Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network

Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin d...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cell stem cell 2010-06, Vol.6 (6), p.591-602
Hauptverfasser: Aiden, Aviva Presser, Rivera, Miguel N., Rheinbay, Esther, Ku, Manching, Coffman, Erik J., Truong, Thanh T., Vargas, Sara O., Lander, Eric S., Haber, Daniel A., Bernstein, Bradley E.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 602
container_issue 6
container_start_page 591
container_title Cell stem cell
container_volume 6
creator Aiden, Aviva Presser
Rivera, Miguel N.
Rheinbay, Esther
Ku, Manching
Coffman, Erik J.
Truong, Thanh T.
Vargas, Sara O.
Lander, Eric S.
Haber, Daniel A.
Bernstein, Bradley E.
description Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin domains previously observed in ESCs. In the cancer, these domains frequently correspond to genes that are critical for kidney development and expressed in the renal stem cell compartment. Wilms cells also express “embryonic” chromatin regulators and maintain stem cell-like p16 silencing. Finally, Wilms and ESCs both exhibit “bivalent” chromatin modifications at silent promoters that may be poised for activation. In Wilms tumor, bivalent promoters correlate to genes expressed in specific kidney compartments and point to a kidney-specific differentiation program arrested at an early-progenitor stage. We suggest that Wilms cells share a transcriptional and epigenetic landscape with a normal renal stem cell, which is inherently susceptible to transformation and may represent a cell of origin for this disease. ► Chromatin profiles of primary Wilms tumors compared to normal cells ► Tumor cells resemble renal progenitors with arrested differentiation ► Data point to renal stem cells being the cell of origin for this disease
doi_str_mv 10.1016/j.stem.2010.03.016
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2897075</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1934590910001451</els_id><sourcerecordid>754531362</sourcerecordid><originalsourceid>FETCH-LOGICAL-c582t-30233c043ac0b38f171306f9b3b3382d53d850c3c4eb84e78a13fe22835d26ee3</originalsourceid><addsrcrecordid>eNp9kU2PFCEQhjtG437oH_BguBhPPQLVNHRiTDaj65ps1Ogaj4Smq3cY6WYEZoz_XiYzrnoxhFBUPfUBb1U9YXTBKGtfrBcp47TgtDgoLIrrXnXKlBR1J6W8X-wOmlp0tDupzlJaUyoko_JhdcKpaLuyTiv91fkpkZvtFCJZrmKYTHYz-RjD6DwmcuVuV77sTD6XXmSJ3u-DG4zZlbCZB2LIJ5yNJ69xhz5sJpxzub3H_CPEb4-qB6PxCR8fz_Pqy-Wbm-VVff3h7bvlxXVtheK5BsoBLG3AWNqDGplkQNux66EHUHwQMChBLdgGe9WgVIbBiJwrEANvEeG8enWou9n2Ew62DBGN15voJhN_6mCc_jcyu5W-DTvNVSepFKXA82OBGL5vMWU9uWTLc82MYZu0FI0ABi0vJD-QNoaUIo53XRjVe2H0Wu-F0XthNAVdXCXp6d_z3aX8VqIAz46ASdb4MZrZuvSHgwJyIQv38sBh-c2dw6iTdThbHFxEm_UQ3P_m-AWY9K1m</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>754531362</pqid></control><display><type>article</type><title>Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via ScienceDirect (Elsevier)</source><creator>Aiden, Aviva Presser ; Rivera, Miguel N. ; Rheinbay, Esther ; Ku, Manching ; Coffman, Erik J. ; Truong, Thanh T. ; Vargas, Sara O. ; Lander, Eric S. ; Haber, Daniel A. ; Bernstein, Bradley E.</creator><creatorcontrib>Aiden, Aviva Presser ; Rivera, Miguel N. ; Rheinbay, Esther ; Ku, Manching ; Coffman, Erik J. ; Truong, Thanh T. ; Vargas, Sara O. ; Lander, Eric S. ; Haber, Daniel A. ; Bernstein, Bradley E.</creatorcontrib><description>Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin domains previously observed in ESCs. In the cancer, these domains frequently correspond to genes that are critical for kidney development and expressed in the renal stem cell compartment. Wilms cells also express “embryonic” chromatin regulators and maintain stem cell-like p16 silencing. Finally, Wilms and ESCs both exhibit “bivalent” chromatin modifications at silent promoters that may be poised for activation. In Wilms tumor, bivalent promoters correlate to genes expressed in specific kidney compartments and point to a kidney-specific differentiation program arrested at an early-progenitor stage. We suggest that Wilms cells share a transcriptional and epigenetic landscape with a normal renal stem cell, which is inherently susceptible to transformation and may represent a cell of origin for this disease. ► Chromatin profiles of primary Wilms tumors compared to normal cells ► Tumor cells resemble renal progenitors with arrested differentiation ► Data point to renal stem cells being the cell of origin for this disease</description><identifier>ISSN: 1934-5909</identifier><identifier>EISSN: 1875-9777</identifier><identifier>DOI: 10.1016/j.stem.2010.03.016</identifier><identifier>PMID: 20569696</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; Biological and medical sciences ; Cell Differentiation - genetics ; Cell differentiation, maturation, development, hematopoiesis ; Cell physiology ; Cell Transformation, Neoplastic - genetics ; CELLCYCLE ; Chromatin - genetics ; Chromatin - metabolism ; Chromatin Immunoprecipitation ; Chromatin. Chromosome ; Cyclin-Dependent Kinase Inhibitor p16 ; DNA Methylation ; Embryonic Stem Cells - metabolism ; Embryonic Stem Cells - pathology ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Developmental ; Gene Regulatory Networks ; Genome-Wide Association Study ; Humans ; Kidney - metabolism ; Kidney - pathology ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Kidney Neoplasms - physiopathology ; Kidneys ; Medical sciences ; Molecular and cellular biology ; Molecular genetics ; Mutation - genetics ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Nephrology. Urinary tract diseases ; Organ Specificity ; STEMCELL ; Transcription, Genetic ; Tumor Suppressor Proteins - biosynthesis ; Tumor Suppressor Proteins - genetics ; Tumors of the urinary system ; Wilms Tumor - genetics ; Wilms Tumor - pathology ; Wilms Tumor - physiopathology</subject><ispartof>Cell stem cell, 2010-06, Vol.6 (6), p.591-602</ispartof><rights>2010 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c582t-30233c043ac0b38f171306f9b3b3382d53d850c3c4eb84e78a13fe22835d26ee3</citedby><cites>FETCH-LOGICAL-c582t-30233c043ac0b38f171306f9b3b3382d53d850c3c4eb84e78a13fe22835d26ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.stem.2010.03.016$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=23056257$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20569696$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aiden, Aviva Presser</creatorcontrib><creatorcontrib>Rivera, Miguel N.</creatorcontrib><creatorcontrib>Rheinbay, Esther</creatorcontrib><creatorcontrib>Ku, Manching</creatorcontrib><creatorcontrib>Coffman, Erik J.</creatorcontrib><creatorcontrib>Truong, Thanh T.</creatorcontrib><creatorcontrib>Vargas, Sara O.</creatorcontrib><creatorcontrib>Lander, Eric S.</creatorcontrib><creatorcontrib>Haber, Daniel A.</creatorcontrib><creatorcontrib>Bernstein, Bradley E.</creatorcontrib><title>Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network</title><title>Cell stem cell</title><addtitle>Cell Stem Cell</addtitle><description>Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin domains previously observed in ESCs. In the cancer, these domains frequently correspond to genes that are critical for kidney development and expressed in the renal stem cell compartment. Wilms cells also express “embryonic” chromatin regulators and maintain stem cell-like p16 silencing. Finally, Wilms and ESCs both exhibit “bivalent” chromatin modifications at silent promoters that may be poised for activation. In Wilms tumor, bivalent promoters correlate to genes expressed in specific kidney compartments and point to a kidney-specific differentiation program arrested at an early-progenitor stage. We suggest that Wilms cells share a transcriptional and epigenetic landscape with a normal renal stem cell, which is inherently susceptible to transformation and may represent a cell of origin for this disease. ► Chromatin profiles of primary Wilms tumors compared to normal cells ► Tumor cells resemble renal progenitors with arrested differentiation ► Data point to renal stem cells being the cell of origin for this disease</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - genetics</subject><subject>Cell differentiation, maturation, development, hematopoiesis</subject><subject>Cell physiology</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>CELLCYCLE</subject><subject>Chromatin - genetics</subject><subject>Chromatin - metabolism</subject><subject>Chromatin Immunoprecipitation</subject><subject>Chromatin. Chromosome</subject><subject>Cyclin-Dependent Kinase Inhibitor p16</subject><subject>DNA Methylation</subject><subject>Embryonic Stem Cells - metabolism</subject><subject>Embryonic Stem Cells - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Regulatory Networks</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidney Neoplasms - physiopathology</subject><subject>Kidneys</subject><subject>Medical sciences</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutation - genetics</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Organ Specificity</subject><subject>STEMCELL</subject><subject>Transcription, Genetic</subject><subject>Tumor Suppressor Proteins - biosynthesis</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumors of the urinary system</subject><subject>Wilms Tumor - genetics</subject><subject>Wilms Tumor - pathology</subject><subject>Wilms Tumor - physiopathology</subject><issn>1934-5909</issn><issn>1875-9777</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2PFCEQhjtG437oH_BguBhPPQLVNHRiTDaj65ps1Ogaj4Smq3cY6WYEZoz_XiYzrnoxhFBUPfUBb1U9YXTBKGtfrBcp47TgtDgoLIrrXnXKlBR1J6W8X-wOmlp0tDupzlJaUyoko_JhdcKpaLuyTiv91fkpkZvtFCJZrmKYTHYz-RjD6DwmcuVuV77sTD6XXmSJ3u-DG4zZlbCZB2LIJ5yNJ69xhz5sJpxzub3H_CPEb4-qB6PxCR8fz_Pqy-Wbm-VVff3h7bvlxXVtheK5BsoBLG3AWNqDGplkQNux66EHUHwQMChBLdgGe9WgVIbBiJwrEANvEeG8enWou9n2Ew62DBGN15voJhN_6mCc_jcyu5W-DTvNVSepFKXA82OBGL5vMWU9uWTLc82MYZu0FI0ABi0vJD-QNoaUIo53XRjVe2H0Wu-F0XthNAVdXCXp6d_z3aX8VqIAz46ASdb4MZrZuvSHgwJyIQv38sBh-c2dw6iTdThbHFxEm_UQ3P_m-AWY9K1m</recordid><startdate>20100604</startdate><enddate>20100604</enddate><creator>Aiden, Aviva Presser</creator><creator>Rivera, Miguel N.</creator><creator>Rheinbay, Esther</creator><creator>Ku, Manching</creator><creator>Coffman, Erik J.</creator><creator>Truong, Thanh T.</creator><creator>Vargas, Sara O.</creator><creator>Lander, Eric S.</creator><creator>Haber, Daniel A.</creator><creator>Bernstein, Bradley E.</creator><general>Elsevier Inc</general><general>Cell Press</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20100604</creationdate><title>Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network</title><author>Aiden, Aviva Presser ; Rivera, Miguel N. ; Rheinbay, Esther ; Ku, Manching ; Coffman, Erik J. ; Truong, Thanh T. ; Vargas, Sara O. ; Lander, Eric S. ; Haber, Daniel A. ; Bernstein, Bradley E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c582t-30233c043ac0b38f171306f9b3b3382d53d850c3c4eb84e78a13fe22835d26ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - genetics</topic><topic>Cell differentiation, maturation, development, hematopoiesis</topic><topic>Cell physiology</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>CELLCYCLE</topic><topic>Chromatin - genetics</topic><topic>Chromatin - metabolism</topic><topic>Chromatin Immunoprecipitation</topic><topic>Chromatin. Chromosome</topic><topic>Cyclin-Dependent Kinase Inhibitor p16</topic><topic>DNA Methylation</topic><topic>Embryonic Stem Cells - metabolism</topic><topic>Embryonic Stem Cells - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Gene Regulatory Networks</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Kidney Neoplasms - physiopathology</topic><topic>Kidneys</topic><topic>Medical sciences</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutation - genetics</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Organ Specificity</topic><topic>STEMCELL</topic><topic>Transcription, Genetic</topic><topic>Tumor Suppressor Proteins - biosynthesis</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumors of the urinary system</topic><topic>Wilms Tumor - genetics</topic><topic>Wilms Tumor - pathology</topic><topic>Wilms Tumor - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aiden, Aviva Presser</creatorcontrib><creatorcontrib>Rivera, Miguel N.</creatorcontrib><creatorcontrib>Rheinbay, Esther</creatorcontrib><creatorcontrib>Ku, Manching</creatorcontrib><creatorcontrib>Coffman, Erik J.</creatorcontrib><creatorcontrib>Truong, Thanh T.</creatorcontrib><creatorcontrib>Vargas, Sara O.</creatorcontrib><creatorcontrib>Lander, Eric S.</creatorcontrib><creatorcontrib>Haber, Daniel A.</creatorcontrib><creatorcontrib>Bernstein, Bradley E.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell stem cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aiden, Aviva Presser</au><au>Rivera, Miguel N.</au><au>Rheinbay, Esther</au><au>Ku, Manching</au><au>Coffman, Erik J.</au><au>Truong, Thanh T.</au><au>Vargas, Sara O.</au><au>Lander, Eric S.</au><au>Haber, Daniel A.</au><au>Bernstein, Bradley E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network</atitle><jtitle>Cell stem cell</jtitle><addtitle>Cell Stem Cell</addtitle><date>2010-06-04</date><risdate>2010</risdate><volume>6</volume><issue>6</issue><spage>591</spage><epage>602</epage><pages>591-602</pages><issn>1934-5909</issn><eissn>1875-9777</eissn><abstract>Wilms tumor is the most common pediatric kidney cancer. To identify transcriptional and epigenetic mechanisms that drive this disease, we compared genome-wide chromatin profiles of Wilms tumors, embryonic stem cells (ESCs), and normal kidney. Wilms tumors prominently exhibit large active chromatin domains previously observed in ESCs. In the cancer, these domains frequently correspond to genes that are critical for kidney development and expressed in the renal stem cell compartment. Wilms cells also express “embryonic” chromatin regulators and maintain stem cell-like p16 silencing. Finally, Wilms and ESCs both exhibit “bivalent” chromatin modifications at silent promoters that may be poised for activation. In Wilms tumor, bivalent promoters correlate to genes expressed in specific kidney compartments and point to a kidney-specific differentiation program arrested at an early-progenitor stage. We suggest that Wilms cells share a transcriptional and epigenetic landscape with a normal renal stem cell, which is inherently susceptible to transformation and may represent a cell of origin for this disease. ► Chromatin profiles of primary Wilms tumors compared to normal cells ► Tumor cells resemble renal progenitors with arrested differentiation ► Data point to renal stem cells being the cell of origin for this disease</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>20569696</pmid><doi>10.1016/j.stem.2010.03.016</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1934-5909
ispartof Cell stem cell, 2010-06, Vol.6 (6), p.591-602
issn 1934-5909
1875-9777
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2897075
source MEDLINE; Cell Press Free Archives; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via ScienceDirect (Elsevier)
subjects Adaptor Proteins, Signal Transducing
Biological and medical sciences
Cell Differentiation - genetics
Cell differentiation, maturation, development, hematopoiesis
Cell physiology
Cell Transformation, Neoplastic - genetics
CELLCYCLE
Chromatin - genetics
Chromatin - metabolism
Chromatin Immunoprecipitation
Chromatin. Chromosome
Cyclin-Dependent Kinase Inhibitor p16
DNA Methylation
Embryonic Stem Cells - metabolism
Embryonic Stem Cells - pathology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Developmental
Gene Regulatory Networks
Genome-Wide Association Study
Humans
Kidney - metabolism
Kidney - pathology
Kidney Neoplasms - genetics
Kidney Neoplasms - pathology
Kidney Neoplasms - physiopathology
Kidneys
Medical sciences
Molecular and cellular biology
Molecular genetics
Mutation - genetics
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
Nephrology. Urinary tract diseases
Organ Specificity
STEMCELL
Transcription, Genetic
Tumor Suppressor Proteins - biosynthesis
Tumor Suppressor Proteins - genetics
Tumors of the urinary system
Wilms Tumor - genetics
Wilms Tumor - pathology
Wilms Tumor - physiopathology
title Wilms Tumor Chromatin Profiles Highlight Stem Cell Properties and a Renal Developmental Network
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T00%3A48%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Wilms%20Tumor%20Chromatin%20Profiles%20Highlight%20Stem%20Cell%20Properties%20and%20a%20Renal%20Developmental%20Network&rft.jtitle=Cell%20stem%20cell&rft.au=Aiden,%20Aviva%20Presser&rft.date=2010-06-04&rft.volume=6&rft.issue=6&rft.spage=591&rft.epage=602&rft.pages=591-602&rft.issn=1934-5909&rft.eissn=1875-9777&rft_id=info:doi/10.1016/j.stem.2010.03.016&rft_dat=%3Cproquest_pubme%3E754531362%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=754531362&rft_id=info:pmid/20569696&rft_els_id=S1934590910001451&rfr_iscdi=true