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dbGaP phs001002 Metastatic Castration-resistant Prostate Cancer GWAS - pht005043.v1.p1

- 1/29/25 - 5 forms, 1 itemgroup, 5 items, 1 language
Itemgroup: pht005043
Principal Investigator: Howard McLeod, Moffitt Cancer Center, Tampa, FL, USA MeSH: Prostatic Neoplasms,Neutropenia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001002 The Cancer and Leukemia Group B (CALGB) 90401 trial compared docetaxel and prednisone with or without bevacizumab in men with metastatic castration-resistant prostate cancer. A genome-wide association study using clinical outcomes and toxicities was conducted on the basis of data from CALGB patients who provided consent for pharmacogenomic studies and usable DNA

pht005044.v1.p1

1 itemgroup 31 items

pht005042.v1.p1

1 itemgroup 5 items

Eligibility

1 itemgroup 1 item

pht005045.v1.p1

1 itemgroup 6 items

dbGaP phs000487 Functionally Active Copy Number Variants Associated with Prostate Cancer Risk - Eligibility

- 1/29/25 - 5 forms, 1 itemgroup, 1 item, 1 language
Itemgroup: IG.elig
Principal Investigator: Francesca Demichelis, PhD, Centre for Integrative Biology, University of Trento, Trento, Italy MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000487 Prostate cancer is a leading cause of cancer death in males throughout the world and has the largest estimated effect of heritability among the most common tumor types. Copy Number Variants (CNVs) are a recently recognized class of human germline polymorphisms (Iafrate AJ, et al. (2004) Nat Genet 36, 949-951; Sebat J, et al. (2004) Science 305, 525-528.) and are associated with a variety of human diseases, including cancer. This study characterized 1,903 individuals from the Tyrol Early Prostate Cancer Detection Program (Bartsch G, et al. (2008) BJU Int 101, 809-816) using a computational framework (Banerjee S, et al. (2011) PLoS One 29;6(3)). The study results establish non-coding and coding germline CNVs as significant risk factors for prostate cancer susceptibility and implicate their role in disease development and progression. The study "Identification of functionally active, low frequency copy number variants at 15q21.3 and 12q21.31 associated with prostate cancer risk," Demichelis F, Setlur SR, Proc Natl Acad Sci U S A. 2012 Apr 24;109(17):6686-91.

pht002923.v1.p1

1 itemgroup 5 items

pht002924.v1.p1

1 itemgroup 5 items

pht002925.v1.p1

1 itemgroup 7 items

pht003118.v1.p1

1 itemgroup 5 items

dbGaP phs000443 Molecular Profiling of Cancer - pht002530.v1.p1

- 1/29/25 - 4 forms, 1 itemgroup, 4 items, 1 language
Itemgroup: pht002530
Principal Investigator: Arul Chinnaiyan, M.D., Ph.D, University of Michigan MeSH: prostate cancer https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000443 Noncoding RNAs (ncRNAs) are emerging as key molecules in human cancer, with the potential to serve as novel markers of disease and to reveal uncharacterized aspects of tumor biology. Here we discover 121 unannotated prostate cancer-associated ncRNA transcripts (PCATs) by *ab initio* assembly of high-throughput sequencing of polyA+ RNA (RNA-Seq) from a cohort of 102 prostate tissues and cells lines. We characterized one ncRNA, PCAT-1, as a prostate-specific regulator of cell proliferation and show that it is a target of the polycomb repressive complex 2 (PRC2). We further found that patterns of PCAT-1 and PRC2 expression stratified patient tissues into molecular subtypes distinguished by expression signatures of PCAT-1-repressed target genes. Taken together, our findings suggest that PCAT-1 is a transcriptional repressor implicated in a subset of prostate cancer patients. These findings establish the utility of RNA-Seq to identify disease-associated ncRNAs that may improve the stratification of cancer subtypes.

pht002531.v1.p1

1 itemgroup 5 items

pht002532.v1.p1

1 itemgroup 2 items

pht002533.v1.p1

1 itemgroup 11 items

dbGaP phs000942 Use of WGS for Diagnosis and Discovery in the Cancer Genetics Clinic - Eligibility

- 11/27/24 - 5 forms, 1 itemgroup, 1 item, 1 language
Itemgroup: IG.elig
Principal Investigator: Theodora S. Ross, MD, PhD, Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX, USA, and Department of Cancer Genetics, UT Southwestern Medical Center, Dallas, TX, USA MeSH: Neoplasms,Breast Neoplasms,Ovarian Neoplasms,Peritoneal Neoplasms,Skin Neoplasms,Esophageal Neoplasms,Thyroid Neoplasms,Urinary Bladder Neoplasms,Endometrial Neoplasms,Fallopian Tube Neoplasms,Melanoma,Testicular Neoplasms,Bile Duct Neoplasms,Lung Neoplasms,Colonic Neoplasms,Adrenocortical Carcinoma,Carcinoma, Renal Cell,Colonic Polyps,Adenomatous Polyposis Coli,Lymphoma, Large B-Cell, Diffuse,Pheochromocytoma,Paraganglioma,Leiomyoma,Hemangioblastoma,Hyperparathyroidism,Pancreatic Neoplasms,Vulvar Neoplasms,Brain Neoplasms,Liver Neoplasms,Kidney Neoplasms,Prostatic Neoplasms,Glioblastoma,Oncocytoma, renal https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000942 Despite the potential of whole-genome sequencing (WGS) to improve patient diagnosis and care, the empirical value of WGS in the cancer genetics clinic is unknown. We performed WGS on members of two cohorts of cancer genetics patients: those with BRCA1/2 mutations (n = 176) and those without (n = 82). Initial analysis of potentially pathogenic variants (PPVs, defined as nonsynonymous variants with allele frequency 1% in ESP6500) in 163 clinically-relevant genes suggested that WGS will provide useful clinical results. This is despite the fact that a majority of PPVs were novel missense variants likely to be classified as variants of unknown significance (VUS). Furthermore, previously reported pathogenic missense variants did not always associate with their predicted diseases in our patients. This suggests that the clinical use of WGS will require large-scale efforts to consolidate WGS and patient data to improve accuracy of interpretation of rare variants. While loss-of-function (LoF) variants represented only a small fraction of PPVs, WGS identified additional cancer risk LoF PPVs in patients with known BRCA1/2 mutations and led to cancer risk diagnoses in 21% of non-BRCA cancer genetics patients after expanding our analysis to 3209 ClinVar genes. These data illustrate how WGS can be used to improve our ability to discover patients' cancer genetic risks. "Reprinted from doi:10.1016/j.ebiom.2014.12.003, with permission from EBioMedicine."

pht004834.v1.p1

1 itemgroup 5 items

pht004835.v1.p1

1 itemgroup 5 items

pht004836.v1.p1

1 itemgroup 16 items

pht004837.v1.p1

1 itemgroup 5 items

dbGaP phs000915 Integrative Clinical Sequencing Analysis of Metastatic Castration Resistant Prostate Cancer Reveals a High Frequency of Clinical Actionability - pht004944.v2.p2

- 4/14/24 - 4 forms, 1 itemgroup, 2 items, 1 language
Itemgroup: pht004944
Principal Investigator: Arul Chinnaiyan, University of Michigan, MI, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000915 Most prostate cancer deaths are caused by metastatic, castration resistant disease (mCRPC). To develop a precision medicine framework for mCRPC, we established a multi-institutional, international clinical sequencing infrastructure to enroll and carry out prospective whole exome and transcriptome sequencing of tumors from a cohort of mCRPC patients. We obtained high quality DNA and RNA sequence data from 150 bone or soft tissue biopsies. Central pathology revealed high-grade adenocarcinoma with only four cases (3.6%) showing neuroendocrine differentiation. Aberrations of AR, ETS genes, TP53 and PTEN were frequent (40-60% of cases), with TP53 and AR alterations being the most enriched in mCRPC compared to primary prostate cancer. We identified novel genomic alterations in PIK3CA/B (fusions and mutations); R-spondin, BRAF and RAF1 (fusions); APC (inactivating mutations); delta-catenin (missense mutations); and ZBTB16/PLZF (homozygous deletions). Aberrations of BRCA2, BRCA1 and ATM were observed at substantially higher frequencies (19.3% overall) than seen in primary prostate cancers, with 56% of these being exclusively somatic. Putative driver gene alterations were identified in nearly all patients, and over half also harbored driver gene fusions, homozygous deletions and/or amplifications. Moreover, 89% of patients harbored a clinically actionable aberration including 62.7% with aberrations in AR, 65% in other cancer-related genes, and 8% with actionable pathogenic germline alterations. Overall, integrative clinical sequencing analysis can be safely and efficiently performed in mCRPC, yields findings that may be actionable for enrolling patients in clinical trials of targeted therapies, and may inform the basis of individual clinical responses.

pht004945.v2.p2

1 itemgroup 3 items

pht004946.v2.p2

1 itemgroup 2 items

pht004947.v2.p2

1 itemgroup 3 items

dbGaP phs000909 Neuroendocrine Prostate Cancer (Trento/Cornell/Broad 2015) - pht005250.v1.p1

- 4/8/24 - 5 forms, 1 itemgroup, 2 items, 1 language
Itemgroup: pht005250
Principal Investigator: Himisha Beltran, Weill Cornell Medical College, New York, NY, USA MeSH: Adenocarcinoma,Prostatic Neoplasms,Neuroendocrine tumors https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000909 A subset of advanced prostate cancers can progress from an androgen receptor (AR)-driven state to AR independence, often associated with low or absent AR expression and extensive neuroendocrine differentiation. Once neuroendocrine prostate cancer (NEPC) develops, patients typically demonstrate an aggressive clinical course and poor overall survival. Early diagnosis is important but remains challenging as the clinical and pathologic features associate with AR independence and NEPC are poorly defined. We performed whole exome sequencing of 114 metastatic tumors from 81 patients (35 with morphologic features of NEPC). Serial or synchronous samples were included to characterize heterogeneity and the transition from adenocarcinoma to NEPC. Computational analysis of clonality and allele specific quantification were performed using CLONET. Quantitative mRNA assessment including AR signaling genes and DNA methylation were evaluated in the context of genomic changes.

pht004874.v1.p1

1 itemgroup 3 items

pht004876.v1.p1

1 itemgroup 6 items

Eligibility

1 itemgroup 1 item

pht004875.v1.p1

1 itemgroup 3 items

dbGaP phs000882 Prostate Cancer Genome-Wide Association Study for Uncommon Susceptibility Loci (PEGASUS) - pht005713.v1.p1

- 3/26/24 - 5 forms, 1 itemgroup, 3 items, 1 language
Itemgroup: pht005713
Principal Investigator: Sonja Berndt, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000882 This genome-wide association study was funded by the National Cancer Institute (NCI) to identify uncommon susceptibility loci for prostate cancer. A total of 4,600 prostate cancer cases and 2,840 controls of European ancestry from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial were genotyped using the Illumina HumanOmni2.5 and passed rigorous quality control filters. Additional genotype data (available in dbGap under other accession numbers) from 101 independent controls of European ancestry scanned with the HumanOmni2.5 were also included, resulting in a total of 4,600 cases and 2,941 controls for the published analysis. SNPs from the most promising regions, as determined by rank p-value, under multiple different models as well as select candidate genes were taken forward for replication using a custom Iselect chip in 6,575 cases and 6,392 controls of European ancestry. Results from the primary scan after imputation were then meta-analyzed with the Iselect results as well as results from previous GWAS. In a combined meta-analysis of the primary scan together with the custom Iselect replication and a previous GWAS, thirteen loci reached genome-wide significance (P 5 x 10sup-8/sup) for prostate cancer overall; however, each of them confirmed a previously reported locus. Although they did not reach genome-wide significance, we found evidence for two new suggestive loci at chromosome 16q22.2 (PKD1L3, rs12597458, P = 9.67 x 10sup-8/sup) and 6p22.3 (CDKAL1, rs12198220, P = 2.13 x 10sup-7/sup). In a combined case-only analysis of 12,518 prostate cancer cases, we identified two loci associated with Gleason score, a pathological measure of disease aggressiveness: rs35148638 at 5q14.3 (RASA1, P=6.49x10sup-9/sup) and rs78943174 at 3q26.31 (NAALADL2, P=4.18x10sup-8/sup). In a stratified case-control analysis, the SNP at 5q14.3 appears specific for aggressive prostate cancer (P=8.85x10sup-5/sup) with no association for non-aggressive prostate cancer compared to controls (P=0.57). Only the cases and controls genotyped on the HumanOmni2.5 specifically for this study are included under this accession number. Controls (n=101) genotyped with the HumanOmni2.5 for another study are posted under a different accession number. Please note that the majority of prostate cancer cases and controls genotyped in CGEMS (and posted under a different accession number) are included in this study.

pht005714.v1.p1

1 itemgroup 7 items

pht005715.v1.p1

1 itemgroup 5 items

pht005712.v1.p1

1 itemgroup 3 items

Eligibility

1 itemgroup 1 item

dbGaP phs000838 Ghana Prostate Study - Eligibility

- 3/9/24 - 5 forms, 1 itemgroup, 2 items, 1 language
Itemgroup: IG.elig
Principal Investigator: Michael B Cook, PhD, National Cancer Institute, NIH, Rockville, MD, USA MeSH: Prostatic Neoplasms,Prostatic Hyperplasia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000838 Participants were recruited through the Ghana Prostate Study-a population-based component, and a clinical component. The population-based component was a probability sample designed using the 2000 Ghana Population and Housing Census data in an attempt to recruit approximately 1,000 men aged 50-74 years in the Greater Accra region (~3 million people), which successfully recruited 1,037 healthy men between 2004 and 2006 with a response percentage of 98.8 %. Consented individuals underwent an in-person interview, and within 7 days had a digital rectal examination (DRE) and provided an overnight fasting blood sample for prostate-specific antigen (PSA) testing, biomarker assays, and genetic analysis. Subjects who had a positive screen by PSA (2.5 ng/ml) or DRE underwent a transrectal ultrasound-guided biopsy. A total of 73 histologically confirmed prostate cancer cases were identified through the population-based screening component of the Ghana Prostate Study and were included in the case population in the published GWAS (Cook et al., Human genetics, 2013). From the remaining 964 screen-negative individuals, 836 had at least 20 μg DNA extracted and available for analysis, and 500 of these were matched to cases for analysis by age (in 5-year categories). In the Ghana Prostate Study, we recruited 676 prostate cancer cases at Korle Bu Teaching Hospital in Accra, Ghana, between 2008 and 2012. All consented cases were interviewed and provided an overnight fasting blood sample. At the time of selection for this analysis we had recruited 582 prostate cancer cases, from which we selected 427 for analysis. Combined with the 73 cases diagnosed through the population-based component of the study, this yielded 500 available prostate cancer cases for analysis.

pht004796.v1.p1

1 itemgroup 3 items

pht004797.v1.p1

1 itemgroup 3 items

pht004798.v1.p1

1 itemgroup 7 items

pht004799.v1.p1

1 itemgroup 5 items

dbGaP phs001105 NHGRI-Mayo Clinic Whole Genome Sequencing of Aggressive Prostate Tumors - Eligibility

- 6/20/23 - 5 forms, 1 itemgroup, 1 item, 1 language
Itemgroup: IG.elig
Principal Investigator: Elaine A Ostrander, PhD, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001105 We collected DNA from fresh frozen prostate tumor samples and matched peripheral blood from 10 subjects with aggressive, Gleason score ≥8 disease. Tumor and normal samples were sequenced on the Illumina HiSeq 2000 to mean depths of 95.3X and 48.3X, respectively.

pht006836.v1.p1

1 itemgroup 5 items

pht006837.v1.p1

1 itemgroup 5 items

pht006838.v1.p1

1 itemgroup 13 items

pht006839.v1.p1

1 itemgroup 10 items

dbGaP phs001141 PROstate Cancer Medically Optimized Genome Enhanced ThErapy (PROMOTE) - Eligibility

- 6/16/23 - 5 forms, 1 itemgroup, 5 items, 1 language
Itemgroup: IG.elig
Principal Investigator: Manish Kohli, MD, Mayo Clinic, Rochester, MN, USA MeSH: Prostatic Neoplasms, Castration-Resistant,Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001141 The Prostate Cancer Medically Optimized Genome-Enhanced Therapy (PROMOTE) study uses genetic clues in castration-resistant prostate cancer that may identify an individualized treatment approach for men with the disease. Understanding the molecular biology behind castration-resistant prostate cancer has led to more treatment options, but there are still no definite conclusions about which specific drug best treats patients - maximum suppression of cancer growth while minimizing side effects. The PROMOTE study explores the genetic characteristics of each tumor to predict these treatment paradigms for the future, resulting in more effective and less toxic options for patients. Our long-term goal is to improve treatments for men with advanced prostate cancer by using genomic sequencing to increase life span and quality of life. We also will uncover novel vulnerable targets in the cancer genome that may provide new drug therapies. **PARTICIPATION** Eligible participants are men: - With castration-resistant prostate cancer or prostate cancer not responding to hormone treatments - About to begin abiraterone acetate therapy - Agreeable to undergoing two tumor biopsies During the study, participants travel to Mayo Clinic for an initial biopsy (before beginning abiraterone acetate) and a second biopsy approximately three months later. The cell tissue collected is analyzed to identify gene alterations in the tumor that could eventually be targeted with treatments. Tissue is preserved for future research. Participants can continue to be treated by their local cancer care team during this period and beyond. In addition, the Mayo team carefully monitors participants' cancer via follow-up studies and the genetic signature of tumors that were biopsied so that patients may benefit from future treatments.

pht005599.v1.p1

1 itemgroup 5 items

pht005600.v1.p1

1 itemgroup 5 items

pht005601.v1.p1

1 itemgroup 5 items

pht005602.v1.p1

1 itemgroup 12 items

dbGaP phs001185 Genome-Wide Scan of Early-onset Prostate Cancer - pht005762.v1.p1

- 6/2/23 - 5 forms, 1 itemgroup, 3 items, 1 language
Itemgroup: pht005762
Principal Investigator: Kathleen Cooney, University of Michigan Ann Arbor, MI, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001185 This is a genome-wide association scan of 931 early-onset prostate cancer cases of European ancestry. The samples were selected from prostate cancer studies at the University of Michigan. Controls were previously genotyped individuals selected from the Cancer Genetics Markers of Susceptibility (CGEMS) and Illumina's iControlDB database.

pht005763.v1.p1

1 itemgroup 4 items

pht005764.v1.p1

1 itemgroup 3 items

pht005765.v1.p1

1 itemgroup 4 items

Eligibility

1 itemgroup 1 item

dbGaP phs001221 ProHealth: Kaiser Permanente GWAS of Prostate Cancer - Eligibility

- 5/16/23 - 7 forms, 1 itemgroup, 7 items, 1 language
Itemgroup: IG.elig
Principal Investigator: John S. Witte, PhD, University of California, San Francisco, CA, USA MeSH: Prostatic Neoplasms https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001221 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 MAF0.01, with a call rate95%, or with Hardy-Weinberg Equilibrium (HWE) p-value in homogeneous groups1x10ˆ-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 p1x10ˆ-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 p0.05 (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.

pht007157.v1.p1

1 itemgroup 4 items

pht007158.v1.p1

1 itemgroup 6 items

pht007159.v1.p1

1 itemgroup 3 items

pht007160.v1.p1

1 itemgroup 42 items

pht007161.v1.p1

1 itemgroup 11 items

pht007162.v1.p1

1 itemgroup 6 items

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