Histone Methyltransferase Gene SETD2 Is a Novel Tumor Suppressor Gene in Clear Cell Renal Cell Carcinoma
Sporadic clear cell renal cell carcinoma (cRCC) is genetically characterized by the recurrent loss of the short arm of chromosome 3, with a hotspot for copy number loss in the 3p21 region. We applied a method called "gene identification by nonsense-mediated mRNA decay inhibition" to a pane...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2010-06, Vol.70 (11), p.4287-4291 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | DUNS, Gerben VAN DEN BERG, Eva VAN DUIVENBODE, Inge OSINGA, Jan HOLLEMA, Harry HOFSTRA, Robert M. W KOK, Klaas |
| description | Sporadic clear cell renal cell carcinoma (cRCC) is genetically characterized by the recurrent loss of the short arm of chromosome 3, with a hotspot for copy number loss in the 3p21 region. We applied a method called "gene identification by nonsense-mediated mRNA decay inhibition" to a panel of 10 cRCC cell lines with 3p21 copy number loss to identify biallelic inactivated genes located at 3p21. This revealed inactivation of the histone methyltransferase gene SETD2, located on 3p21.31, as a common event in cRCC cells. SETD2 is nonredundantly responsible for trimethylation of the histone mark H3K36. Consistent with this function, we observed loss or a decrease of H3K36me3 in 7 out of the 10 cRCC cell lines. Identification of missense mutations in 2 out of 10 primary cRCC tumor samples added support to the involvement of loss of SETD2 function in the development of cRCC tumors. |
| doi_str_mv | 10.1158/0008-5472.can-10-0120 |
| format | Article |
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Identification of missense mutations in 2 out of 10 primary cRCC tumor samples added support to the involvement of loss of SETD2 function in the development of cRCC tumors.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.can-10-0120</identifier><identifier>PMID: 20501857</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adenocarcinoma, Clear Cell - enzymology ; Adenocarcinoma, Clear Cell - genetics ; Antineoplastic agents ; Biological and medical sciences ; Carcinoma, Renal Cell - enzymology ; Carcinoma, Renal Cell - genetics ; Cell Line, Tumor ; Chromosomes, Human, Pair 3 ; Comparative Genomic Hybridization ; DNA Methylation ; DNA Mutational Analysis ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Histone-Lysine N-Methyltransferase - genetics ; Humans ; Kidney Neoplasms - enzymology ; Kidney Neoplasms - genetics ; Kidneys ; Medical sciences ; Nephrology. Urinary tract diseases ; Oligonucleotide Array Sequence Analysis ; Pharmacology. Drug treatments ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tumors ; Tumors of the urinary system</subject><ispartof>Cancer research (Chicago, Ill.), 2010-06, Vol.70 (11), p.4287-4291</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright 2010 AACR.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-3f6f66485f08f7ec8b236236e30afe8a210cc928d4f8d80cf2836e8e1d22ca643</citedby><cites>FETCH-LOGICAL-c451t-3f6f66485f08f7ec8b236236e30afe8a210cc928d4f8d80cf2836e8e1d22ca643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22853074$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20501857$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DUNS, Gerben</creatorcontrib><creatorcontrib>VAN DEN BERG, Eva</creatorcontrib><creatorcontrib>VAN DUIVENBODE, Inge</creatorcontrib><creatorcontrib>OSINGA, Jan</creatorcontrib><creatorcontrib>HOLLEMA, Harry</creatorcontrib><creatorcontrib>HOFSTRA, Robert M. W</creatorcontrib><creatorcontrib>KOK, Klaas</creatorcontrib><title>Histone Methyltransferase Gene SETD2 Is a Novel Tumor Suppressor Gene in Clear Cell Renal Cell Carcinoma</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Sporadic clear cell renal cell carcinoma (cRCC) is genetically characterized by the recurrent loss of the short arm of chromosome 3, with a hotspot for copy number loss in the 3p21 region. We applied a method called "gene identification by nonsense-mediated mRNA decay inhibition" to a panel of 10 cRCC cell lines with 3p21 copy number loss to identify biallelic inactivated genes located at 3p21. This revealed inactivation of the histone methyltransferase gene SETD2, located on 3p21.31, as a common event in cRCC cells. SETD2 is nonredundantly responsible for trimethylation of the histone mark H3K36. Consistent with this function, we observed loss or a decrease of H3K36me3 in 7 out of the 10 cRCC cell lines. Identification of missense mutations in 2 out of 10 primary cRCC tumor samples added support to the involvement of loss of SETD2 function in the development of cRCC tumors.</description><subject>Adenocarcinoma, Clear Cell - enzymology</subject><subject>Adenocarcinoma, Clear Cell - genetics</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Renal Cell - enzymology</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Cell Line, Tumor</subject><subject>Chromosomes, Human, Pair 3</subject><subject>Comparative Genomic Hybridization</subject><subject>DNA Methylation</subject><subject>DNA Mutational Analysis</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Histone-Lysine N-Methyltransferase - genetics</subject><subject>Humans</subject><subject>Kidney Neoplasms - enzymology</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidneys</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Pharmacology. Drug treatments</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkG1LwzAQgIMobk5_gpIv4qfOvDRt_Djq3AZzgpufS5ZeWKVvJq2wf2_q5oSDXO6eu4QHoVtKxpQK-UgIkYEIYzbWqgooCQhl5AwNqeAyiMNQnKPhiRmgK-c-_VVQIi7RgBFBqBTxEO3muWvrCvArtLt90VpVOQNWOcAz8OX1dPPM8MJhhVf1NxR405W1xeuuaSw459NfLK9wUoCyOIGiwO9QqeKQJsrqvKpLdY0ujCoc3BzPEfp4mW6SebB8my2SyTLQoaBtwE1koiiUwhBpYtByy3jkAzhRBqRilGj9xGQWGplJog2TvimBZoxpFYV8hB4Oextbf3Xg2rTMnfZfURXUnUtjzimLJeWeFAdS29o5CyZtbF4qu08pSXvHae8v7f2lyWTVV3vHfu7u-EK3LSE7Tf1J9cD9EVBOq8J4pzp3_xyTgpM45D96JYOy</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>DUNS, Gerben</creator><creator>VAN DEN BERG, Eva</creator><creator>VAN DUIVENBODE, Inge</creator><creator>OSINGA, Jan</creator><creator>HOLLEMA, Harry</creator><creator>HOFSTRA, Robert M. 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Urinary tract diseases</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Pharmacology. Drug treatments</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DUNS, Gerben</creatorcontrib><creatorcontrib>VAN DEN BERG, Eva</creatorcontrib><creatorcontrib>VAN DUIVENBODE, Inge</creatorcontrib><creatorcontrib>OSINGA, Jan</creatorcontrib><creatorcontrib>HOLLEMA, Harry</creatorcontrib><creatorcontrib>HOFSTRA, Robert M. 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This revealed inactivation of the histone methyltransferase gene SETD2, located on 3p21.31, as a common event in cRCC cells. SETD2 is nonredundantly responsible for trimethylation of the histone mark H3K36. Consistent with this function, we observed loss or a decrease of H3K36me3 in 7 out of the 10 cRCC cell lines. Identification of missense mutations in 2 out of 10 primary cRCC tumor samples added support to the involvement of loss of SETD2 function in the development of cRCC tumors.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>20501857</pmid><doi>10.1158/0008-5472.can-10-0120</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma, Clear Cell - enzymology Adenocarcinoma, Clear Cell - genetics Antineoplastic agents Biological and medical sciences Carcinoma, Renal Cell - enzymology Carcinoma, Renal Cell - genetics Cell Line, Tumor Chromosomes, Human, Pair 3 Comparative Genomic Hybridization DNA Methylation DNA Mutational Analysis Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Histone-Lysine N-Methyltransferase - genetics Humans Kidney Neoplasms - enzymology Kidney Neoplasms - genetics Kidneys Medical sciences Nephrology. Urinary tract diseases Oligonucleotide Array Sequence Analysis Pharmacology. Drug treatments RNA, Messenger - genetics RNA, Messenger - metabolism Tumors Tumors of the urinary system |
| title | Histone Methyltransferase Gene SETD2 Is a Novel Tumor Suppressor Gene in Clear Cell Renal Cell Carcinoma |
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