DNA methylation profiles in chronic lymphocytic leukemia patients treated with chemoimmunotherapy
In order to gain insight into the contribution of DNA methylation to disease progression of chronic lymphocytic leukemia (CLL), using 450K Illumina arrays, we determined the DNA methylation profiles in paired pre-treatment/relapse samples from 34 CLL patients treated with chemoimmunotherapy, mostly...
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| Veröffentlicht in: | Clinical epigenetics 2019-12, Vol.11 (1), p.177-177, Article 177 |
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| creator | Tsagiopoulou, Maria Papakonstantinou, Nikos Moysiadis, Theodoros Mansouri, Larry Ljungström, Viktor Duran-Ferrer, Martí Malousi, Andigoni Queirós, Ana C Plevova, Karla Bhoi, Sujata Kollia, Panagoula Oscier, David Anagnostopoulos, Achilles Trentin, Livio Ritgen, Matthias Pospisilova, Sarka Stavroyianni, Niki Ghia, Paolo Martin-Subero, Jose I Pott, Christiane Rosenquist, Richard Stamatopoulos, Kostas |
| description | In order to gain insight into the contribution of DNA methylation to disease progression of chronic lymphocytic leukemia (CLL), using 450K Illumina arrays, we determined the DNA methylation profiles in paired pre-treatment/relapse samples from 34 CLL patients treated with chemoimmunotherapy, mostly (n = 31) with the fludarabine-cyclophosphamide-rituximab (FCR) regimen.
The extent of identified changes in CLL cells versus memory B cells from healthy donors was termed "epigenetic burden" (EB) whereas the number of changes between the pre-treatment versus the relapse sample was termed "relapse changes" (RC). Significant (p < 0.05) associations were identified between (i) high EB and short time-to-first-treatment (TTFT); and, (ii) few RCs and short time-to-relapse. Both the EB and the RC clustered in specific genomic regions and chromatin states, including regulatory regions containing binding sites of transcription factors implicated in B cell and CLL biology.
Overall, we show that DNA methylation in CLL follows different dynamics in response to chemoimmunotherapy. These epigenetic alterations were linked with specific clinical and biological features. |
| doi_str_mv | 10.1186/s13148-019-0783-1 |
| format | Article |
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The extent of identified changes in CLL cells versus memory B cells from healthy donors was termed "epigenetic burden" (EB) whereas the number of changes between the pre-treatment versus the relapse sample was termed "relapse changes" (RC). Significant (p < 0.05) associations were identified between (i) high EB and short time-to-first-treatment (TTFT); and, (ii) few RCs and short time-to-relapse. Both the EB and the RC clustered in specific genomic regions and chromatin states, including regulatory regions containing binding sites of transcription factors implicated in B cell and CLL biology.
Overall, we show that DNA methylation in CLL follows different dynamics in response to chemoimmunotherapy. These epigenetic alterations were linked with specific clinical and biological features.</description><identifier>ISSN: 1868-7075</identifier><identifier>ISSN: 1868-7083</identifier><identifier>EISSN: 1868-7083</identifier><identifier>EISSN: 1868-7075</identifier><identifier>DOI: 10.1186/s13148-019-0783-1</identifier><identifier>PMID: 31791414</identifier><language>eng</language><publisher>Germany: BioMed Central</publisher><subject>Binding sites ; Chemoimmunotherapy ; Chromatin ; Chronic lymphocytic leukemia ; CLL ; Cyclophosphamide ; Deoxyribonucleic acid ; DNA ; DNA methylation ; Epigenetics ; Evolution ; Fludarabine ; Genes ; Immunological memory ; Lymphatic leukemia ; Lymphocytes B ; Memory cells ; Microarray analysis ; Monoclonal antibodies ; Patients ; Regulatory sequences ; Relapse ; Rituximab ; Targeted cancer therapy ; Transcription factors</subject><ispartof>Clinical epigenetics, 2019-12, Vol.11 (1), p.177-177, Article 177</ispartof><rights>2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c502t-9d76cbd68458cdcb24f92a858f61d6adfc0970cb4797cdf0fececacf63cb19683</citedby><cites>FETCH-LOGICAL-c502t-9d76cbd68458cdcb24f92a858f61d6adfc0970cb4797cdf0fececacf63cb19683</cites><orcidid>0000-0001-8529-640X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889736/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889736/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,550,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31791414$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-400829$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:142504163$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsagiopoulou, Maria</creatorcontrib><creatorcontrib>Papakonstantinou, Nikos</creatorcontrib><creatorcontrib>Moysiadis, Theodoros</creatorcontrib><creatorcontrib>Mansouri, Larry</creatorcontrib><creatorcontrib>Ljungström, Viktor</creatorcontrib><creatorcontrib>Duran-Ferrer, Martí</creatorcontrib><creatorcontrib>Malousi, Andigoni</creatorcontrib><creatorcontrib>Queirós, Ana C</creatorcontrib><creatorcontrib>Plevova, Karla</creatorcontrib><creatorcontrib>Bhoi, Sujata</creatorcontrib><creatorcontrib>Kollia, Panagoula</creatorcontrib><creatorcontrib>Oscier, David</creatorcontrib><creatorcontrib>Anagnostopoulos, Achilles</creatorcontrib><creatorcontrib>Trentin, Livio</creatorcontrib><creatorcontrib>Ritgen, Matthias</creatorcontrib><creatorcontrib>Pospisilova, Sarka</creatorcontrib><creatorcontrib>Stavroyianni, Niki</creatorcontrib><creatorcontrib>Ghia, Paolo</creatorcontrib><creatorcontrib>Martin-Subero, Jose I</creatorcontrib><creatorcontrib>Pott, Christiane</creatorcontrib><creatorcontrib>Rosenquist, Richard</creatorcontrib><creatorcontrib>Stamatopoulos, Kostas</creatorcontrib><title>DNA methylation profiles in chronic lymphocytic leukemia patients treated with chemoimmunotherapy</title><title>Clinical epigenetics</title><addtitle>Clin Epigenetics</addtitle><description>In order to gain insight into the contribution of DNA methylation to disease progression of chronic lymphocytic leukemia (CLL), using 450K Illumina arrays, we determined the DNA methylation profiles in paired pre-treatment/relapse samples from 34 CLL patients treated with chemoimmunotherapy, mostly (n = 31) with the fludarabine-cyclophosphamide-rituximab (FCR) regimen.
The extent of identified changes in CLL cells versus memory B cells from healthy donors was termed "epigenetic burden" (EB) whereas the number of changes between the pre-treatment versus the relapse sample was termed "relapse changes" (RC). Significant (p < 0.05) associations were identified between (i) high EB and short time-to-first-treatment (TTFT); and, (ii) few RCs and short time-to-relapse. Both the EB and the RC clustered in specific genomic regions and chromatin states, including regulatory regions containing binding sites of transcription factors implicated in B cell and CLL biology.
Overall, we show that DNA methylation in CLL follows different dynamics in response to chemoimmunotherapy. These epigenetic alterations were linked with specific clinical and biological features.</description><subject>Binding sites</subject><subject>Chemoimmunotherapy</subject><subject>Chromatin</subject><subject>Chronic lymphocytic leukemia</subject><subject>CLL</subject><subject>Cyclophosphamide</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>Epigenetics</subject><subject>Evolution</subject><subject>Fludarabine</subject><subject>Genes</subject><subject>Immunological memory</subject><subject>Lymphatic leukemia</subject><subject>Lymphocytes B</subject><subject>Memory cells</subject><subject>Microarray analysis</subject><subject>Monoclonal antibodies</subject><subject>Patients</subject><subject>Regulatory sequences</subject><subject>Relapse</subject><subject>Rituximab</subject><subject>Targeted cancer therapy</subject><subject>Transcription 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patients treated with chemoimmunotherapy</title><author>Tsagiopoulou, Maria ; Papakonstantinou, Nikos ; Moysiadis, Theodoros ; Mansouri, Larry ; Ljungström, Viktor ; Duran-Ferrer, Martí ; Malousi, Andigoni ; Queirós, Ana C ; Plevova, Karla ; Bhoi, Sujata ; Kollia, Panagoula ; Oscier, David ; Anagnostopoulos, Achilles ; Trentin, Livio ; Ritgen, Matthias ; Pospisilova, Sarka ; Stavroyianni, Niki ; Ghia, Paolo ; Martin-Subero, Jose I ; Pott, Christiane ; Rosenquist, Richard ; Stamatopoulos, Kostas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c502t-9d76cbd68458cdcb24f92a858f61d6adfc0970cb4797cdf0fececacf63cb19683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Binding sites</topic><topic>Chemoimmunotherapy</topic><topic>Chromatin</topic><topic>Chronic lymphocytic leukemia</topic><topic>CLL</topic><topic>Cyclophosphamide</topic><topic>Deoxyribonucleic 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epigenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsagiopoulou, Maria</au><au>Papakonstantinou, Nikos</au><au>Moysiadis, Theodoros</au><au>Mansouri, Larry</au><au>Ljungström, Viktor</au><au>Duran-Ferrer, Martí</au><au>Malousi, Andigoni</au><au>Queirós, Ana C</au><au>Plevova, Karla</au><au>Bhoi, Sujata</au><au>Kollia, Panagoula</au><au>Oscier, David</au><au>Anagnostopoulos, Achilles</au><au>Trentin, Livio</au><au>Ritgen, Matthias</au><au>Pospisilova, Sarka</au><au>Stavroyianni, Niki</au><au>Ghia, Paolo</au><au>Martin-Subero, Jose I</au><au>Pott, Christiane</au><au>Rosenquist, Richard</au><au>Stamatopoulos, Kostas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA methylation profiles in chronic lymphocytic leukemia patients treated with chemoimmunotherapy</atitle><jtitle>Clinical epigenetics</jtitle><addtitle>Clin Epigenetics</addtitle><date>2019-12-02</date><risdate>2019</risdate><volume>11</volume><issue>1</issue><spage>177</spage><epage>177</epage><pages>177-177</pages><artnum>177</artnum><issn>1868-7075</issn><issn>1868-7083</issn><eissn>1868-7083</eissn><eissn>1868-7075</eissn><abstract>In order to gain insight into the contribution of DNA methylation to disease progression of chronic lymphocytic leukemia (CLL), using 450K Illumina arrays, we determined the DNA methylation profiles in paired pre-treatment/relapse samples from 34 CLL patients treated with chemoimmunotherapy, mostly (n = 31) with the fludarabine-cyclophosphamide-rituximab (FCR) regimen.
The extent of identified changes in CLL cells versus memory B cells from healthy donors was termed "epigenetic burden" (EB) whereas the number of changes between the pre-treatment versus the relapse sample was termed "relapse changes" (RC). Significant (p < 0.05) associations were identified between (i) high EB and short time-to-first-treatment (TTFT); and, (ii) few RCs and short time-to-relapse. Both the EB and the RC clustered in specific genomic regions and chromatin states, including regulatory regions containing binding sites of transcription factors implicated in B cell and CLL biology.
Overall, we show that DNA methylation in CLL follows different dynamics in response to chemoimmunotherapy. These epigenetic alterations were linked with specific clinical and biological features.</abstract><cop>Germany</cop><pub>BioMed Central</pub><pmid>31791414</pmid><doi>10.1186/s13148-019-0783-1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-8529-640X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical epigenetics, 2019-12, Vol.11 (1), p.177-177, Article 177 |
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| language | eng |
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| source | Springer Nature - Complete Springer Journals; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SWEPUB Freely available online; PubMed Central Open Access; Springer Nature OA Free Journals |
| subjects | Binding sites Chemoimmunotherapy Chromatin Chronic lymphocytic leukemia CLL Cyclophosphamide Deoxyribonucleic acid DNA DNA methylation Epigenetics Evolution Fludarabine Genes Immunological memory Lymphatic leukemia Lymphocytes B Memory cells Microarray analysis Monoclonal antibodies Patients Regulatory sequences Relapse Rituximab Targeted cancer therapy Transcription factors |
| title | DNA methylation profiles in chronic lymphocytic leukemia patients treated with chemoimmunotherapy |
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