Dataset Information

National Cancer Institute (NCI) TARGET: Therapeutically Applicable Research to Generate Effective Treatments

ABSTRACT:

The Therapeutically Applicable Research to Generate Effective Treatments (TARGET) Initiative seeks to accelerate research in novel marker and drug development, along with understanding the molecular basis of pediatric malignancy, through identification of genomic changes associated with the following childhood cancers:

Acute Lymphoblastic Leukemia (ALL) - A fast-growing type of blood cancer in which too many immature white blood cells are found in the blood and bone marrow.
Acute Myeloid Leukemia (AML) - Another type of blood cancer marked by too many myeloblasts, an alternate type of immature white blood cell, are found in the blood and bone marrow.
Neuroblastoma (NBL) - Cancer of cells of the sympathetic nervous system.
Osteosarcoma (OS) - A cancer of the bone that primarily affects children and adolescents.
Wilms' Tumor (WT) - A cancer of cells in the kidney that can spread to the liver, lung and lymph nodes.

Together these cancers account for the majority of the more than 10,000 childhood cancer cases diagnosed in the United States each year.

TARGET is employing a set of advanced and complementary genome analysis technologies, including large scale 2nd and 3rd generation genome sequencing, to strategically characterize alterations in both gene expression and in genomic structure (such as deletions and amplification) that are involved in childhood cancers. The goal of this coordinated effort is a comprehensive genomic and transcriptomic profile of each cancer. Integrated analysis of the TARGET data will identify those genes that are either altered in their expression level or mapped to the chromosome regions of deletion/amplification/translocation, as these genes represent strong candidates for therapeutic targeting. To learn more about the TARGET project, visit the website at http://target.cancer.gov/.

*Additional renal tumors are being added to the TARGET Initiative (clear cell sarcoma of the kidney - CCSK, and rhabdoid tumor - RT), along with some sequencing of cell lines and xenografts in conjunction with the NCI PPTP project.

TARGET primary genomic sequencing datasets (controlled-access) and limited phenotype data (open-access) are available from this site. TARGET characterization data will be deposited into the TARGET Data Coordinating Center (DCC) database, which is supported by the cancer bioinformatics grid (caBIG), while the sequence data is deposited either into the NCBI's trace repository or the sequence read archive (SRA). Comprehensive access to TARGET datasets, including molecular characterization (e.g. gene expression, copy number variation and epigenetics), full clinical information, and targeted sequencing linking tables, is available via the TARGET Data Portal.

OTHER RELATED OMICS DATASETS IN: PRJNA105689PRJNA283848PRJNA283537

PROVIDER: phs000218.v5.p1 | EGA |

REPOSITORIES: EGA

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Publications

The genetic landscape of high-risk neuroblastoma.

Pugh Trevor J TJ Morozova Olena O Attiyeh Edward F EF Asgharzadeh Shahab S Wei Jun S JS Auclair Daniel D Carter Scott L SL Cibulskis Kristian K Hanna Megan M Kiezun Adam A Kim Jaegil J Lawrence Michael S MS Lichenstein Lee L McKenna Aaron A Pedamallu Chandra Sekhar CS Ramos Alex H AH Shefler Erica E Sivachenko Andrey A Sougnez Carrie C Stewart Chip C Ally Adrian A Birol Inanc I Chiu Readman R Corbett Richard D RD Hirst Martin M Jackman Shaun D SD Kamoh Baljit B Khodabakshi Alireza Hadj AH Krzywinski Martin M Lo Allan A Moore Richard A RA Mungall Karen L KL Qian Jenny J Tam Angela A Thiessen Nina N Zhao Yongjun Y Cole Kristina A KA Diamond Maura M Diskin Sharon J SJ Mosse Yael P YP Wood Andrew C AC Ji Lingyun L Sposto Richard R Badgett Thomas T London Wendy B WB Moyer Yvonne Y Gastier-Foster Julie M JM Smith Malcolm A MA Guidry Auvil Jaime M JM Gerhard Daniela S DS Hogarty Michael D MD Jones Steven J M SJ Lander Eric S ES Gabriel Stacey B SB Getz Gad G Seeger Robert C RC Khan Javed J Marra Marco A MA Meyerson Matthew M Maris John M JM

Nature genetics 20130120 3

Neuroblastoma is a malignancy of the developing sympathetic nervous system that often presents with widespread metastatic disease, resulting in survival rates of less than 50%. To determine the spectrum of somatic mutation in high-risk neuroblastoma, we studied 240 affected individuals (cases) using a combination of whole-exome, genome and transcriptome sequencing as part of the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) initiative. Here we report a low median ...[more]

PMID: 23334666

Publication: 1/9

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Project description:The Therapeutically Applicable Research to Generate Effective Treatments (TARGET) Initiative seeks to accelerate research in novel marker and drug development, along with understanding the molecular basis of pediatric malignancy, through identification of genomic changes associated with the following childhood cancers: <ul> <li>Acute Lymphoblastic Leukemia (ALL) - A fast-growing type of blood cancer in which too many immature white blood cells are found in the blood and bone marrow.</li> <li>Acute Myeloid Leukemia (AML) - Another type of blood cancer marked by too many myeloblasts, an alternate type of immature white blood cell, are found in the blood and bone marrow.</li> <li>Neuroblastoma (NBL) - Cancer of cells of the sympathetic nervous system.</li> <li>Osteosarcoma (OS) - A cancer of the bone that primarily affects children and adolescents.</li> <li>Wilms' Tumor (WT) - A cancer of cells in the kidney that can spread to the liver, lung and lymph nodes.</li> </ul> *Additional renal and AML tumors are being added to the TARGET Initiative (clear cell sarcoma of the kidney - CCSK, rhabdoid tumor - RT, and AML cases that fail to respond to standard treatment called induction - AML-IF), along with some sequencing of cell lines and xenografts including some that are being sequenced in conjunction with the NCI PPTP project (model systems substudy - MDLS). More information can be found about each TARGET subproject by following the links on the righthand side of this page. Together these cancers account for the majority of the more than 10,000 childhood cancer cases diagnosed in the United States each year. TARGET is employing a set of advanced and complementary genome analysis technologies, including large scale 2nd and 3rd generation genome sequencing, to strategically characterize alterations in both gene expression and in genomic structure (such as deletions and amplification) that are involved in childhood cancers. The goal of this coordinated effort is a comprehensive genomic and transcriptomic profile of each cancer. Integrated analysis of the TARGET data will identify those genes that are either altered in their expression level or mapped to the chromosome regions of deletion/amplification/translocation, as these genes represent strong candidates for therapeutic targeting. To learn more about the TARGET project, visit the website at <a href="http://ocg.cancer.gov/programs/target" target="_blank">http://ocg.cancer.gov/programs/target</a>. TARGET primary genomic sequencing datasets (controlled-access) and limited phenotype data (open-access) are available from this site. TARGET characterization data will be deposited into the TARGET Data Coordinating Center (DCC) database, while the sequence data is deposited either into the NCBI's trace repository or the sequence read archive (SRA). Comprehensive access to TARGET datasets, including molecular characterization (e.g. gene expression, copy number variation and epigenetics), fully annotated clinical information, and targeted sequencing linking tables, is available via the TARGET <a href="http://target.nci.nih.gov/dataMatrix/" target="_blank">Data Matrix</a>. Please see the TARGET Publication Guidelines at the <a href="http://ocg.cancer.gov/programs/target/target-publication-guidelines" target="_blank">OCG website</a> for updated details on sharing of any TARGET substudy data.

Project description:The Cancer Genome Atlas (TCGA) is a comprehensive and coordinated effort to accelerate our understanding of the molecular basis of cancer through the application of genome analysis technologies, including large-scale genome sequencing. TCGA is a joint effort of the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), which are both part of the National Institutes of Health, U.S. Department of Health and Human Services. TCGA projects are organized by cancer type or subtype. Click <a href="http://cancergenome.nih.gov/cancersselected" target="_blank">here</a> for a current list of cancer types selected for study in TCGA. Data from TCGA (e.g., gene expression, copy number variation and clinical information), are available via the <a href="https://tcga-data.nci.nih.gov/tcga/" target="_blank">TCGA Data Portal</a>, EXCEPT for the genomic sequence data (.bam files), which are hosted at the <a href="https://cghub.ucsc.edu/" target="_blank">Cancer Genomics Hub (CGHub)</a>. Data from TCGA projects are organized into two tiers: Open Access and Controlled Access. <ul> <li>Open Access data tier contains data that cannot be attributed to an individual research participant. The Open Access data tier does not require user certification. Data in Open Access tier are available in the TCGA Data Portal.</li> <li>Controlled Access data tier contains individual-level genotype data that are unique to an individual. Access to data in the Controlled Access data tier requires user certification through <a href="https://dbgap.ncbi.nlm.nih.gov/aa/wga.cgi?login=&page=login" target="_blank">dbGaP Authorized Access</a>.</li> <li>Controlled Access data types consist of the following: <ul> <li>Individual germline variant data (SNP .cel files)</li> <li>Primary sequence data (.bam files), which are available at CGHub</li> <li>Clinical free text fields</li> <li>Exon Array files (for Glioblastoma and Ovarian projects only)</li> </ul> </li> </ul> NOTE: TCGA strives to release most data in the open access tier. Individual genotype or sequence files are prominent exceptions. Commonly requested files such as descriptions of somatic mutations or clinical data are open access. The TCGA study is utilized in the following dbGaP substudies. To view genotypes and other molecular data collected in these substudies, please click on the following substudies below or in the "Substudies" box located on the right hand side of this top-level study page phs000178 TCGA study. <ul> <li><a href="./study.cgi?study_id=phs000441">phs000441</a> Integrated Genomic Analyses of Ovarian Carcinoma (OV)</li> <li><a href="./study.cgi?study_id=phs000489">phs000489</a> Comprehensive Genomic Characterization Defines Human Glioblastoma Genes and Core Pathways</li> </ul>

Project description:<a href="https://cptac-data-portal.georgetown.edu/study-summary/S056" target="_blank">Proteogenomics of Lung Adenocarcinoma, Gillette et al., 2020 publication is here</a> Lung cancer is a leading cause of cancer death in the United States and in 2019 it is estimated that there will be over 228,000 new cases (<a href="https://www.cancer.org/cancer/non-small-cell-lung-cancer/about/key-statistics.html" target="_blank">American Cancer Society</a>). There are two main types, small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). A majority of patients (85%) have NSCLC, with a significant portion of those individuals having a histological subtype lung adenocarcinoma (LUAD) <a href="https://www.ncbi.nlm.nih.gov/pubmed/29364287" target="_blank">Herbst et al., 2018 Nature</a>. To advance the proteogenomic understanding of LUAD, the CPTAC program has investigated 111 tumors, (with 102 tumors paired with normal adjacent tissue samples) and subjected these samples to global proteome and phosphoproteome analysis. An optimized workflow for mass spectrometry of tissues using isobaric tags (TMT (tandem mass tags)-10) was used (<a href="https://www.ncbi.nlm.nih.gov/pubmed/29988108" target="_blank">Mertins et al., Nature Protocols 2018</a>). Proteome and phosphoproteome data from the LUAD discovery cohort is available below along with peptide spectrum matches (PSMs) and protein summary reports from the CPTAC common data analysis pipeline (CDAP).Clinical Data for LUAD tumors are provided below. Updates will be available as the LUAD cohort characterization proceeds. Genomic Data for LUAD tumors is available from the NCI Genomic Data Commons (GDC), <a href="https://portal.gdc.cancer.gov/projects/CPTAC-3" target="_blank">here</a> Imaging Data for LUAD tumors is available from NCI, The Cancer Imaging Archive (TCIA), <a href="https://wiki.cancerimagingarchive.net/display/Public/CPTAC-LUAD" target="_blank">here</a> This release includes over 4500 files and 914 GB of data. <ul><li>Dataset imported into MassIVE from <a href="https://cptac-data-portal.georgetown.edu/study-summary/S046">https://cptac-data-portal.georgetown.edu/study-summary/S046</a> on 01/29/21</li></ul>

Project description:Bone development and regeneration is associated with the Wnt signaling pathway that, according to literature, can be modulated by lithium ions (Li+). The aim of this study was to evaluate the gene expression profile during peri-implant healing of poly(lactic-co-glycolic acid) (PLGA) implants with incorporated Li+, while PLGA without Li+ was used as control, and a special attention was then paid to the Wnt signaling pathway. The implants were inserted in rat tibia for 7 or 28 days and the gene expression profile was investigated using a genome-wide microarray analysis. The results were verified by qPCR and immunohistochemistry. Histomorphometry was used to evaluate the possible effect of Li+ on bone regeneration. The microarray analysis revealed a large number of significantly differentially regulated genes over time within the two implant groups. The Wnt signaling pathway was significantly affected by Li+, with approximately 34% of all Wnt-related markers regulated over time, compared to 22% for non-Li+ containing (control; Ctrl) implants. Functional cluster analysis indicated skeletal system morphogenesis, cartilage development and condensation as related to Li+. The downstream Wnt target gene, FOSL1, and the extracellular protein-encoding gene, ASPN, were significantly upregulated by Li+ compared with Ctrl. The presence of β-catenin, FOSL1 and ASPN positive cells was confirmed around implants of both groups. Interestingly, a significantly reduced bone area was observed over time around both implant groups. The presence of periostin and calcitonin receptor-positive cells was observed at both time points. This study is to the best of the authors’ knowledge the first report evaluating the effect of a local release of Li+ from PLGA at the fracture site. The present study shows that during the current time frame and with the present dose of Li+ in PLGA implants, Li+ is not an enhancer of early bone growth, although it affects the Wnt signaling pathway.

Dataset Information

National Cancer Institute (NCI) TARGET: Therapeutically Applicable Research to Generate Effective Treatments

Publications

The genetic landscape of high-risk neuroblastoma.

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