DNA methylation epigenotype and clinical features of NRAS‐mutation(+) colorectal cancer
Sporadic colorectal cancer (CRC) is classified into several molecular subtypes. We previously established two groups of DNA methylation markers through genome‐wide DNA methylation analysis to classify CRC into distinct subgroups: high‐, intermediate‐, and low‐methylation epigenotypes (HME, IME, and...
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| Veröffentlicht in: | Cancer medicine (Malden, MA) MA), 2017-05, Vol.6 (5), p.1023-1035 |
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| creator | Takane, Kiyoko Akagi, Kiwamu Fukuyo, Masaki Yagi, Koichi Takayama, Tadatoshi Kaneda, Atsushi |
| description | Sporadic colorectal cancer (CRC) is classified into several molecular subtypes. We previously established two groups of DNA methylation markers through genome‐wide DNA methylation analysis to classify CRC into distinct subgroups: high‐, intermediate‐, and low‐methylation epigenotypes (HME, IME, and LME, respectively). HME CRC, also called CpG island methylator phenotype (CIMP)‐high CRC, shows methylation of both Group 1 markers (CIMP markers) and Group 2 markers, while IME/CIMP‐low CRC shows methylation of Group 2, but not of Group 1 markers, and LME CRC shows no methylation of either Group 1 or Group 2 markers. While BRAF‐ and KRAS‐mutation(+) CRC strongly correlated with HME and IME, respectively, clinicopathological features of NRAS‐mutation(+) CRC, including association with DNA methylation, remain unclear. To characterize NRAS‐mutation(+) CRC, the methylation levels of 19 methylation marker genes (6 Group 1 and 13 Group 2) were analyzed in 61 NRAS‐mutation(+) and 144 NRAS‐mutation(−) CRC cases by pyrosequencing, and their correlation with clinicopathological features was investigated. Different from KRAS‐mutation(+) CRC, NRAS‐mutation(+) CRC significantly correlated with LME. NRAS‐mutation(+) CRC showed significantly better prognosis than KRAS‐mutation(+) CRC (P = 3 × 10−4). NRAS‐mutation(+) CRC preferentially occurred in elder patients (P = 0.02) and at the distal colon (P = 0.006), showed significantly less lymph vessel invasion (P = 0.002), and correlated with LME (P = 8 × 10−5). DNA methylation significantly accumulated at the proximal colon. NRAS‐mutation(+) CRC may constitute a different subgroup from KRAS‐mutation(+) CRC, showing significant correlation with LME, older age, distal colon, and relatively better prognosis.
Genetic and epigenetic analyses of colorectal cancer (CRC) were conducted to clarify molecular and clinicopathological features of NRAS‐mutation(+) CRC compared to KRAS‐mutation(+) and other subgroups of CRC. NRAS‐mutation(+) CRC presented a low‐methylation epigenotype, occurred in elder patients and at the distal colon, and showed relatively better prognosis |
| doi_str_mv | 10.1002/cam4.1061 |
| format | Article |
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Genetic and epigenetic analyses of colorectal cancer (CRC) were conducted to clarify molecular and clinicopathological features of NRAS‐mutation(+) CRC compared to KRAS‐mutation(+) and other subgroups of CRC. NRAS‐mutation(+) CRC presented a low‐methylation epigenotype, occurred in elder patients and at the distal colon, and showed relatively better prognosis</description><identifier>ISSN: 2045-7634</identifier><identifier>EISSN: 2045-7634</identifier><identifier>DOI: 10.1002/cam4.1061</identifier><identifier>PMID: 28378457</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Age Factors ; Aged ; Aged, 80 and over ; BRAF mutation ; Clinical Cancer Research ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; CpG Islands ; Deoxyribonucleic acid ; DNA ; DNA Methylation ; Epigenesis, Genetic ; Female ; Genes ; Genomes ; GTP Phosphohydrolases - genetics ; Humans ; KRAS mutation ; Male ; Membrane Proteins - genetics ; Middle Aged ; Mutation ; Neoplasm Invasiveness ; NRAS mutation ; Original Research ; Phenotypes ; Prognosis ; Proto-Oncogene Proteins p21(ras) - genetics ; Sequence Analysis, DNA ; Survival Analysis</subject><ispartof>Cancer medicine (Malden, MA), 2017-05, Vol.6 (5), p.1023-1035</ispartof><rights>2017 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2017 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.</rights><rights>2017. This work is published 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4741-b3769d07910239a5fa611c34259d0aab43422d7cc5509354cfd4d98a509ddae53</citedby><cites>FETCH-LOGICAL-c4741-b3769d07910239a5fa611c34259d0aab43422d7cc5509354cfd4d98a509ddae53</cites><orcidid>0000-0002-6980-5515</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/PMC5430106/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5430106/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28378457$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takane, Kiyoko</creatorcontrib><creatorcontrib>Akagi, Kiwamu</creatorcontrib><creatorcontrib>Fukuyo, Masaki</creatorcontrib><creatorcontrib>Yagi, Koichi</creatorcontrib><creatorcontrib>Takayama, Tadatoshi</creatorcontrib><creatorcontrib>Kaneda, Atsushi</creatorcontrib><title>DNA methylation epigenotype and clinical features of NRAS‐mutation(+) colorectal cancer</title><title>Cancer medicine (Malden, MA)</title><addtitle>Cancer Med</addtitle><description>Sporadic colorectal cancer (CRC) is classified into several molecular subtypes. We previously established two groups of DNA methylation markers through genome‐wide DNA methylation analysis to classify CRC into distinct subgroups: high‐, intermediate‐, and low‐methylation epigenotypes (HME, IME, and LME, respectively). HME CRC, also called CpG island methylator phenotype (CIMP)‐high CRC, shows methylation of both Group 1 markers (CIMP markers) and Group 2 markers, while IME/CIMP‐low CRC shows methylation of Group 2, but not of Group 1 markers, and LME CRC shows no methylation of either Group 1 or Group 2 markers. While BRAF‐ and KRAS‐mutation(+) CRC strongly correlated with HME and IME, respectively, clinicopathological features of NRAS‐mutation(+) CRC, including association with DNA methylation, remain unclear. To characterize NRAS‐mutation(+) CRC, the methylation levels of 19 methylation marker genes (6 Group 1 and 13 Group 2) were analyzed in 61 NRAS‐mutation(+) and 144 NRAS‐mutation(−) CRC cases by pyrosequencing, and their correlation with clinicopathological features was investigated. Different from KRAS‐mutation(+) CRC, NRAS‐mutation(+) CRC significantly correlated with LME. NRAS‐mutation(+) CRC showed significantly better prognosis than KRAS‐mutation(+) CRC (P = 3 × 10−4). NRAS‐mutation(+) CRC preferentially occurred in elder patients (P = 0.02) and at the distal colon (P = 0.006), showed significantly less lymph vessel invasion (P = 0.002), and correlated with LME (P = 8 × 10−5). DNA methylation significantly accumulated at the proximal colon. NRAS‐mutation(+) CRC may constitute a different subgroup from KRAS‐mutation(+) CRC, showing significant correlation with LME, older age, distal colon, and relatively better prognosis.
Genetic and epigenetic analyses of colorectal cancer (CRC) were conducted to clarify molecular and clinicopathological features of NRAS‐mutation(+) CRC compared to KRAS‐mutation(+) and other subgroups of CRC. NRAS‐mutation(+) CRC presented a low‐methylation epigenotype, occurred in elder patients and at the distal colon, and showed relatively better prognosis</description><subject>Age Factors</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>BRAF mutation</subject><subject>Clinical Cancer Research</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>CpG Islands</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Epigenesis, Genetic</subject><subject>Female</subject><subject>Genes</subject><subject>Genomes</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>Humans</subject><subject>KRAS mutation</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Invasiveness</subject><subject>NRAS mutation</subject><subject>Original Research</subject><subject>Phenotypes</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>Sequence Analysis, DNA</subject><subject>Survival Analysis</subject><issn>2045-7634</issn><issn>2045-7634</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kdFKHDEUhoO0VLFe9AXKQG-UsppMksnMTWFZ2ypYBW0vvApnM2c0kknWZMayd32EPmOfxKxrxRbMTf6cfPk5Jz8h7xjdZ5SWBwZ6kVXFNshWSYWcqIqLV8_0JtlJ6YbmpWhZKfaGbJY1V7WQaotcHp5Oix6H66WDwQZf4MJeoQ_DcoEF-LYwznprwBUdwjBGTEXoitPz6cWfX7_7cXh4tPtxrzDBhYhmyKQBbzC-Ja87cAl3Hvdt8uPL5--zo8nJ2dfj2fRkYoQSbDLnqmpaqhpGS96A7KBizHBRylwFmIssy1YZIyVtuBSma0Xb1JBPbQso-Tb5tPZdjPMeW4N-iOD0Itoe4lIHsPrfG2-v9VW401Jwmv8tG-w-GsRwO2IadG-TQefAYxiTZnUthCop4xn98B96E8bo83iZauqKNlUtMrW3pkwMKUXsnpphVK8y06vM9CqzzL5_3v0T-TehDBysgZ_W4fJlJz2bfhMPlvenFaBw</recordid><startdate>201705</startdate><enddate>201705</enddate><creator>Takane, Kiyoko</creator><creator>Akagi, Kiwamu</creator><creator>Fukuyo, Masaki</creator><creator>Yagi, Koichi</creator><creator>Takayama, Tadatoshi</creator><creator>Kaneda, Atsushi</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6980-5515</orcidid></search><sort><creationdate>201705</creationdate><title>DNA methylation epigenotype and clinical features of NRAS‐mutation(+) colorectal cancer</title><author>Takane, Kiyoko ; Akagi, Kiwamu ; Fukuyo, Masaki ; Yagi, Koichi ; Takayama, Tadatoshi ; Kaneda, Atsushi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4741-b3769d07910239a5fa611c34259d0aab43422d7cc5509354cfd4d98a509ddae53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Age Factors</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>BRAF mutation</topic><topic>Clinical Cancer Research</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>CpG Islands</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Epigenesis, Genetic</topic><topic>Female</topic><topic>Genes</topic><topic>Genomes</topic><topic>GTP Phosphohydrolases - genetics</topic><topic>Humans</topic><topic>KRAS mutation</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Invasiveness</topic><topic>NRAS mutation</topic><topic>Original Research</topic><topic>Phenotypes</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>Sequence Analysis, DNA</topic><topic>Survival Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takane, Kiyoko</creatorcontrib><creatorcontrib>Akagi, Kiwamu</creatorcontrib><creatorcontrib>Fukuyo, Masaki</creatorcontrib><creatorcontrib>Yagi, Koichi</creatorcontrib><creatorcontrib>Takayama, Tadatoshi</creatorcontrib><creatorcontrib>Kaneda, Atsushi</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer medicine (Malden, MA)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takane, Kiyoko</au><au>Akagi, Kiwamu</au><au>Fukuyo, Masaki</au><au>Yagi, Koichi</au><au>Takayama, Tadatoshi</au><au>Kaneda, Atsushi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA methylation epigenotype and clinical features of NRAS‐mutation(+) colorectal cancer</atitle><jtitle>Cancer medicine (Malden, MA)</jtitle><addtitle>Cancer Med</addtitle><date>2017-05</date><risdate>2017</risdate><volume>6</volume><issue>5</issue><spage>1023</spage><epage>1035</epage><pages>1023-1035</pages><issn>2045-7634</issn><eissn>2045-7634</eissn><abstract>Sporadic colorectal cancer (CRC) is classified into several molecular subtypes. We previously established two groups of DNA methylation markers through genome‐wide DNA methylation analysis to classify CRC into distinct subgroups: high‐, intermediate‐, and low‐methylation epigenotypes (HME, IME, and LME, respectively). HME CRC, also called CpG island methylator phenotype (CIMP)‐high CRC, shows methylation of both Group 1 markers (CIMP markers) and Group 2 markers, while IME/CIMP‐low CRC shows methylation of Group 2, but not of Group 1 markers, and LME CRC shows no methylation of either Group 1 or Group 2 markers. While BRAF‐ and KRAS‐mutation(+) CRC strongly correlated with HME and IME, respectively, clinicopathological features of NRAS‐mutation(+) CRC, including association with DNA methylation, remain unclear. To characterize NRAS‐mutation(+) CRC, the methylation levels of 19 methylation marker genes (6 Group 1 and 13 Group 2) were analyzed in 61 NRAS‐mutation(+) and 144 NRAS‐mutation(−) CRC cases by pyrosequencing, and their correlation with clinicopathological features was investigated. Different from KRAS‐mutation(+) CRC, NRAS‐mutation(+) CRC significantly correlated with LME. NRAS‐mutation(+) CRC showed significantly better prognosis than KRAS‐mutation(+) CRC (P = 3 × 10−4). NRAS‐mutation(+) CRC preferentially occurred in elder patients (P = 0.02) and at the distal colon (P = 0.006), showed significantly less lymph vessel invasion (P = 0.002), and correlated with LME (P = 8 × 10−5). DNA methylation significantly accumulated at the proximal colon. NRAS‐mutation(+) CRC may constitute a different subgroup from KRAS‐mutation(+) CRC, showing significant correlation with LME, older age, distal colon, and relatively better prognosis.
Genetic and epigenetic analyses of colorectal cancer (CRC) were conducted to clarify molecular and clinicopathological features of NRAS‐mutation(+) CRC compared to KRAS‐mutation(+) and other subgroups of CRC. NRAS‐mutation(+) CRC presented a low‐methylation epigenotype, occurred in elder patients and at the distal colon, and showed relatively better prognosis</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>28378457</pmid><doi>10.1002/cam4.1061</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-6980-5515</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Age Factors Aged Aged, 80 and over BRAF mutation Clinical Cancer Research Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology CpG Islands Deoxyribonucleic acid DNA DNA Methylation Epigenesis, Genetic Female Genes Genomes GTP Phosphohydrolases - genetics Humans KRAS mutation Male Membrane Proteins - genetics Middle Aged Mutation Neoplasm Invasiveness NRAS mutation Original Research Phenotypes Prognosis Proto-Oncogene Proteins p21(ras) - genetics Sequence Analysis, DNA Survival Analysis |
| title | DNA methylation epigenotype and clinical features of NRAS‐mutation(+) colorectal cancer |
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