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...
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Veröffentlicht in: | Cell stem cell 2010-06, Vol.6 (6), p.591-602 |
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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 |
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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>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23056257$$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> |
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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 |
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