Search Results - EGA European Genome-Phenome Archive

NCI's Collection of Datasets for Pediatric and Adolescent and Young Adults Research

This collection contains a compilation of NIH authorized individual-level datasets on childhood cancers currently in dbGaP with various data use limitations (DULs) such as Pediatric Cancer Research without the NPU modifier. The collection has been created to streamline access to pediatric, and adolescent and young adults (AYA) cancer datasets under the purview of NCI DAC and other NIH IC DACs with permission and will include any additional authorized individual-level datasets as they become available. To request access to this study collection, select phs003964 in the dbGaP Authorized Access System.

Study phs003964

NCTN: Phase III Trial of Tamoxifen Alone vs. Tamoxifen Plus Radiation Therapy for Good Risk Duct Carcinoma In-Situ (DCIS) of the Female Breast (RTOG-98-04)

Study ID: RTOG-98-04 NCT Number: NCT00003857 NRG Oncology Submitted in collaboration with the NCTN/NCORP Data Archive Trial Title: NCTN: Phase III Trial of Tamoxifen Alone vs. Tamoxifen plus Radiation Therapy for Good Risk Duct Carcinoma In-Situ (DCIS) of the Female Breast (RTOG-98-04) Trial Description: RATIONALE: Radiation therapy uses high-energy x-rays to damage tumor cells. Estrogen can stimulate the growth of breast cancer cells. Hormone therapy using tamoxifen may fight breast cancer by blocking the uptake of estrogen by the tumor cells. It is not yet known if radiation therapy is more effective than observation, with or without tamoxifen, in treating ductal carcinoma in situ. PURPOSE: Randomized phase III trial to compare the effectiveness of radiation therapy with that of observation, with or without tamoxifen, in treating women who have ductal carcinoma in situ.Clinical data presented in the following publication(s): • PMID 25605856 Disease type(s): Breast Neoplasm - Breast Neoplasm, Miscellaneous Clinical Dataset(s) included: • NCT00003857-D1 (PMID 25605856): This dataset is for RTOG-98-04's primary publication 25605856. The dataset contains reasons for exclusion, baseline characteristics, survival, local failure, distant metastasis, salvage mastectomy, and toxicity data. You are encouraged to view the PDF data dictionaries found in the “Documents” tab of the dbGaP study page, which may contain additional information regarding the data or the associated publication(s).

Study phs004264

Real-Time Genomic Characterization of Advanced Pancreatic Cancer to Enable Precision Medicine

Clinically relevant subtypes exist for pancreatic ductal adenocarcinoma (PDAC), but molecular characterization is not yet standard in clinical care. We implemented a biopsy protocol to perform time-sensitive whole exome sequencing (WES) and RNA-sequencing (RNA-Seq) for patients with advanced PDAC. Therapeutically relevant genomic alterations were identified in 48% (34/71) and pathogenic/likely pathogenic germline alterations in 18% (13/71) of patients. Overall, 30% (21/71) of enrolled patients experienced a change in clinical management as a result of genomic data. Twenty-six patients had germline and/or somatic alterations in DNA-damage repair genes, and 5 additional patients had mutational signatures of homologous recombination deficiency but no identified causal genomic alteration. Two patients had oncogenic in-frame BRAF deletions, and we report the first clinical evidence that this alteration confers sensitivity to MAP-kinase pathway inhibition. Moreover, we identified tumor/stroma gene expression signatures with clinical relevance. Collectively, these data demonstrate the feasibility and value of real-time genomic characterization of advanced PDAC.

Study phs001652

Blood and Marrow Transplant Clinical Trials Network - Randomized Multicenter Trial Comparing Sirolimus Plus Prednisone and Sirolimus/Calcineurin Inhibitor Plus Prednisone for the Treatment of Chronic Graft-versus-Host Disease (BMT-CTN-0801-BioLINCC)

Data Access NOTE: Please refer to the “Authorized Access” section below for information about how access to the data from this accession differs from many other dbGaP accessions. ObjectivesFor the phase II component, to compare the responses of patients with graft-versus-host disease who received sirolimus/calcineurin inhibitor plus prednisone versus sirolimus plus prednisone after 6 months of therapy. For the phase III component, to compare the proportion of subjects with complete resolution of all reversible manifestations at 24 months after starting therapy.BackgroundChronic graft-versus-host disease (cGVHD) is the major treatment-related complication among patients who survive after allogeneic hematopoietic cell transplantation (HCT). Standard immunosuppressive therapy (IST) with prednisone ± a calcineurin inhibitor (CNI) has not changed for three decades, but most patients respond inadequately with slow and most often incomplete control of their disease. Renewed understanding of regulatory T cells (Tregs) led to the hypothesis that experimental therapies permissive of Treg expansion would better abrogate GVHD than CNI-containing (control) IST. Sirolimus and extracorporeal photopheresis (ECP) are permissive of Treg expansion. Because of their acceptance in clinical practice, sirolimus and ECP were considered good candidates for adding to prednisone in clinical trials in cGVHD.ParticipantsAdult and pediatric allogeneic HCT recipients were eligible if they had classic cGVHD ± acute GVHD (overlap subtype) that met 2005 NIH diagnostic consensus criteria. This included newly diagnosed patients, defined as individuals who had received One hundred patients were evaluated for the phase II primary endpoint after all had completed 6 months of follow-up. All 151 enrolled subjects were followed for phase III endpoints. 77 patients were randomized to the prednisone/sirolimus arm and 74 patients to the prednisone/sirolimus/CNI arm.DesignThe trial was designed as an adaptive phase II/III randomized, open-label, prospective study of three treatments for chronic GVHD. Phase II was to include two parallel, 100-patient, randomized trials, comparing prednisone/sirolimus or prednisone/sirolimus/ECP versus identical (prednisone/sirolimus/CNI) comparator arms, where centers selected only one trial in which to participate. However, the prednisone/sirolimus/ECP arm was closed prematurely due to poor accrual. Comparison of complete/partial response rates did not support proceeding to phase III and further accrual was suspended.The starting dose of prednisone (or prednisone-equivalent) was 1 mg/kg once daily, unless contraindicated, in which case the prednisone dose began at 0.5–1 mg/kg once daily. It was recommended that the dose of prednisone was tapered down, over 4–8 weeks to reach a dose of 0.5–1 mg/kg every other day, with the tapering starting within 2 weeks after the first evidence of GVHD improvement. Once an every-other-day prednisone (or equivalent) regimen was achieved, this dose remained constant for 10–12 weeks until all reversible chronic GVHD manifestations resolved. The sirolimus therapy began at a dose of 2 mg orally once daily (1 mg/m2 per day if the patient weighed Health-related quality of life was measured by self-report instruments, including the Functional Assessment of Cancer Therapy Bone Marrow Transplantation (FACT-BMT), Short Form-36 (SF-36).For phase II, the primary outcome was complete or partial response after 6 months of therapy. For phase III, the primary outcome was complete response at 24 months.ConclusionsInitial therapy of chronic GVHD with prednisone/sirolimus is an acceptable alternative and better tolerated than therapy with prednisone/sirolimus/CNI.Carpenter PA, Logan BR, Lee SJ, et al. A phase II/III randomized, multicenter trial of prednisone/sirolimus versus prednisone/ sirolimus/calcineurin inhibitor for the treatment of chronic graft-versus-host disease: BMT CTN 0801 (Carpenter PA et al. Haematologica, 2018).

Study phs004641

Field Effect-Informed Urine Liquid Biopsy Analysis for Assessment of Adjuvant BCG Response in Non-Muscle Invasive Bladder Cancer

The goal of this study was to develop a urine tumor DNA-based minimal residual disease liquid biopsy assay for bladder cancer that improves specificity by considering field effect mutations. We performed targeted cell free DNA sequencing on tumor, adjacent normal, and urine cell free DNA (cfDNA) from non-muscle invasive bladder cancer patients and urine cfDNA from healthy controls. We developed a method called RePhyNERX and used it to identify three molecular response classes: complete responders to surgery, responders to adjuvant Bacillus Calmette-Guérin immunotherapy, and non-responders. These molecular classifications correlated with patient outcome. We also performed RNA sequencing on tumor tissues to identify expression differences between the response classes.

Study phs004110

NCTN: A Phase III Protocol of Androgen Suppression (AS) and 3DCRT/IMRT Vs AS and 3DCTR/IMRT Followed by Chemotherapy with Docetaxel and Prednisone for Localized, High-Risk, Prostate Cancer (RTOG-0521)

Study ID: RTOG-0521 NCT Number: NCT00288080 NRG Oncology Submitted in collaboration with the NCTN/NCORP Data Archive Trial Title: NCTN: A Phase III Protocol of Androgen Suppression (AS) and 3DCRT/IMRT vs AS and 3DCTR/IMRT followed by Chemotherapy with Docetaxel and Prednisone for Localized, High-Risk, Prostate Cancer (RTOG-0521) Trial Description: RATIONALE: Androgens can cause the growth of prostate cancer cells. Hormone therapy using drugs, such as leuprolide, goserelin, flutamide, or bicalutamide, may fight prostate cancer by lowering the amount of androgens the body makes. Radiation therapy uses high-energy x-rays to kill tumor cells. Drugs used in chemotherapy, such as docetaxel and prednisone, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. It is not yet known whether giving hormone therapy and radiation therapy together with chemotherapy is more effective than giving hormone therapy together with radiation therapy in treating prostate cancer. PURPOSE: This randomized phase III trial is studying hormone therapy and radiation therapy followed by docetaxel and prednisone to see how well it works compared to hormone therapy and radiation therapy in treating patients with localized prostate cancer. Clinical data presented in the following publication(s): PMID 30860948Disease type(s): Reproductive System Neoplasm, Male - Prostate Cancer Clinical Dataset(s) included: NCT00288080-D1 (PMID 30860948): This dataset, NCT00288080-D1, contains the data presented in the RTOG-0521 primary publication (PMID: 30860948). The dataset includes reasons for exclusion, treatment arm, baseline characteristics, treatment compliance, adverse event, survival, cause of death, biochemical failure, and distant metastases data. You are encouraged to view the PDF data dictionaries found in the “Documents” tab of the dbGaP study page, which may contain additional information regarding the data or the associated publication(s).

Study phs004255

Whole-Exome Sequencing of Acute Myeloid Leukemia

The Fanconi anemia (FA) pathway is a tumor-suppressive network comprised of at least 22 genes. We demonstrate that the FA pathway disruption sensitizes Acute Myeloid Leukemia (AML) cells to PLK1 inhibition (iPLK1). We obtained cryopreserved mononuclear cells (MNCs) derived from the bone marrow of 16 adult AML patients from the Indiana University Simon Comprehensive Cancer Center (IUSCCC) Biospecimen Collection and Banking Core as a panel for comparative volasertib (iPLK1) sensitivity assessment. Through whole-exome sequencing (WES), we identified multiple pathogenic mutations in FA pathway and FA pathway-associated genes. We found that higher FA pathway mutation burden correlated with sensitivity to volasertib.

Study phs003966

NCTN: CHAARTED: ChemoHormonal Therapy Versus Androgen Ablation Randomized Trial for Extensive Disease in Prostate Cancer (E3805)

Study ID: E3805 NCT Number: NCT00309985ECOG-ACRIN Cancer Research GroupSubmitted in collaboration with the NCTN/NCORP Data ArchiveTrial Title: NCTN: CHAARTED: ChemoHormonal Therapy versus Androgen Ablation Randomized Trial for Extensive Disease in Prostate Cancer Trial Description: RATIONALE: Androgens can cause the growth of prostate cancer cells. Androgen ablation therapy may stop the adrenal glands from making androgens. Drugs used in chemotherapy, such as docetaxel, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. It is not yet known whether androgen-ablation therapy is more effective with or without docetaxel in treating metastatic prostate cancer. PURPOSE: This randomized phase III trial is studying androgen-ablation therapy and chemotherapy to see how well they work compared to androgen-ablation therapy alone in treating patients with metastatic prostate cancer.Data presented in the following publication(s):PMID 26244877PMID 29384722PMID 34129855Additional unpublished data from E3805Disease type(s): Reproductive System Neoplasm, Male - Prostate Cancer Dataset(s) included: NCT00309985-D1 (PMID 26244877): There are 2 datasets (NCT00309985-D1 and -D2) associated with E3805's primary publication (PMID 26244877). This dataset, NCT00309985-D1, contains baseline characteristics (e.g., age, baseline PSA value, Gleason score, etc.), stratification factors, follow-up data, progression data (e.g., post-progression treatment), dose modification information, and outcome data (overall survival, progression-free survival, PSA complete response).NCT00309985-D2 (PMID 26244877): There are 2 datasets (NCT00309985-D1 and -D2) associated with E3805's primary publication (PMID 26244877). This dataset, NCT00309985-D2, contains treatment-related toxicity data.NCT00309985-D3 (PMID 29384722): There are two datasets (NCT00309985-D3 and -D4) associated with PMID 29384722, a publication analyzing the long-term follow-up of ECOG-ACRIN trial E3805. This dataset, NCT00309985-D3, contains updated outcome data. Data that are identical to those presented in NCT00309985-D1 are not duplicated in this dataset.NCT00309985-D4 (PMID 29384722): There are two datasets (NCT00309985-D3 and -D4) associated with PMID 29384722, a publication analyzing the long-term follow-up of ECOG-ACRIN trial E3805. This dataset, NCT00309985-D4, contains data describing the reasons patients never started protocol treatment. Data that are identical to those presented in NCT00309985-D1 are not duplicated in this dataset.NCT00309985-D5 (Unpublished data): This dataset, NCT00309985-D5, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D5 contains unpublished baseline data (including prior treatments, patient characteristics and disease factors), treatment data, and PSA progression data.NCT00309985-D6 (Unpublished data): This dataset, NCT00309985-D6, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D6 contains longitudinal PSA data. NCT00309985-D7 (Unpublished data): This dataset, NCT00309985-D7, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D7 contains chemotherapy total dose data. NCT00309985-D8 (Unpublished data): This dataset, NCT00309985-D8 contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D8 contains the year of randomization for each patient. NCT00309985-D9 (Unpublished data): This dataset, NCT00309985-D9, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D9 contains more baseline data (including pathologic stage, PSA, prior treatments, etc.) and non-protocol treatment data.NCT00309985-D10 (Unpublished data): This dataset, NCT00309985-D10, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D10 contains testosterone data.NCT00309985-D11 (Unpublished data): This dataset, NCT00309985-D11, contains data collected on ECOG-ACRIN trial E3805, which are not published in the primary, long-term follow-up, or gene expression publication for the trial. NCT00309985-D11 contains fasting AM glucose and HDL data.NCT00309985-D12 (PMID 34129855): This dataset, NCT00309985-D12, contains gene expression data reported in PMID 34129855, a secondary publication of E3805 presenting transcriptional profiling associations with clinical outcomes.You are encouraged to view the PDF data dictionaries found in the "Documents" tab of the dbGaP study page, which may contain additional information regarding the data or the associated publication(s).

Study phs004201

HINTS Geo-Coded Data 2011 (HINTS 4 Cycle 1)

The Health Information National Trends Survey (HINTS) is a nationally representative survey which has been administered every few years by the National Cancer Institute since 2003. HINTS 4 includes four mail-mode data collection cycles over the course of three years. The first of these cycles (Cycle 1) was conducted from October 2011 through February 2012, including a total of 3,959 respondents.

Study phs004212

Spindle Assembly Checkpoint Competency Determines Sensitivity to KIF18A Inhibition in Small-Cell Lung Cancer

This study examined the biological determinants of response to KIF18A inhibition in small-cell lung cancer (SCLC), a chromosomal instability-high cancer. The study used patient tumor datasets, SCLC cell line models, genomic and transcriptomic profiling, drug sensitivity testing, live-cell imaging, genetic perturbation, and pharmacologic inhibition to assess chromosomal instability, mitotic regulation, and spindle assembly checkpoint function. Although KIF18A expression was elevated in SCLC and associated with chromosomal instability, proliferation, and neuroendocrine transcriptional programs, these features did not predict drug sensitivity. Instead, response to KIF18A inhibition was primarily determined by spindle assembly checkpoint competency, with SAC-proficient cells undergoing sustained mitotic arrest and apoptosis and SAC-defective cells showing resistance. The dbGaP-accessible data will include de-identified RNA-seq-derived expression data and associated sample metadata for the NIH/NCI patient-derived SCLC cell line component of the study. These data were used to assess selected gene expression features, including KIF18A-related expression and a neuroendocrine-related score based on Neuroendocrine-associated genes. No direct participant identifiers will be included.

Study phs004869

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