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{
  "results": [
    {
      "dataset.Disease": ["Cancer"],
      "dataset.Institution": ["Memorial Sloan Kettering Cancer Center"],
      "dataset.Internal_Name": ["Prostate cancer-MSKCC"],
      "dataset.Number_of_Samples": [261],
      "dataset.Posting_Restriction": ["unspecified"],
      "dataset.QC_statistician": ["Solly Sieberts"],
      "dataset.Species": ["Human"],
      "dataset.Tissue_Tumor": ["Prostate"],
      "dataset.Type": ["GCD"],
      "dataset.accessControlList": "/repo/v1/dataset/3733/acl",
      "dataset.citation": ["Integrative genomic profiling of human prostate cancer. Taylor BS et al., Cancer Cell. 2010 Jul 13;18(1):11-22.  "],
      "dataset.creationDate": 1312573506326,
      "dataset.creator": "Charles Sawyers",
      "dataset.curator": ["Matt Furia"],
      "dataset.description": "Genetic and epigenetic alterations have been identified that lead to transcriptional Annotation of prostate cancer genomes provides a foundation for discoveries that can impact disease understanding and treatment. Concordant assessment of DNA copy number, mRNA expression, and focused exon resequencing in the 218 prostate cancer tumors represented in this dataset haveidentified the nuclear receptor coactivator NCOA2 as an oncogene in approximately 11% of tumors. Additionally, the androgen-driven TMPRSS2-ERG fusion was associated with a previously unrecognized, prostate-specific deletion at chromosome 3p14 that implicates FOXP1, RYBP, and SHQ1 as potential cooperative tumor suppressors. DNA copy-number data from primary tumors revealed that copy-number alterations robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score.  ",
      "dataset.eulaId": "3732",
      "dataset.hasClinicalData": true,
      "dataset.hasExpressionData": true,
      "dataset.hasGeneticData": true,
      "dataset.id": "3733",
      "dataset.last_modified_date": [1243987200000],
      "dataset.layers": "/repo/v1/dataset/3733/layer",
      "dataset.locations": "/repo/v1/dataset/3733/location",
      "dataset.name": "MSKCC Prostate Cancer",
      "dataset.number_of_downloads": [32],
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      "dataset.parentId": "3731",
      "dataset.pubmed_id": [20579941],
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      "dataset.status": "Current",
      "dataset.version": "1.0.0"
    },
    {
      "dataset.Disease": ["Metabolic Disease"],
      "dataset.Institution": ["UCLA/  Merck & Co."],
      "dataset.Internal_Name": ["BxD"],
      "dataset.Number_of_Samples": [111],
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      "dataset.QC_statistician": ["Solly Sieberts"],
      "dataset.Species": ["Mouse"],
      "dataset.Tissue_Tumor": ["Liver"],
      "dataset.Type": ["GCD"],
      "dataset.accessControlList": "/repo/v1/dataset/3735/acl",
      "dataset.citation": ["Genetic loci determining bone density in mice with diet-induced atherosclerosis.  Drake TA, Schadt E, Hannani K, Kabo JM, Krass K, Colinayo V, Greaser LE 3rd, Goldin J, Lusis AJ. Physiol Genomics. 2001 Apr 27;5(4):205-15. PMID: 11328966   Genetics of gene expression surveyed in maize, mouse and man. Schadt EE, Monks SA, Drake TA, Lusis AJ, Che N, Colinayo V, Ruff TG, Milligan SB, Lamb JR, Cavet G, Linsley PS, Mao M, Stoughton RB, Friend SH. Nature. 2003 Mar 20;422(6929):297-302.PMID: 12646919 "],
      "dataset.creationDate": 1312573523697,
      "dataset.creator": "Jake Lusis/ Merck & Co.",
      "dataset.curator": ["Matt Furia"],
      "dataset.description": "111 female F2 progeny of a C57BL/6J and DBA/2J intercross were examined for multiple measures of femoral bone mass, density, and biomechanical properties using both computerized tomographic and radiographic methods. In addition, body weight and length, adipose tissue mass, plasma lipids and insulin, and aortic fatty lesions were assessed. Mice were on a rodent chow diet up to 12 months of age, and then switched to an atherogenic high-fat, high-cholesterol diet for another 4 months. Mice were killed at 16 months of age.  Liver tissue was profiled for expression traits using a custom mouse gene oligonucleotide microarray (Rosetta Inpharmatics) that contained 23,574 non-control oligonucleotide probes for mouse genes and 2,186 control probes. All microarrays were custom ink-jet microarrays fabricated by Agilent Technologies. A complete linkage map for all chromosomes except Y in mouse was constructed at an average density of 13cM using microsatellite markers. ",
      "dataset.eulaId": "3732",
      "dataset.hasClinicalData": true,
      "dataset.hasExpressionData": true,
      "dataset.hasGeneticData": true,
      "dataset.id": "3735",
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      "dataset.layers": "/repo/v1/dataset/3735/layer",
      "dataset.locations": "/repo/v1/dataset/3735/location",
      "dataset.name": "Mouse Model of Diet-Induced Atherosclerosis",
      "dataset.number_of_downloads": [60],
      "dataset.number_of_followers": [101],
      "dataset.parentId": "3731",
      "dataset.pubmed_id": [18406497],
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      "dataset.status": "Current",
      "dataset.version": "1.0.0"
    },
    {
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      "dataset.Institution": ["UCLA/  Merck & Co."],
      "dataset.Internal_Name": ["BxH ApoE"],
      "dataset.Number_of_Samples": [334],
      "dataset.Posting_Restriction": ["No Restriction"],
      "dataset.QC_statistician": ["Solly Sieberts"],
      "dataset.Species": ["Mouse"],
      "dataset.Tissue_Tumor": [
        "Adipose",
        "Liver",
        "Brain",
        "Muscle"
      ],
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      "dataset.accessControlList": "/repo/v1/dataset/3736/acl",
      "dataset.citation": ["Integrating genetic and network analysis to characterize genes related to mouse weight. Ghazalpour, A., et al., PLoS Genet, 2006. 2(8): p. e130.  Dosage compensation is less effective in birds than in mammals. Itoh, Y., et al., J Biol, 2007. 6(1): p. 2.  Elucidating the murine brain transcriptional network in a segregating mouse population to identify core functional modules for obesity and diabetes.  Lum, P.Y., et al., J Neurochem, 2006. 97 Suppl 1: p. 50-62.  Identification of Abcc6 as the major causal gene for dystrophic cardiac calcification in mice through integrative genomics. Meng, H., et al. Proc Natl Acad Sci U S A, 2007. 104(11): p. 4530-5.  Mapping the genetic architecture of gene expression in human liver. Schadt, E.E., et al.,  PLoS Biol, 2008. 6(5): p. e107.  Elucidating the role of gonadal hormones in sexually dimorphic gene coexpression networks.  van Nas, A., et al., Endocrinology, 2009. 150(3): p. 1235-49.  Identification of pathways for atherosclerosis in mice: integration of quantitative trait locus analysis and global gene expression data. Wang, S.S., et al., Circ Res, 2007. 101(3): p. e11-30.  Tissue-specific expression and regulation of sexually dimorphic genes in mice. Yang, X., et al., Genome Res, 2006. 16(8): p. 995-1004. "],
      "dataset.creationDate": 1312573525824,
      "dataset.creator": "Jake Lusis/ Merck & Co.",
      "dataset.curator": ["Matt Furia"],
      "dataset.description": "C57BL/6J and C3H/HeJ inbred mouse strains exhibit dramatically different cardiovascular and metabolic phenotypes on the hyperlipidemic apolipoprotein E (Apoe) null background.  In order to identify the genes that contribute to these differences, we constructed an F2 intercross between the B6.Apoe-/- and C3H.Apoe-/- strains consisting of 334 animals.  The mice were fed on a chow diet until 8 weeks of age, then fed a high fat (42% fat) \"western\" diet for 16 weeks to exacerbate the phenotypes and euthanized at 24 weeks of age via cervical dislocation.  Prior to death, mice were fasted for 4 hours in the morning, anesthetized using Isoflurane, and weighed.   Blood was collected by retro-orbital bleed; plasma was frozen at -800C.  We measured plasma cholesterol, HDL, LDL, triglycerides, free fatty acids, glucose, insulin, leptin, adiponectin and PON1 activity levels.  Liver, brain, skeletal muscle (hamstring) and adipose (gonadal fat pad) were flash frozen in liquid nitrogen. RNA was isolated from the tissues using the Trizol method and utilized in microarray analysis on a custom 60mer Agilent chip (reference for chip would be useful).  Hepatic cholesterol, triglyceride and free fatty acid levels were also measured.  Hearts and aortae were extracted, perfused and fixed for atherosclerotic lesion analysis.  The aortic arch was serially sectioned through to the aortic sinus with every fifth 10um section stained with hematoxylin and oil-red-o, which specifically stains lipids.  Slides were examined by light microscopy.  The fatty streak lesion area was quantified using an ocular with a grid; forty sections per mouse were quantified and averaged.  Vascular calcification and aneurysm formation were also measured in a semi-quantitative manner based on presence or absence and size or severity. DNA was isolated from kidney using a phenol chloroform extraction method.  The mice were genotyped at 1500 SNPs using the ParAllele molecular inversion probe technology; 1353 SNPs passed quality control for a final marker density of 1.5cM. ",
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    "dataset.Species": ["Human"],
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    "dataset.description": "Genetic and epigenetic alterations have been identified that lead to transcriptional Annotation of prostate cancer genomes provides a foundation for discoveries that can impact disease understanding and treatment. Concordant assessment of DNA copy number, mRNA expression, and focused exon resequencing in the 218 prostate cancer tumors represented in this dataset haveidentified the nuclear receptor coactivator NCOA2 as an oncogene in approximately 11% of tumors. Additionally, the androgen-driven TMPRSS2-ERG fusion was associated with a previously unrecognized, prostate-specific deletion at chromosome 3p14 that implicates FOXP1, RYBP, and SHQ1 as potential cooperative tumor suppressors. DNA copy-number data from primary tumors revealed that copy-number alterations robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score.  ",
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    "dataset.pubmed_id": [20579941],
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}

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      "layer.name": "CNV",
      "layer.numSamples": 230,
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      "layer.platform": "Agilent 244K array comparative genomic hybridization (aCGH) microarrays",
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    {
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      "layer.colDesc_age": ["Age at diagnosis.."],
      "layer.colDesc_bcr_event": ["was a biochemical recurrance event detected"],
      "layer.colDesc_bcr_freetime": ["elapsed time before bichemical recurrance"],
      "layer.colDesc_chemotx": ["chemotherapy treatment"],
      "layer.colDesc_clinical_gleason_score": ["clinical tertiary gleason score"],
      "layer.colDesc_clinical_primary_gleason": ["clinical gleason score of the majority of the tumor"],
      "layer.colDesc_clinical_secondary_gleason": ["clinical gleason score of the minority of the tumor"],
      "layer.colDesc_clinical_tnm_stage_t": ["Cancer stage based on the Tumor, Node, Metastasis scoring system"],
      "layer.colDesc_copy_number_cluster": ["copy number cluster size"],
      "layer.colDesc_ethnicity": ["ethnicity of the individual"],
      "layer.colDesc_event": ["Cause of death"],
      "layer.colDesc_expression_array_tissue_source": ["Source of tissue used for expression profiling"],
      "layer.colDesc_extra_capsular_extension": ["extra-capsular extension: cancer extending beyond the prostate capsule"],
      "layer.colDesc_hormtx": ["Hormone treatment"],
      "layer.colDesc_metastatic_site": ["Site in the body where metastatic tumor was detected."],
      "layer.colDesc_metsevent": ["metastatic event"],
      "layer.colDesc_neoadjradtx": ["neo-adjuvant treatment"],
      "layer.colDesc_nomogram_nomopred_extra_capsular_extension": ["probability of extra capsular extension"],
      "layer.colDesc_nomogram_nomopred_lni": ["probability of lymph node involvement"],
      "layer.colDesc_nomogram_nomopred_ocd": ["probability of organ confined disease"],
      "layer.colDesc_nomogram_nomopred_seminal_vesicle_invasion": ["probability of seminal vesicle invasion"],
      "layer.colDesc_nomogram_pfp_postrp": ["nomogram progression-free probability post radical prostatectomy"],
      "layer.colDesc_number_nodes_positive": ["number node-positive nodes"],
      "layer.colDesc_number_nodes_removed": ["Number of cancerous nodes removed"],
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      "layer.colDesc_pathologic_tnm_stage_t": ["pathologic TNM \"T\" stage"],
      "layer.colDesc_pre_treatment_psa": ["Prostate specific antigen level prior to treatment"],
      "layer.colDesc_predxbxpsa": ["PSA prior to diagnostic biopsy"],
      "layer.colDesc_radtxtype": ["radiation treatment type"],
      "layer.colDesc_rp_type": ["Surgical treatment. RP=radical prostatectomy, LP=laproscopic prostatectomy, SALRP=Salvage radical prostatectomy"],
      "layer.colDesc_sample_type": ["Type of sample that was profiled. One of: Benign=benign tumor ,CELL LINE=cancer cell line , MET=metastatic tumor, PRIMARY=primary tumor or XENOGRAFT. "],
      "layer.colDesc_seminal_vesicle_invasion": ["seminal vesicle invasion. Either \"positive\" or \"negative\""],
      "layer.colDesc_sms": ["somatostatin"],
      "layer.colDesc_survtime": ["Survival time post-diagnosis"],
      "layer.colDesc_tnm_stage_n": ["TNM \"N\" stage"],
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      "layer.colUnits_bcr_event": ["factor"],
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  "agreement": "Copyright 2011 Sage Bionetworks\n\nLicensed under the Apache License, Version 2.0 (the \"License\"). You may not use this file except in compliance with the License. You may obtain a copy of the License at\n\n  http://www.apache.org/licenses/LICENSE-2.0\n\nUnless required by applicable law or agreed to in writing, software distributed under the License is distributed on an \"AS IS\" BASIS, WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied. See the License for the specific language governing permissions andlimitations under the License.\n\n1. Definitions.\n\n\"License\" shall mean the terms and conditions for use, reproduction, and distribution as defined by Sections 1 through 9 of this document.\n\n\"Licensor\" shall mean the copyright owner or entity authorized by the copyright owner that is granting the License.\n\n\"Legal Entity\" shall mean the union of the acting entity and all other entities that control, are controlled by, or are under common control with that entity. For the purposes of this definition, \"control\" means (i) the power, direct or indirect, to cause the direction or management of such entity, whether by contract or otherwise, or (ii) ownership of fifty percent (50%) or more of the outstanding shares, or (iii) beneficial ownership of such entity.\n\n\"You\" (or \"Your\") shall mean an individual or Legal Entity exercising permissions granted by this License.\n\n\"Source\" form shall mean the preferred form for making modifications, including but not limited to software source code, documentation source, and configuration files.\n\n\"Object\" form shall mean any form resulting from mechanical transformation or translation of a Source form, including but not limited to compiled object code, generated documentation, and conversions to other media types.\n\n\"Work\" shall mean the work of authorship, whether in Source or Object form, made available under the License, as indicated by a copyright notice that is included in or attached to the work (an example is provided in the Appendix below).\n\n\"Derivative Works\" shall mean any work, whether in Source or Object form, that is based on (or derived from) the Work and for which the editorial revisions, annotations, elaborations, or other modifications represent, as a whole, an original work of authorship. For the purposes of this License, Derivative Works shall not include works that remain separable from, or merely link (or bind by name) to the interfaces of, the Work and Derivative Works thereof.\n\n\"Contribution\" shall mean any work of authorship, including the original version of the Work and any modifications or additions to that Work or Derivative Works thereof, that is intentionally submitted to Licensor for inclusion in the Work by the copyright owner or by an individual or Legal Entity authorized to submit on behalf of the copyright owner. For the purposes of this definition, \"submitted\" means any form of electronic, verbal, or written communication sent to the Licensor or its representatives, including but not limited to communication on electronic mailing lists, source code control systems, and issue tracking systems that are managed by, or on behalf of, the Licensor for the purpose of discussing and improving the Work, but excluding communication that is conspicuously marked or otherwise designated in writing by the copyright owner as \"Not a Contribution.\"\n\n\"Contributor\" shall mean Licensor and any individual or Legal Entity on behalf of whom a Contribution has been received by Licensor and subsequently incorporated within the Work.\n\n2. Grant of Copyright License. Subject to the terms and conditions of this License, each Contributor hereby grants to You a perpetual, worldwide, non-exclusive, no-charge, royalty-free, irrevocable copyright license to reproduce, prepare Derivative Works of, publicly display, publicly perform, sublicense, and distribute the Work and such Derivative Works in Source or Object form.\n\n3. Grant of Patent License. Subject to the terms and conditions of this License, each Contributor hereby grants to You a perpetual, worldwide, non-exclusive, no-charge, royalty-free, irrevocable (except as stated in this section) patent license to make, have made, use, offer to sell, sell, import, and otherwise transfer the Work, where such license applies only to those patent claims licensable by such Contributor that are necessarily infringed by their Contribution(s) alone or by combination of their Contribution(s) with the Work to which such Contribution(s) was submitted. If You institute patent litigation against any entity (including a cross-claim or counterclaim in a lawsuit) alleging that the Work or a Contribution incorporated within the Work constitutes direct or contributory patent infringement, then any patent licenses granted to You under this License for that Work shall terminate as of the date such litigation is filed.\n\n4. Redistribution. You may reproduce and distribute copies of the Work or Derivative Works thereof in any medium, with or without modifications, and in Source or Object form, provided that You meet the following conditions:\n\nYou must give any other recipients of the Work or Derivative Works a copy of this License; and\n\nYou must cause any modified files to carry prominent notices stating that You changed the files; and\n\nYou must retain, in the Source form of any Derivative Works that You distribute, all copyright, patent, trademark, and attribution notices from the Source form of the Work, excluding those notices that do not pertain to any part of the Derivative Works; and\n\nIf the Work includes a \"NOTICE\" text file as part of its distribution, then any Derivative Works that You distribute must include a readable copy of the attribution notices contained within such NOTICE file, excluding those notices that do not pertain to any part of the Derivative Works, in at least one of the following places: within a NOTICE text file distributed as part of the Derivative Works; within the Source form or documentation, if provided along with the Derivative Works; or, within a display generated by the Derivative Works, if and wherever such third-party notices normally appear. The contents of the NOTICE file are for informational purposes only and do not modify the License. You may add Your own attribution notices within Derivative Works that You distribute, alongside or as an addendum to the NOTICE text from the Work, provided that such additional attribution notices cannot be construed as modifying the License. You may add Your own copyright statement to Your modifications and may provide additional or different license terms and conditions for use, reproduction, or distribution of Your modifications, or for any such Derivative Works as a whole, provided Your use, reproduction, and distribution of the Work otherwise complies with the conditions stated in this License.\n\n5. Submission of Contributions. Unless You explicitly state otherwise, any Contribution intentionally submitted for inclusion in the Work by You to the Licensor shall be under the terms and conditions of this License, without any additional terms or conditions. Notwithstanding the above, nothing herein shall supersede or modify the terms of any separate license agreement you may have executed with Licensor regarding such Contributions.\n\n6. Trademarks. This License does not grant permission to use the trade names, trademarks, service marks, or product names of the Licensor, except as required for reasonable and customary use in describing the origin of the Work and reproducing the content of the NOTICE file.\n\n7. Disclaimer of Warranty. Unless required by applicable law or agreed to in writing, Licensor provides the Work (and each Contributor provides its Contributions) on an \"AS IS\" BASIS, WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied, including, without limitation, any warranties or conditions of TITLE, NON-INFRINGEMENT, MERCHANTABILITY, or FITNESS FOR A PARTICULAR PURPOSE. You are solely responsible for determining the appropriateness of using or redistributing the Work an
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Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:06 GMT
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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
ETag: 0
Server: Apache-Coyote/1.1
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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

{
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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

{
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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

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HTTP/1.1 200 OK
Content-Type: application/json
Date: Wed, 05 Oct 2011 16:35:07 GMT
Server: Apache-Coyote/1.1
transfer-encoding: chunked
Connection: keep-alive

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