratios of 1.32 (P < 1X10-17) for both SNPs. These two SNPs mapped to a region of strong linkage disequilibrium within 15q25.1 containing PSMA4 and the nicotinic acetylcholine receptor subunit genes CHRNA3 and CHRNA5. (Nat Genet. 2008 May;40(5):616-22. PMID:18385676)

  Study phs000753

• Ischemic Stroke Genetics Study (ISGS)

  The third leading cause of death in the United States, stroke is an acute neurological event leading to death of neural tissues. Although the majority of strokes are ischemic strokes, meaning there is oxygen deprivation to the brain, almost 20% of strokes are hemorrhagic, resulting from bleeding into the brain. Stroke is a complex disorder and likely multigenic in nature, resulting from a combination of genetic and environmental factors. These well characterized risk factors that contribute to the incidence of stroke include hypertension, cardiac disease, sickle cell disease, hyperhomocysteinemia, family history of stroke and smoking. ISGS aim is to perform a prospective genetic association study of ischemic stroke focusing on the hemostatic system. ISGS is a 5-center case-control study of first-ever ischemic stroke cases and concurrent controls individually matched for age, sex and recruitment site. This data includes that from subjects both banked in the NINDS repository with biologicals publicly available, and those whose samples are not banked/not available. Important links to apply for individual-level data Data Use Certification Requirements (DUC) Apply here for controlled access to individual level data Participant Protection Policy FAQ --> This study utilized the NINDS Repository Cerebrovascular/Stroke Study, and neurologically normal controls from the sample population which are banked in the National Institute of Neurological Disorders and Stroke (NINDS Repository) collection for a first stage whole genome analysis.

  Study phs000102

• Natural History, Pathogenesis and Outcome of Melorheostosis

  Melorheostosis is a rare osteosclerotic disease resulting in exuberant excessive bone growth with a characteristic radiographic appearance often described as "dripping candle wax". As a result of these bony formations, patients report mild to moderate pain that interferes with their routine activities. It is usually diagnosed on radiographs but bone biopsy may be performed to exclude other osteosclerotic diseases and/or osteosarcoma. Deformities, limb-length discrepancy, muscle atrophy, neurological deficit have been reported as complications. A subset of patients have somatic mutations in MAP2K1. The cause of this disease is not known in all patients, the natural history poorly described and there is no clearly-defined systemic therapy. We propose a prospective observational study to investigate the natural history and pathogenesis of the disease. Subjects will undergo standardized initial evaluation and medically indicated testing. Skin biopsies may be performed to test for known mutations related to melorheostosis, and if negative affected bone and/or skin may be sent for genetic testing for acquired somatic mutations in genes that control bone homeostasis. Enrolled subjects will be followed every two to three years for assessment of disease progression and receive clinically indicated testing and treatment. The study of this rare bone disease offers the potential to generate new insights, provide answers as well as generate new questions into the biology of the skeletal and mineral metabolism.

  Study phs001976

• Genomic Analyses in Neoadjuvant Immunotherapy-Treated Head and Neck Cancers

  This is a phase 2 multicenter interventional trial involving the preoperative (neoadjuvant) administration of pembrolizumab, an anti-programmed cell death protein-1 (anti-PD-1) agent, to patients with pathologically confirmed, surgically resectable advanced head and neck squamous cell carcinoma (HNSCC). Participating centers were Dana-Farber/Harvard Cancer Center, Alvin J. Siteman Cancer Center, Washington University and Memorial Sloan Kettering Cancer Center. The trial (NCT02296684) consisted of two cohorts: Cohort 1 enrolled and treated patients received one dose of pembrolizumab prior to surgical resection with curative intent, and adjuvant pembrolizumab was planned for patients with high risk pathological features (positive margins and/or extranodal extension) in the surgical specimen. Cohort 2 enrolled and treated patients received 2 doses of pembrolizumab prior to surgical resection with curative intent. Adjuvant treatment was not dictated by the trial protocol for Cohort 2. The primary endpoint was rate of at least 50% pathological tumor response (pTR), defined as the presence of tumor necrosis/keratinous debris in the tumor bed following neoadjuvant pembrolizumab. pTR was graded as follows: pTR0 (<10%), pTR1 (10-49%) and pTR2 (≥50%). Baseline, pre-treatment tumor biopsy and post-neoadjuvant pembrolizumab surgically resected tumor specimens were dissociated, and CD3+CD45+ cells were analyzed for T cell receptor (TCR) expression and 5' gene expression analysis using single cell sequencing technologies for a subset of patients.

  Study phs002864