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Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long‐term follow‐up study
Changes of DNA methylation in gastric mucosae after eradication of Helicobacter pylori have not been clarified yet. From this background, we investigated time course of DNA methylation following H. pylori eradication in 221 successfully H. pylori eradicated subjects with endoscopic follow‐up at leas...
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| Published in: | International journal of cancer 2013-11, Vol.133 (9), p.2034-2042 |
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| container_end_page | 2042 |
| container_issue | 9 |
| container_start_page | 2034 |
| container_title | International journal of cancer |
| container_volume | 133 |
| creator | Shin, Cheol Min Kim, Nayoung Lee, Hye Seung Park, Ji Hyun Ahn, Soyeon Kang, Gyeong Hoon Kim, Jung Mogg Kim, Joo Sung Lee, Dong Ho Jung, Hyun Chae |
| description | Changes of DNA methylation in gastric mucosae after eradication of Helicobacter pylori have not been clarified yet. From this background, we investigated time course of DNA methylation following H. pylori eradication in 221 successfully H. pylori eradicated subjects with endoscopic follow‐up at least for 6 months, including 114 controls, 53 subjects with gastric dysplasia and 54 patients with early gastric cancer. All dysplasia and gastric cancer patients underwent endoscopic resection at the time of enrollment. The methylation levels in LOX, APC and MOS genes from noncancerous gastric mucosae using quantitative methylation‐specific PCR, as well as the histologic findings of gastric mucosae, were compared before and after eradication. Average follow‐up duration was 26.0 months (range: 6 to 76 months). H. pylori eradication decreased methylation levels in LOX (p‐value for slope |
| doi_str_mv | 10.1002/ijc.28219 |
| format | article |
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What's new?
While eradication of Helicobacter pylori, a known risk factor for gastric cancer, can prevent disease progression in animal models, its eradication in gastric cancer patients has yielded inconsistent results, possibly owing to the persistence of aberrant changes in DNA methylation. In this study, methylation of the gene MOS was correlated with severity of intestinal metaplasia, a risk factor for progression to gastric cancer. MOS methylation level was persistently higher in subjects with intestinal metaplasia, dysplasia, or gastric cancer, even after H. pylori eradication. The findings strongly support the epigenetic field defect hypothesis for gastric cancer.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.28219</identifier><identifier>PMID: 23595635</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken, NJ: Wiley-Blackwell</publisher><subject>Adenomatous Polyposis Coli Protein - genetics ; Biological and medical sciences ; Biomarkers, Tumor - genetics ; Cancer ; Cancer therapies ; Case-Control Studies ; Deoxyribonucleic acid ; DNA ; DNA - analysis ; DNA - genetics ; DNA Methylation ; Epigenetics ; Female ; Follow-Up Studies ; Gastric cancer ; Gastric Mucosa - metabolism ; Gastric Mucosa - microbiology ; Gastric Mucosa - pathology ; Gastritis - etiology ; Gastritis - pathology ; Gastroenterology. Liver. Pancreas. Abdomen ; Helicobacter Infections - complications ; Helicobacter Infections - genetics ; Helicobacter Infections - microbiology ; Helicobacter pylori ; Helicobacter pylori - pathogenicity ; Humans ; Infections ; inflammation ; Intestines - microbiology ; Intestines - pathology ; Male ; Medical research ; Medical sciences ; Metaplasia - etiology ; Metaplasia - pathology ; methylation ; Middle Aged ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Neoplasm Grading ; Polymerase Chain Reaction ; Precancerous Conditions - etiology ; Precancerous Conditions - pathology ; Prognosis ; Proto-Oncogene Proteins c-mos - genetics ; Scavenger Receptors, Class E - genetics ; Stomach Neoplasms - etiology ; Stomach Neoplasms - pathology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Tumors ; Ulcers</subject><ispartof>International journal of cancer, 2013-11, Vol.133 (9), p.2034-2042</ispartof><rights>2013 UICC</rights><rights>2014 INIST-CNRS</rights><rights>2013 UICC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5179-d9bdf07bf49b17ab2d6e77602cb0d3e0a8ee31086a95e398a8052a7f65d930e33</citedby><cites>FETCH-LOGICAL-c5179-d9bdf07bf49b17ab2d6e77602cb0d3e0a8ee31086a95e398a8052a7f65d930e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27663225$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23595635$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Cheol Min</creatorcontrib><creatorcontrib>Kim, Nayoung</creatorcontrib><creatorcontrib>Lee, Hye Seung</creatorcontrib><creatorcontrib>Park, Ji Hyun</creatorcontrib><creatorcontrib>Ahn, Soyeon</creatorcontrib><creatorcontrib>Kang, Gyeong Hoon</creatorcontrib><creatorcontrib>Kim, Jung Mogg</creatorcontrib><creatorcontrib>Kim, Joo Sung</creatorcontrib><creatorcontrib>Lee, Dong Ho</creatorcontrib><creatorcontrib>Jung, Hyun Chae</creatorcontrib><title>Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long‐term follow‐up study</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Changes of DNA methylation in gastric mucosae after eradication of Helicobacter pylori have not been clarified yet. From this background, we investigated time course of DNA methylation following H. pylori eradication in 221 successfully H. pylori eradicated subjects with endoscopic follow‐up at least for 6 months, including 114 controls, 53 subjects with gastric dysplasia and 54 patients with early gastric cancer. All dysplasia and gastric cancer patients underwent endoscopic resection at the time of enrollment. The methylation levels in LOX, APC and MOS genes from noncancerous gastric mucosae using quantitative methylation‐specific PCR, as well as the histologic findings of gastric mucosae, were compared before and after eradication. Average follow‐up duration was 26.0 months (range: 6 to 76 months). H. pylori eradication decreased methylation levels in LOX (p‐value for slope < 0.001) but not in APC. In MOS, decrease of its methylation level following H. pylori eradication was significant among controls without intestinal metaplasia (IM) (p‐value for slope < 0.05); however, it was not observed among patients with IM or those with dysplasia or gastric cancer. After H. pylori eradication, methylation level in MOS persistently increased in patients with dysplasia or gastric cancer (p < 0.01). In conclusion, H. pylori eradication decreases aberrant DNA methylation with gene‐specific manner. Methylation level in MOS is associated with IM and may be used as a surrogate marker for gastric cancer risk, regardless of H. pylori eradication history.
What's new?
While eradication of Helicobacter pylori, a known risk factor for gastric cancer, can prevent disease progression in animal models, its eradication in gastric cancer patients has yielded inconsistent results, possibly owing to the persistence of aberrant changes in DNA methylation. In this study, methylation of the gene MOS was correlated with severity of intestinal metaplasia, a risk factor for progression to gastric cancer. MOS methylation level was persistently higher in subjects with intestinal metaplasia, dysplasia, or gastric cancer, even after H. pylori eradication. The findings strongly support the epigenetic field defect hypothesis for gastric cancer.</description><subject>Adenomatous Polyposis Coli Protein - genetics</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Case-Control Studies</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA - analysis</subject><subject>DNA - genetics</subject><subject>DNA Methylation</subject><subject>Epigenetics</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gastric cancer</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - microbiology</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastritis - etiology</subject><subject>Gastritis - pathology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Helicobacter Infections - complications</subject><subject>Helicobacter Infections - genetics</subject><subject>Helicobacter Infections - microbiology</subject><subject>Helicobacter pylori</subject><subject>Helicobacter pylori - pathogenicity</subject><subject>Humans</subject><subject>Infections</subject><subject>inflammation</subject><subject>Intestines - microbiology</subject><subject>Intestines - pathology</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metaplasia - etiology</subject><subject>Metaplasia - pathology</subject><subject>methylation</subject><subject>Middle Aged</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Neoplasm Grading</subject><subject>Polymerase Chain Reaction</subject><subject>Precancerous Conditions - etiology</subject><subject>Precancerous Conditions - pathology</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins c-mos - genetics</subject><subject>Scavenger Receptors, Class E - genetics</subject><subject>Stomach Neoplasms - etiology</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Tumors</subject><subject>Ulcers</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqN0c1u1DAQB3ALUdGlcOAFkCWERA9p_RHbMbfVQmlRBRc4R44zab1y4sVOVOXGI_CMPAlOd6ESEhKn0Wh-mtHoj9ALSs4oIezcbe0ZqxjVj9CKEq0Kwqh4jFZ5RgpFuTxGT1PaEkKpIOUTdMy40EJysULbza0ZbiBhN2DTQIxmGPG7T2vcw3g7ezO6kAfdCBFfgnc2NMYuzW72IToM0bTO3qu3eI19GG5-fv-RQY-74H24y920w2mc2vkZOuqMT_D8UE_Q14v3XzaXxfXnD1eb9XVhBVW6aHXTdkQ1XakbqkzDWglKScJsQ1oOxFQAnJJKGi2A68pURDCjOilazQlwfoLe7PfuYvg2QRrr3iUL3psBwpRqWvKScKY5_Q_KpBKUiYW--otuwxSH_MiiKlkywVRWp3tlY0gpQlfvoutNnGtK6iWrOmdV32eV7cvDxqnpof0jf4eTwesDMMka3-VsrEsPTknJGVvc-d7dOQ_zvy_WVx83-9O_AFbLq2k</recordid><startdate>201311</startdate><enddate>201311</enddate><creator>Shin, Cheol Min</creator><creator>Kim, Nayoung</creator><creator>Lee, Hye Seung</creator><creator>Park, Ji Hyun</creator><creator>Ahn, Soyeon</creator><creator>Kang, Gyeong Hoon</creator><creator>Kim, Jung Mogg</creator><creator>Kim, Joo Sung</creator><creator>Lee, Dong Ho</creator><creator>Jung, Hyun Chae</creator><general>Wiley-Blackwell</general><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>7QL</scope><scope>7TM</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope></search><sort><creationdate>201311</creationdate><title>Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long‐term follow‐up study</title><author>Shin, Cheol Min ; Kim, Nayoung ; Lee, Hye Seung ; Park, Ji Hyun ; Ahn, Soyeon ; Kang, Gyeong Hoon ; Kim, Jung Mogg ; Kim, Joo Sung ; Lee, Dong Ho ; Jung, Hyun Chae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5179-d9bdf07bf49b17ab2d6e77602cb0d3e0a8ee31086a95e398a8052a7f65d930e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenomatous Polyposis Coli Protein - genetics</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Case-Control Studies</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA - analysis</topic><topic>DNA - genetics</topic><topic>DNA Methylation</topic><topic>Epigenetics</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gastric cancer</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - microbiology</topic><topic>Gastric Mucosa - pathology</topic><topic>Gastritis - etiology</topic><topic>Gastritis - pathology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Helicobacter Infections - complications</topic><topic>Helicobacter Infections - genetics</topic><topic>Helicobacter Infections - microbiology</topic><topic>Helicobacter pylori</topic><topic>Helicobacter pylori - pathogenicity</topic><topic>Humans</topic><topic>Infections</topic><topic>inflammation</topic><topic>Intestines - microbiology</topic><topic>Intestines - pathology</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Metaplasia - etiology</topic><topic>Metaplasia - pathology</topic><topic>methylation</topic><topic>Middle Aged</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Neoplasm Grading</topic><topic>Polymerase Chain Reaction</topic><topic>Precancerous Conditions - etiology</topic><topic>Precancerous Conditions - pathology</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins c-mos - genetics</topic><topic>Scavenger Receptors, Class E - genetics</topic><topic>Stomach Neoplasms - etiology</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Tumors</topic><topic>Ulcers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Cheol Min</creatorcontrib><creatorcontrib>Kim, Nayoung</creatorcontrib><creatorcontrib>Lee, Hye Seung</creatorcontrib><creatorcontrib>Park, Ji Hyun</creatorcontrib><creatorcontrib>Ahn, Soyeon</creatorcontrib><creatorcontrib>Kang, Gyeong Hoon</creatorcontrib><creatorcontrib>Kim, Jung Mogg</creatorcontrib><creatorcontrib>Kim, Joo Sung</creatorcontrib><creatorcontrib>Lee, Dong Ho</creatorcontrib><creatorcontrib>Jung, Hyun Chae</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>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Cheol Min</au><au>Kim, Nayoung</au><au>Lee, Hye Seung</au><au>Park, Ji Hyun</au><au>Ahn, Soyeon</au><au>Kang, Gyeong Hoon</au><au>Kim, Jung Mogg</au><au>Kim, Joo Sung</au><au>Lee, Dong Ho</au><au>Jung, Hyun Chae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long‐term follow‐up study</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2013-11</date><risdate>2013</risdate><volume>133</volume><issue>9</issue><spage>2034</spage><epage>2042</epage><pages>2034-2042</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Changes of DNA methylation in gastric mucosae after eradication of Helicobacter pylori have not been clarified yet. From this background, we investigated time course of DNA methylation following H. pylori eradication in 221 successfully H. pylori eradicated subjects with endoscopic follow‐up at least for 6 months, including 114 controls, 53 subjects with gastric dysplasia and 54 patients with early gastric cancer. All dysplasia and gastric cancer patients underwent endoscopic resection at the time of enrollment. The methylation levels in LOX, APC and MOS genes from noncancerous gastric mucosae using quantitative methylation‐specific PCR, as well as the histologic findings of gastric mucosae, were compared before and after eradication. Average follow‐up duration was 26.0 months (range: 6 to 76 months). H. pylori eradication decreased methylation levels in LOX (p‐value for slope < 0.001) but not in APC. In MOS, decrease of its methylation level following H. pylori eradication was significant among controls without intestinal metaplasia (IM) (p‐value for slope < 0.05); however, it was not observed among patients with IM or those with dysplasia or gastric cancer. After H. pylori eradication, methylation level in MOS persistently increased in patients with dysplasia or gastric cancer (p < 0.01). In conclusion, H. pylori eradication decreases aberrant DNA methylation with gene‐specific manner. Methylation level in MOS is associated with IM and may be used as a surrogate marker for gastric cancer risk, regardless of H. pylori eradication history.
What's new?
While eradication of Helicobacter pylori, a known risk factor for gastric cancer, can prevent disease progression in animal models, its eradication in gastric cancer patients has yielded inconsistent results, possibly owing to the persistence of aberrant changes in DNA methylation. In this study, methylation of the gene MOS was correlated with severity of intestinal metaplasia, a risk factor for progression to gastric cancer. MOS methylation level was persistently higher in subjects with intestinal metaplasia, dysplasia, or gastric cancer, even after H. pylori eradication. The findings strongly support the epigenetic field defect hypothesis for gastric cancer.</abstract><cop>Hoboken, NJ</cop><pub>Wiley-Blackwell</pub><pmid>23595635</pmid><doi>10.1002/ijc.28219</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of cancer, 2013-11, Vol.133 (9), p.2034-2042 |
| issn | 0020-7136 1097-0215 |
| language | eng |
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| source | Wiley-Blackwell Read & Publish Collection |
| subjects | Adenomatous Polyposis Coli Protein - genetics Biological and medical sciences Biomarkers, Tumor - genetics Cancer Cancer therapies Case-Control Studies Deoxyribonucleic acid DNA DNA - analysis DNA - genetics DNA Methylation Epigenetics Female Follow-Up Studies Gastric cancer Gastric Mucosa - metabolism Gastric Mucosa - microbiology Gastric Mucosa - pathology Gastritis - etiology Gastritis - pathology Gastroenterology. Liver. Pancreas. Abdomen Helicobacter Infections - complications Helicobacter Infections - genetics Helicobacter Infections - microbiology Helicobacter pylori Helicobacter pylori - pathogenicity Humans Infections inflammation Intestines - microbiology Intestines - pathology Male Medical research Medical sciences Metaplasia - etiology Metaplasia - pathology methylation Middle Aged Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Neoplasm Grading Polymerase Chain Reaction Precancerous Conditions - etiology Precancerous Conditions - pathology Prognosis Proto-Oncogene Proteins c-mos - genetics Scavenger Receptors, Class E - genetics Stomach Neoplasms - etiology Stomach Neoplasms - pathology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors Ulcers |
| title | Changes in aberrant DNA methylation after Helicobacter pylori eradication: A long‐term follow‐up study |
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