The SFRP family of WNT inhibitors function as novel tumor suppressor genes epigenetically silenced in medulloblastoma
Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Dysregulation of WNT signaling occurs in up to 20% of cases. Using a genome-wide approach, we identified the secreted frizzled-related protein 1, 2 and 3 ( SFRP1, SFRP2 and SFRP3 ) family of WNT inhibitors as putative tumor sup...
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description | Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Dysregulation of WNT signaling occurs in up to 20% of cases. Using a genome-wide approach, we identified the
secreted frizzled-related protein 1, 2 and 3
(
SFRP1, SFRP2
and
SFRP3
) family of WNT inhibitors as putative tumor suppressor genes silenced by promoter region methylation in MB.
SFRP1, SFRP2
and
SFRP3
expression increased after 5-aza-2′-deoxycytidine treatment.
SFRP1
,
SFRP2
and
SFRP3
methylation was identified in 23.5, 3.9 and 15.7% of primary MB specimens, respectively, by methylation-specific PCR. Stable
SFRP1, SFRP2
and
SFRP3
expression reduced phospho-DVL2 levels and hindered MB cell proliferation and colony formation in soft agar
in vitro
. In 60% of primary tumors,
SFRP1
was expressed at levels twofold lower than that in normal cerebellum.
SFRP1
expression impaired tumor formation
in vivo
in flank and orthotopic intracerebellar xenograft models and conferred a significant survival advantage (
P |
doi_str_mv | 10.1038/onc.2010.32 |
format | Article |
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secreted frizzled-related protein 1, 2 and 3
(
SFRP1, SFRP2
and
SFRP3
) family of WNT inhibitors as putative tumor suppressor genes silenced by promoter region methylation in MB.
SFRP1, SFRP2
and
SFRP3
expression increased after 5-aza-2′-deoxycytidine treatment.
SFRP1
,
SFRP2
and
SFRP3
methylation was identified in 23.5, 3.9 and 15.7% of primary MB specimens, respectively, by methylation-specific PCR. Stable
SFRP1, SFRP2
and
SFRP3
expression reduced phospho-DVL2 levels and hindered MB cell proliferation and colony formation in soft agar
in vitro
. In 60% of primary tumors,
SFRP1
was expressed at levels twofold lower than that in normal cerebellum.
SFRP1
expression impaired tumor formation
in vivo
in flank and orthotopic intracerebellar xenograft models and conferred a significant survival advantage (
P
<0.0001). We identify for the first time tumor suppressor gene function of
SFRP
genes in MB, and suggest that loss of WNT pathway inhibition due to
SFRP
gene silencing is an additional mechanism that may contribute to excessive WNT signaling in this disease.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2010.32</identifier><identifier>PMID: 20208569</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/208/176/2016 ; 631/67/1922 ; 631/67/581 ; 631/80/86 ; Adaptor Proteins, Signal Transducing - antagonists & inhibitors ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Apoptosis ; Biological and medical sciences ; Brain cancer ; Brain tumors ; Cell Biology ; Cell Line, Tumor ; Cell physiology ; Cell proliferation ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cellular signal transduction ; Cerebellum ; Cerebellum - metabolism ; Cerebellum - pathology ; Dishevelled protein ; Dishevelled Proteins ; DNA Methylation ; Frizzled protein ; Frizzled-related protein ; Frizzled-related protein 1 ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genes ; Genes, Tumor Suppressor - physiology ; Genetic aspects ; Genomes ; Genomics ; Glycoproteins - genetics ; Glycoproteins - metabolism ; Health aspects ; Human Genetics ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; Intercellular Signaling Peptides and Proteins - metabolism ; Internal Medicine ; Medical sciences ; Medicine ; Medicine & Public Health ; Medulloblastoma ; Medulloblastoma - genetics ; Medulloblastoma - metabolism ; Medulloblastoma - pathology ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Nude ; Molecular and cellular biology ; Neurology ; Oncology ; Pediatrics ; Phosphoproteins - antagonists & inhibitors ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Phosphorylation ; Physiological aspects ; Promoter Regions, Genetic ; Proteins ; Risk factors ; short-communication ; Signal transduction ; Survival Rate ; Tumor suppressor genes ; Tumors of the nervous system. Phacomatoses ; Wnt protein ; Wnt Proteins - metabolism ; Xenograft Model Antitumor Assays ; Xenografts</subject><ispartof>Oncogene, 2010-05, Vol.29 (20), p.3017-3024</ispartof><rights>Macmillan Publishers Limited 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2010.</rights><rights>Copyright Nature Publishing Group May 20, 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-2d0f472ae85ab6ad59ab69da2b09f7733052a065be1827e42624b3c8817d6ea83</citedby><cites>FETCH-LOGICAL-c509t-2d0f472ae85ab6ad59ab69da2b09f7733052a065be1827e42624b3c8817d6ea83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2010.32$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2010.32$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22838451$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20208569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kongkham, P N</creatorcontrib><creatorcontrib>Northcott, P A</creatorcontrib><creatorcontrib>Croul, S E</creatorcontrib><creatorcontrib>Smith, C A</creatorcontrib><creatorcontrib>Taylor, M D</creatorcontrib><creatorcontrib>Rutka, J T</creatorcontrib><title>The SFRP family of WNT inhibitors function as novel tumor suppressor genes epigenetically silenced in medulloblastoma</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Dysregulation of WNT signaling occurs in up to 20% of cases. Using a genome-wide approach, we identified the
secreted frizzled-related protein 1, 2 and 3
(
SFRP1, SFRP2
and
SFRP3
) family of WNT inhibitors as putative tumor suppressor genes silenced by promoter region methylation in MB.
SFRP1, SFRP2
and
SFRP3
expression increased after 5-aza-2′-deoxycytidine treatment.
SFRP1
,
SFRP2
and
SFRP3
methylation was identified in 23.5, 3.9 and 15.7% of primary MB specimens, respectively, by methylation-specific PCR. Stable
SFRP1, SFRP2
and
SFRP3
expression reduced phospho-DVL2 levels and hindered MB cell proliferation and colony formation in soft agar
in vitro
. In 60% of primary tumors,
SFRP1
was expressed at levels twofold lower than that in normal cerebellum.
SFRP1
expression impaired tumor formation
in vivo
in flank and orthotopic intracerebellar xenograft models and conferred a significant survival advantage (
P
<0.0001). We identify for the first time tumor suppressor gene function of
SFRP
genes in MB, and suggest that loss of WNT pathway inhibition due to
SFRP
gene silencing is an additional mechanism that may contribute to excessive WNT signaling in this disease.</description><subject>631/208/176/2016</subject><subject>631/67/1922</subject><subject>631/67/581</subject><subject>631/80/86</subject><subject>Adaptor Proteins, Signal Transducing - antagonists & inhibitors</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell physiology</subject><subject>Cell proliferation</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cellular signal transduction</subject><subject>Cerebellum</subject><subject>Cerebellum - metabolism</subject><subject>Cerebellum - pathology</subject><subject>Dishevelled protein</subject><subject>Dishevelled Proteins</subject><subject>DNA Methylation</subject><subject>Frizzled protein</subject><subject>Frizzled-related protein</subject><subject>Frizzled-related protein 1</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Genes</subject><subject>Genes, Tumor Suppressor - physiology</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - metabolism</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Internal Medicine</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Medulloblastoma</subject><subject>Medulloblastoma - genetics</subject><subject>Medulloblastoma - metabolism</subject><subject>Medulloblastoma - pathology</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular and cellular biology</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Pediatrics</subject><subject>Phosphoproteins - antagonists & inhibitors</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Promoter Regions, Genetic</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>short-communication</subject><subject>Signal transduction</subject><subject>Survival Rate</subject><subject>Tumor suppressor genes</subject><subject>Tumors of the nervous system. Phacomatoses</subject><subject>Wnt protein</subject><subject>Wnt Proteins - metabolism</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkt9rFDEQxxdRbK0--S5BER_0zuwk2U0eS7EqFBU98TFks7PXlGxyTXaF_vfmvNNDqUgeZkI-853Mj6p6XNNlTZl8HYNdAi03Bneq45q3zUIIxe9Wx1QJulDA4Kh6kPMVpbRVFO5XR0CBStGo42peXSL5cv75ExnM6PwNiQP59mFFXLh0nZtiymSYg51cDMRkEuJ39GSax5hInjebhDkXd40BM8GN2zqTs8YXpew8Bot90SIj9rP3sfMmT3E0D6t7g_EZH-3tSfX1_M3q7N3i4uPb92enFwsrqJoW0NOBt2BQCtM1pheqGNUb6Kga2pYxKsDQRnRYS2iRQwO8Y1bKuu0bNJKdVC92upsUr2fMkx5dtui9CRjnrFvOm1pIBv8nGWO8UXyr-fQv8irOKZQyNKsBGlGaW6Bn_4Kg4TWnnIE6UGvjUbswxCkZu02sTwHaRjDZikItb6HK6XF0NgYcSqP_DHi5C7Ap5pxw0JvkRpNudE31dmV0WRm9XRn9s_In-6_OXRnTb_bXjhTg-R4wuUx2SCZYlw8cSCa5qAv3asfl8hTWmA4135b3Bxvb1XE</recordid><startdate>20100520</startdate><enddate>20100520</enddate><creator>Kongkham, P N</creator><creator>Northcott, P A</creator><creator>Croul, S E</creator><creator>Smith, C A</creator><creator>Taylor, M D</creator><creator>Rutka, J T</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100520</creationdate><title>The SFRP family of WNT inhibitors function as novel tumor suppressor genes epigenetically silenced in medulloblastoma</title><author>Kongkham, P N ; Northcott, P A ; Croul, S E ; Smith, C A ; Taylor, M D ; Rutka, J T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-2d0f472ae85ab6ad59ab69da2b09f7733052a065be1827e42624b3c8817d6ea83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/208/176/2016</topic><topic>631/67/1922</topic><topic>631/67/581</topic><topic>631/80/86</topic><topic>Adaptor Proteins, Signal Transducing - antagonists & inhibitors</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Brain cancer</topic><topic>Brain tumors</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell physiology</topic><topic>Cell proliferation</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cellular signal transduction</topic><topic>Cerebellum</topic><topic>Cerebellum - metabolism</topic><topic>Cerebellum - pathology</topic><topic>Dishevelled protein</topic><topic>Dishevelled Proteins</topic><topic>DNA Methylation</topic><topic>Frizzled protein</topic><topic>Frizzled-related protein</topic><topic>Frizzled-related protein 1</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Genes</topic><topic>Genes, Tumor Suppressor - physiology</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Genomics</topic><topic>Glycoproteins - genetics</topic><topic>Glycoproteins - metabolism</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - metabolism</topic><topic>Internal Medicine</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Medulloblastoma</topic><topic>Medulloblastoma - genetics</topic><topic>Medulloblastoma - metabolism</topic><topic>Medulloblastoma - pathology</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Molecular and cellular biology</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Pediatrics</topic><topic>Phosphoproteins - antagonists & inhibitors</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Promoter Regions, Genetic</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>short-communication</topic><topic>Signal transduction</topic><topic>Survival Rate</topic><topic>Tumor suppressor genes</topic><topic>Tumors of the nervous system. Phacomatoses</topic><topic>Wnt protein</topic><topic>Wnt Proteins - metabolism</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kongkham, P N</creatorcontrib><creatorcontrib>Northcott, P A</creatorcontrib><creatorcontrib>Croul, S E</creatorcontrib><creatorcontrib>Smith, C A</creatorcontrib><creatorcontrib>Taylor, M D</creatorcontrib><creatorcontrib>Rutka, J T</creatorcontrib><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>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kongkham, P N</au><au>Northcott, P A</au><au>Croul, S E</au><au>Smith, C A</au><au>Taylor, M D</au><au>Rutka, J T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The SFRP family of WNT inhibitors function as novel tumor suppressor genes epigenetically silenced in medulloblastoma</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2010-05-20</date><risdate>2010</risdate><volume>29</volume><issue>20</issue><spage>3017</spage><epage>3024</epage><pages>3017-3024</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Dysregulation of WNT signaling occurs in up to 20% of cases. Using a genome-wide approach, we identified the
secreted frizzled-related protein 1, 2 and 3
(
SFRP1, SFRP2
and
SFRP3
) family of WNT inhibitors as putative tumor suppressor genes silenced by promoter region methylation in MB.
SFRP1, SFRP2
and
SFRP3
expression increased after 5-aza-2′-deoxycytidine treatment.
SFRP1
,
SFRP2
and
SFRP3
methylation was identified in 23.5, 3.9 and 15.7% of primary MB specimens, respectively, by methylation-specific PCR. Stable
SFRP1, SFRP2
and
SFRP3
expression reduced phospho-DVL2 levels and hindered MB cell proliferation and colony formation in soft agar
in vitro
. In 60% of primary tumors,
SFRP1
was expressed at levels twofold lower than that in normal cerebellum.
SFRP1
expression impaired tumor formation
in vivo
in flank and orthotopic intracerebellar xenograft models and conferred a significant survival advantage (
P
<0.0001). We identify for the first time tumor suppressor gene function of
SFRP
genes in MB, and suggest that loss of WNT pathway inhibition due to
SFRP
gene silencing is an additional mechanism that may contribute to excessive WNT signaling in this disease.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20208569</pmid><doi>10.1038/onc.2010.32</doi><tpages>8</tpages></addata></record> |
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language | eng |
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source | MEDLINE; SpringerLink Journals; Nature; EZB-FREE-00999 freely available EZB journals |
subjects | 631/208/176/2016 631/67/1922 631/67/581 631/80/86 Adaptor Proteins, Signal Transducing - antagonists & inhibitors Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Animals Apoptosis Biological and medical sciences Brain cancer Brain tumors Cell Biology Cell Line, Tumor Cell physiology Cell proliferation Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cellular signal transduction Cerebellum Cerebellum - metabolism Cerebellum - pathology Dishevelled protein Dishevelled Proteins DNA Methylation Frizzled protein Frizzled-related protein Frizzled-related protein 1 Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation, Neoplastic Gene Silencing Genes Genes, Tumor Suppressor - physiology Genetic aspects Genomes Genomics Glycoproteins - genetics Glycoproteins - metabolism Health aspects Human Genetics Humans Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Internal Medicine Medical sciences Medicine Medicine & Public Health Medulloblastoma Medulloblastoma - genetics Medulloblastoma - metabolism Medulloblastoma - pathology Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Nude Molecular and cellular biology Neurology Oncology Pediatrics Phosphoproteins - antagonists & inhibitors Phosphoproteins - genetics Phosphoproteins - metabolism Phosphorylation Physiological aspects Promoter Regions, Genetic Proteins Risk factors short-communication Signal transduction Survival Rate Tumor suppressor genes Tumors of the nervous system. Phacomatoses Wnt protein Wnt Proteins - metabolism Xenograft Model Antitumor Assays Xenografts |
title | The SFRP family of WNT inhibitors function as novel tumor suppressor genes epigenetically silenced in medulloblastoma |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T03%3A20%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20SFRP%20family%20of%20WNT%20inhibitors%20function%20as%20novel%20tumor%20suppressor%20genes%20epigenetically%20silenced%20in%20medulloblastoma&rft.jtitle=Oncogene&rft.au=Kongkham,%20P%20N&rft.date=2010-05-20&rft.volume=29&rft.issue=20&rft.spage=3017&rft.epage=3024&rft.pages=3017-3024&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2010.32&rft_dat=%3Cgale_proqu%3EA227653875%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2641404329&rft_id=info:pmid/20208569&rft_galeid=A227653875&rfr_iscdi=true |