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Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis
DNA methyltransferase 3A (DNMT3A) catalyzes cytosine methylation of mammalian genomic DNA. In addition to myeloid malignancies, mutations in DNMT3A have been recently reported in T-cell lymphoma and leukemia, implying a possible involvement in the pathogenesis of human diseases. However, the role of...
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Published in: | Oncogene 2015-10, Vol.34 (43), p.5436-5446 |
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description | DNA methyltransferase 3A (DNMT3A) catalyzes cytosine methylation of mammalian genomic DNA. In addition to myeloid malignancies, mutations in DNMT3A have been recently reported in T-cell lymphoma and leukemia, implying a possible involvement in the pathogenesis of human diseases. However, the role of Dnmt3a in T-cell transformation
in vivo
is poorly understood. Here we analyzed the functional consequences of Dnmt3a inactivation in a mouse model of MYC-induced T-cell lymphomagenesis (MTCL). Loss of Dnmt3a delayed tumorigenesis by suppressing cellular proliferation during disease progression. Gene expression profiling and pathway analysis identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b, in Dnmt3a-deficient lymphomas as molecular events potentially responsible for the delayed lymphomagenesis in
Dnmt3a
Δ/Δ
mice. Interestingly, promoter and gene body methylation of these genes was not substantially changed between control and Dnmt3a-deficient lymphomas, suggesting that Dnmt3a may inhibit their expression in a methylation-independent manner. Re-expression of both wild type and catalytically inactive Dnmt3a in
Dnmt3a
Δ/Δ
lymphoma cells
in vitro
inhibited Dnmt3b expression, indicating that Dnmt3b upregulation may be directly repressed by Dnmt3a. Importantly, genetic inactivation of Dnmt3b accelerated lymphomagenesis in
Dnmt3a
Δ/Δ
mice, demonstrating that upregulation of Dnmt3b is a relevant molecular change in Dnmt3a-deficient lymphomas that inhibits disease progression. Collectively, our data demonstrate an unexpected oncogenic role for Dnmt3a in MTCL through methylation-independent repression of Dnmt3b and possibly other tumor suppressor genes. |
doi_str_mv | 10.1038/onc.2014.472 |
format | article |
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in vivo
is poorly understood. Here we analyzed the functional consequences of Dnmt3a inactivation in a mouse model of MYC-induced T-cell lymphomagenesis (MTCL). Loss of Dnmt3a delayed tumorigenesis by suppressing cellular proliferation during disease progression. Gene expression profiling and pathway analysis identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b, in Dnmt3a-deficient lymphomas as molecular events potentially responsible for the delayed lymphomagenesis in
Dnmt3a
Δ/Δ
mice. Interestingly, promoter and gene body methylation of these genes was not substantially changed between control and Dnmt3a-deficient lymphomas, suggesting that Dnmt3a may inhibit their expression in a methylation-independent manner. Re-expression of both wild type and catalytically inactive Dnmt3a in
Dnmt3a
Δ/Δ
lymphoma cells
in vitro
inhibited Dnmt3b expression, indicating that Dnmt3b upregulation may be directly repressed by Dnmt3a. Importantly, genetic inactivation of Dnmt3b accelerated lymphomagenesis in
Dnmt3a
Δ/Δ
mice, demonstrating that upregulation of Dnmt3b is a relevant molecular change in Dnmt3a-deficient lymphomas that inhibits disease progression. Collectively, our data demonstrate an unexpected oncogenic role for Dnmt3a in MTCL through methylation-independent repression of Dnmt3b and possibly other tumor suppressor genes.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2014.472</identifier><identifier>PMID: 25639876</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 13/44 ; 38/39 ; 38/61 ; 631/67/1990/291/1621/1916 ; 64/110 ; 64/60 ; Analysis ; Animals ; Apoptosis ; Carcinogenesis - genetics ; Cell Biology ; Cell Proliferation - genetics ; Cells ; Cytosine ; Deoxyribonucleic acid ; Disease Models, Animal ; Disease Progression ; DNA ; DNA (Cytosine-5-)-Methyltransferases - genetics ; DNA - genetics ; DNA methylation ; DNA Methylation - genetics ; DNA methyltransferase ; DNA Methyltransferase 3A ; DNA Methyltransferase 3B ; Gene expression ; Genes ; Genetic aspects ; Genetic transformation ; Human Genetics ; Internal Medicine ; Leukemia ; Lymphocytes T ; Lymphoma ; Lymphoma, T-Cell - genetics ; Lymphoma, T-Cell - pathology ; Medicine ; Medicine & Public Health ; Methylation ; Methyltransferases ; Mice ; Myc protein ; Non-Hodgkin's lymphomas ; Oncology ; original-article ; Physiological aspects ; Promoter Regions, Genetic - genetics ; Proto-Oncogene Proteins c-myc - genetics ; Risk factors ; Rodents ; T cells ; T-cell lymphoma ; Tetracycline ; Tetracyclines ; Transcriptome - genetics ; Tumor suppressor genes ; Tumorigenesis ; Up-Regulation - genetics</subject><ispartof>Oncogene, 2015-10, Vol.34 (43), p.5436-5446</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Oct 23, 2015</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c715t-f0b8b26d2734f0bc85c1bb8514b785ef3d2923f4b157c9b0afc1281fb56eaf453</citedby><cites>FETCH-LOGICAL-c715t-f0b8b26d2734f0bc85c1bb8514b785ef3d2923f4b157c9b0afc1281fb56eaf453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25639876$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Haney, S L</creatorcontrib><creatorcontrib>Hlady, R A</creatorcontrib><creatorcontrib>Opavska, J</creatorcontrib><creatorcontrib>Klinkebiel, D</creatorcontrib><creatorcontrib>Pirruccello, S J</creatorcontrib><creatorcontrib>Dutta, S</creatorcontrib><creatorcontrib>Datta, K</creatorcontrib><creatorcontrib>Simpson, M A</creatorcontrib><creatorcontrib>Wu, L</creatorcontrib><creatorcontrib>Opavsky, R</creatorcontrib><title>Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>DNA methyltransferase 3A (DNMT3A) catalyzes cytosine methylation of mammalian genomic DNA. In addition to myeloid malignancies, mutations in DNMT3A have been recently reported in T-cell lymphoma and leukemia, implying a possible involvement in the pathogenesis of human diseases. However, the role of Dnmt3a in T-cell transformation
in vivo
is poorly understood. Here we analyzed the functional consequences of Dnmt3a inactivation in a mouse model of MYC-induced T-cell lymphomagenesis (MTCL). Loss of Dnmt3a delayed tumorigenesis by suppressing cellular proliferation during disease progression. Gene expression profiling and pathway analysis identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b, in Dnmt3a-deficient lymphomas as molecular events potentially responsible for the delayed lymphomagenesis in
Dnmt3a
Δ/Δ
mice. Interestingly, promoter and gene body methylation of these genes was not substantially changed between control and Dnmt3a-deficient lymphomas, suggesting that Dnmt3a may inhibit their expression in a methylation-independent manner. Re-expression of both wild type and catalytically inactive Dnmt3a in
Dnmt3a
Δ/Δ
lymphoma cells
in vitro
inhibited Dnmt3b expression, indicating that Dnmt3b upregulation may be directly repressed by Dnmt3a. Importantly, genetic inactivation of Dnmt3b accelerated lymphomagenesis in
Dnmt3a
Δ/Δ
mice, demonstrating that upregulation of Dnmt3b is a relevant molecular change in Dnmt3a-deficient lymphomas that inhibits disease progression. Collectively, our data demonstrate an unexpected oncogenic role for Dnmt3a in MTCL through methylation-independent repression of Dnmt3b and possibly other tumor suppressor genes.</description><subject>13/31</subject><subject>13/44</subject><subject>38/39</subject><subject>38/61</subject><subject>631/67/1990/291/1621/1916</subject><subject>64/110</subject><subject>64/60</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Carcinogenesis - genetics</subject><subject>Cell Biology</subject><subject>Cell Proliferation - genetics</subject><subject>Cells</subject><subject>Cytosine</subject><subject>Deoxyribonucleic acid</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>DNA</subject><subject>DNA (Cytosine-5-)-Methyltransferases - genetics</subject><subject>DNA - genetics</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>DNA methyltransferase</subject><subject>DNA Methyltransferase 3A</subject><subject>DNA Methyltransferase 3B</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic transformation</subject><subject>Human Genetics</subject><subject>Internal Medicine</subject><subject>Leukemia</subject><subject>Lymphocytes T</subject><subject>Lymphoma</subject><subject>Lymphoma, T-Cell - genetics</subject><subject>Lymphoma, T-Cell - pathology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylation</subject><subject>Methyltransferases</subject><subject>Mice</subject><subject>Myc protein</subject><subject>Non-Hodgkin's lymphomas</subject><subject>Oncology</subject><subject>original-article</subject><subject>Physiological aspects</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>T cells</subject><subject>T-cell lymphoma</subject><subject>Tetracycline</subject><subject>Tetracyclines</subject><subject>Transcriptome - genetics</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenesis</subject><subject>Up-Regulation - genetics</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqNks1v1DAQxSMEokvhxhlZ4tIDWWzHjpMLUrV8Sq24lAMny3Ymu64Se7GdSnvnD8dhy7JFVYUiJZb9mzd5z1MULwleElw1b70zS4oJWzJBHxULwkRdct6yx8UCtxyXLa3oSfEsxmuMsWgxfVqcUF5XbSPqRfHzEtJmN6hkvSut62AL-eUSCrANEGPeRr5H792YKo2MdylYPSWIKHmUW_s1OGuQMsne2LQ7sApZh0Y_RUCX31ez8mSgQ1elgWFAw27cbvyocjFEG58XT3o1RHhx-z0tvn38cLX6XF58_fRldX5RGkF4KnusG03rjoqK5bVpuCFaN5wwLRoOfdXRbLZnmnBhWo1VbwhtSK95DapnvDot3u11t5MeoTPZZ1CD3AY7qrCTXll598TZjVz7G5lrq0aQLHB2KxD8jwlikqONsyPlIHuVRNQ5eV4zltHX_6DXfgou25O0qkhNWCvoQxQRlHPOaib-Ums1gLSu9_nvzNxantcEU8xJgx-kWG5JicBzBst7qPx0MNp8v9DbvH9H9r8Kjju82ReY4GMM0B8CJljOIyvz3Mh5ZCX7HcGr40s5wH9mNAPlHoj5yK0hHGV0n-AvwSr0xw</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Haney, S L</creator><creator>Hlady, R A</creator><creator>Opavska, J</creator><creator>Klinkebiel, D</creator><creator>Pirruccello, S J</creator><creator>Dutta, S</creator><creator>Datta, K</creator><creator>Simpson, M A</creator><creator>Wu, L</creator><creator>Opavsky, R</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>Q9U</scope><scope>RC3</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20151001</creationdate><title>Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis</title><author>Haney, S L ; Hlady, R A ; Opavska, J ; Klinkebiel, D ; Pirruccello, S J ; Dutta, S ; Datta, K ; Simpson, M A ; Wu, L ; Opavsky, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c715t-f0b8b26d2734f0bc85c1bb8514b785ef3d2923f4b157c9b0afc1281fb56eaf453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>13/31</topic><topic>13/44</topic><topic>38/39</topic><topic>38/61</topic><topic>631/67/1990/291/1621/1916</topic><topic>64/110</topic><topic>64/60</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Carcinogenesis - genetics</topic><topic>Cell Biology</topic><topic>Cell Proliferation - genetics</topic><topic>Cells</topic><topic>Cytosine</topic><topic>Deoxyribonucleic acid</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>DNA</topic><topic>DNA (Cytosine-5-)-Methyltransferases - genetics</topic><topic>DNA - genetics</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>DNA methyltransferase</topic><topic>DNA Methyltransferase 3A</topic><topic>DNA Methyltransferase 3B</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic transformation</topic><topic>Human Genetics</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Lymphocytes T</topic><topic>Lymphoma</topic><topic>Lymphoma, T-Cell - genetics</topic><topic>Lymphoma, T-Cell - pathology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylation</topic><topic>Methyltransferases</topic><topic>Mice</topic><topic>Myc protein</topic><topic>Non-Hodgkin's lymphomas</topic><topic>Oncology</topic><topic>original-article</topic><topic>Physiological aspects</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Proto-Oncogene Proteins c-myc - genetics</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>T cells</topic><topic>T-cell lymphoma</topic><topic>Tetracycline</topic><topic>Tetracyclines</topic><topic>Transcriptome - genetics</topic><topic>Tumor suppressor genes</topic><topic>Tumorigenesis</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Haney, S L</creatorcontrib><creatorcontrib>Hlady, R A</creatorcontrib><creatorcontrib>Opavska, J</creatorcontrib><creatorcontrib>Klinkebiel, D</creatorcontrib><creatorcontrib>Pirruccello, S J</creatorcontrib><creatorcontrib>Dutta, S</creatorcontrib><creatorcontrib>Datta, K</creatorcontrib><creatorcontrib>Simpson, M A</creatorcontrib><creatorcontrib>Wu, L</creatorcontrib><creatorcontrib>Opavsky, R</creatorcontrib><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>Health & Medical Collection</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)</collection><collection>ProQuest Central</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</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>Research Library</collection><collection>Biological Science Database</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 Basic</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Haney, S L</au><au>Hlady, R A</au><au>Opavska, J</au><au>Klinkebiel, D</au><au>Pirruccello, S J</au><au>Dutta, S</au><au>Datta, K</au><au>Simpson, M A</au><au>Wu, L</au><au>Opavsky, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>34</volume><issue>43</issue><spage>5436</spage><epage>5446</epage><pages>5436-5446</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>DNA methyltransferase 3A (DNMT3A) catalyzes cytosine methylation of mammalian genomic DNA. In addition to myeloid malignancies, mutations in DNMT3A have been recently reported in T-cell lymphoma and leukemia, implying a possible involvement in the pathogenesis of human diseases. However, the role of Dnmt3a in T-cell transformation
in vivo
is poorly understood. Here we analyzed the functional consequences of Dnmt3a inactivation in a mouse model of MYC-induced T-cell lymphomagenesis (MTCL). Loss of Dnmt3a delayed tumorigenesis by suppressing cellular proliferation during disease progression. Gene expression profiling and pathway analysis identified upregulation of 17 putative tumor suppressor genes, including DNA methyltransferase Dnmt3b, in Dnmt3a-deficient lymphomas as molecular events potentially responsible for the delayed lymphomagenesis in
Dnmt3a
Δ/Δ
mice. Interestingly, promoter and gene body methylation of these genes was not substantially changed between control and Dnmt3a-deficient lymphomas, suggesting that Dnmt3a may inhibit their expression in a methylation-independent manner. Re-expression of both wild type and catalytically inactive Dnmt3a in
Dnmt3a
Δ/Δ
lymphoma cells
in vitro
inhibited Dnmt3b expression, indicating that Dnmt3b upregulation may be directly repressed by Dnmt3a. Importantly, genetic inactivation of Dnmt3b accelerated lymphomagenesis in
Dnmt3a
Δ/Δ
mice, demonstrating that upregulation of Dnmt3b is a relevant molecular change in Dnmt3a-deficient lymphomas that inhibits disease progression. Collectively, our data demonstrate an unexpected oncogenic role for Dnmt3a in MTCL through methylation-independent repression of Dnmt3b and possibly other tumor suppressor genes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25639876</pmid><doi>10.1038/onc.2014.472</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/31 13/44 38/39 38/61 631/67/1990/291/1621/1916 64/110 64/60 Analysis Animals Apoptosis Carcinogenesis - genetics Cell Biology Cell Proliferation - genetics Cells Cytosine Deoxyribonucleic acid Disease Models, Animal Disease Progression DNA DNA (Cytosine-5-)-Methyltransferases - genetics DNA - genetics DNA methylation DNA Methylation - genetics DNA methyltransferase DNA Methyltransferase 3A DNA Methyltransferase 3B Gene expression Genes Genetic aspects Genetic transformation Human Genetics Internal Medicine Leukemia Lymphocytes T Lymphoma Lymphoma, T-Cell - genetics Lymphoma, T-Cell - pathology Medicine Medicine & Public Health Methylation Methyltransferases Mice Myc protein Non-Hodgkin's lymphomas Oncology original-article Physiological aspects Promoter Regions, Genetic - genetics Proto-Oncogene Proteins c-myc - genetics Risk factors Rodents T cells T-cell lymphoma Tetracycline Tetracyclines Transcriptome - genetics Tumor suppressor genes Tumorigenesis Up-Regulation - genetics |
title | Methylation-independent repression of Dnmt3b contributes to oncogenic activity of Dnmt3a in mouse MYC-induced T-cell lymphomagenesis |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-26T18%3A26%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Methylation-independent%20repression%20of%20Dnmt3b%20contributes%20to%20oncogenic%20activity%20of%20Dnmt3a%20in%20mouse%20MYC-induced%20T-cell%20lymphomagenesis&rft.jtitle=Oncogene&rft.au=Haney,%20S%20L&rft.date=2015-10-01&rft.volume=34&rft.issue=43&rft.spage=5436&rft.epage=5446&rft.pages=5436-5446&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2014.472&rft_dat=%3Cgale_pubme%3EA433121705%3C/gale_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c715t-f0b8b26d2734f0bc85c1bb8514b785ef3d2923f4b157c9b0afc1281fb56eaf453%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1725554647&rft_id=info:pmid/25639876&rft_galeid=A433121705&rfr_iscdi=true |