Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas
p16(INK4A) and p57(KIP2) are inhibitors of cyclin-dependent kinases and their inactivation by methylation has been reported as a major tumorigenic mechanism in tumors. To examine whether methylation of p16(INK4A) and p57(KIP2) is involved in the development and progression of gastric MALT lymphomas,...
Gespeichert in:
| Veröffentlicht in: | Modern pathology 2006-01, Vol.19 (1), p.141-148 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 148 |
|---|---|
| container_issue | 1 |
| container_start_page | 141 |
| container_title | Modern pathology |
| container_volume | 19 |
| creator | Min, Ki Ouk Seo, Eun Joo Kwon, Hi Jeong Lee, Eui Jin Kim, Won Il Kang, Chang Suk Kim, Kyoung-Mee |
| description | p16(INK4A) and p57(KIP2) are inhibitors of cyclin-dependent kinases and their inactivation by methylation has been reported as a major tumorigenic mechanism in tumors. To examine whether methylation of p16(INK4A) and p57(KIP2) is involved in the development and progression of gastric MALT lymphomas, 24 gastric low-grade lymphomas of MALT, 11 diffuse large B-cell lymphomas, and 10 each case of gastric lymphoid follicles with and without Helicobacter pylori infection were studied. H. pylori infection was positive in 85.7% of the gastric lymphomas. In the gastric lymphoid follicles positive for H. pylori, methylation of p16(INK4A) was detected in 10% of cases, while methylation of p57(KIP2) was not detected. In low-grade MALT lymphomas, p16(INK4A) and p57(KIP2) were methylated in 41.7 and 29.2% of the cases, respectively. In diffuse large B-cell lymphomas, methylation of p16(INK4A) and p57(KIP2) was found in 72.7 and 36.4% of the cases, respectively. All but one case with p16(INK4A) and p57(KIP2) methylation was H. pylori positive and most of them were stage I. Our results indicate that methylation of p16(INK4A) followed by p57(KIP2) methylation involves during the tumorigenesis of gastric MALT lymphomas associated with H. pylori infection. As methylation of these two genes was more frequent in the higher grade (P |
| doi_str_mv | 10.1038/modpathol.3800505 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_67573306</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67573306</sourcerecordid><originalsourceid>FETCH-LOGICAL-p209t-8b06cf937df20e7913fb167bfe34c4698447a39be2750997386b07c599c4ac403</originalsourceid><addsrcrecordid>eNo1kE1PwkAYhPegEUR_gBezJ4OH4rb7fSTEDwKoBzw32_Ytrdl2S3ch4d_bBDzNTPJkMhmEHmIyiwlVL40rOhMqZ2dUEcIJv0JjojSNqObJCN16_0tIzLhKbtAoFpRLxfgY7TcQqpM1oXYtdiXuYjFdfq7Y_BmbtsAdl9PV8jsZUg-4bo_OHqEYDA4V4AKOYF3XQBvOdO92PXh_6doZH_o6x5v5eovtqekq1xh_h65LYz3cX3SCft5et4uPaP31vlzM11GXEB0ilRGRl5rKokwISB3TMouFzEqgLGdCK8akoTqDRHKitaRKZETmXOucmZwROkFP595h1f4APqRN7XOw1rTgDj4VkktKiRjAxwt4yBoo0q6vG9Of0v-T6B9Ee2dr</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67573306</pqid></control><display><type>article</type><title>Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Min, Ki Ouk ; Seo, Eun Joo ; Kwon, Hi Jeong ; Lee, Eui Jin ; Kim, Won Il ; Kang, Chang Suk ; Kim, Kyoung-Mee</creator><creatorcontrib>Min, Ki Ouk ; Seo, Eun Joo ; Kwon, Hi Jeong ; Lee, Eui Jin ; Kim, Won Il ; Kang, Chang Suk ; Kim, Kyoung-Mee</creatorcontrib><description>p16(INK4A) and p57(KIP2) are inhibitors of cyclin-dependent kinases and their inactivation by methylation has been reported as a major tumorigenic mechanism in tumors. To examine whether methylation of p16(INK4A) and p57(KIP2) is involved in the development and progression of gastric MALT lymphomas, 24 gastric low-grade lymphomas of MALT, 11 diffuse large B-cell lymphomas, and 10 each case of gastric lymphoid follicles with and without Helicobacter pylori infection were studied. H. pylori infection was positive in 85.7% of the gastric lymphomas. In the gastric lymphoid follicles positive for H. pylori, methylation of p16(INK4A) was detected in 10% of cases, while methylation of p57(KIP2) was not detected. In low-grade MALT lymphomas, p16(INK4A) and p57(KIP2) were methylated in 41.7 and 29.2% of the cases, respectively. In diffuse large B-cell lymphomas, methylation of p16(INK4A) and p57(KIP2) was found in 72.7 and 36.4% of the cases, respectively. All but one case with p16(INK4A) and p57(KIP2) methylation was H. pylori positive and most of them were stage I. Our results indicate that methylation of p16(INK4A) followed by p57(KIP2) methylation involves during the tumorigenesis of gastric MALT lymphomas associated with H. pylori infection. As methylation of these two genes was more frequent in the higher grade (P<0.05), it may contribute to the malignant progression of gastric MALT lymphomas.</description><identifier>ISSN: 0893-3952</identifier><identifier>DOI: 10.1038/modpathol.3800505</identifier><identifier>PMID: 16357845</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; Aged ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-Dependent Kinase Inhibitor p57 - genetics ; Disease Progression ; DNA Methylation ; Female ; Helicobacter Infections - complications ; Humans ; Lymphoma, B-Cell, Marginal Zone - complications ; Lymphoma, B-Cell, Marginal Zone - genetics ; Lymphoma, B-Cell, Marginal Zone - pathology ; Male ; Middle Aged ; Polymerase Chain Reaction - methods ; Stomach Neoplasms - complications ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology</subject><ispartof>Modern pathology, 2006-01, Vol.19 (1), p.141-148</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16357845$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Min, Ki Ouk</creatorcontrib><creatorcontrib>Seo, Eun Joo</creatorcontrib><creatorcontrib>Kwon, Hi Jeong</creatorcontrib><creatorcontrib>Lee, Eui Jin</creatorcontrib><creatorcontrib>Kim, Won Il</creatorcontrib><creatorcontrib>Kang, Chang Suk</creatorcontrib><creatorcontrib>Kim, Kyoung-Mee</creatorcontrib><title>Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas</title><title>Modern pathology</title><addtitle>Mod Pathol</addtitle><description>p16(INK4A) and p57(KIP2) are inhibitors of cyclin-dependent kinases and their inactivation by methylation has been reported as a major tumorigenic mechanism in tumors. To examine whether methylation of p16(INK4A) and p57(KIP2) is involved in the development and progression of gastric MALT lymphomas, 24 gastric low-grade lymphomas of MALT, 11 diffuse large B-cell lymphomas, and 10 each case of gastric lymphoid follicles with and without Helicobacter pylori infection were studied. H. pylori infection was positive in 85.7% of the gastric lymphomas. In the gastric lymphoid follicles positive for H. pylori, methylation of p16(INK4A) was detected in 10% of cases, while methylation of p57(KIP2) was not detected. In low-grade MALT lymphomas, p16(INK4A) and p57(KIP2) were methylated in 41.7 and 29.2% of the cases, respectively. In diffuse large B-cell lymphomas, methylation of p16(INK4A) and p57(KIP2) was found in 72.7 and 36.4% of the cases, respectively. All but one case with p16(INK4A) and p57(KIP2) methylation was H. pylori positive and most of them were stage I. Our results indicate that methylation of p16(INK4A) followed by p57(KIP2) methylation involves during the tumorigenesis of gastric MALT lymphomas associated with H. pylori infection. As methylation of these two genes was more frequent in the higher grade (P<0.05), it may contribute to the malignant progression of gastric MALT lymphomas.</description><subject>Adult</subject><subject>Aged</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p57 - genetics</subject><subject>Disease Progression</subject><subject>DNA Methylation</subject><subject>Female</subject><subject>Helicobacter Infections - complications</subject><subject>Humans</subject><subject>Lymphoma, B-Cell, Marginal Zone - complications</subject><subject>Lymphoma, B-Cell, Marginal Zone - genetics</subject><subject>Lymphoma, B-Cell, Marginal Zone - pathology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Stomach Neoplasms - complications</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><issn>0893-3952</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kE1PwkAYhPegEUR_gBezJ4OH4rb7fSTEDwKoBzw32_Ytrdl2S3ch4d_bBDzNTPJkMhmEHmIyiwlVL40rOhMqZ2dUEcIJv0JjojSNqObJCN16_0tIzLhKbtAoFpRLxfgY7TcQqpM1oXYtdiXuYjFdfq7Y_BmbtsAdl9PV8jsZUg-4bo_OHqEYDA4V4AKOYF3XQBvOdO92PXh_6doZH_o6x5v5eovtqekq1xh_h65LYz3cX3SCft5et4uPaP31vlzM11GXEB0ilRGRl5rKokwISB3TMouFzEqgLGdCK8akoTqDRHKitaRKZETmXOucmZwROkFP595h1f4APqRN7XOw1rTgDj4VkktKiRjAxwt4yBoo0q6vG9Of0v-T6B9Ee2dr</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Min, Ki Ouk</creator><creator>Seo, Eun Joo</creator><creator>Kwon, Hi Jeong</creator><creator>Lee, Eui Jin</creator><creator>Kim, Won Il</creator><creator>Kang, Chang Suk</creator><creator>Kim, Kyoung-Mee</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200601</creationdate><title>Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas</title><author>Min, Ki Ouk ; Seo, Eun Joo ; Kwon, Hi Jeong ; Lee, Eui Jin ; Kim, Won Il ; Kang, Chang Suk ; Kim, Kyoung-Mee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p209t-8b06cf937df20e7913fb167bfe34c4698447a39be2750997386b07c599c4ac403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p57 - genetics</topic><topic>Disease Progression</topic><topic>DNA Methylation</topic><topic>Female</topic><topic>Helicobacter Infections - complications</topic><topic>Humans</topic><topic>Lymphoma, B-Cell, Marginal Zone - complications</topic><topic>Lymphoma, B-Cell, Marginal Zone - genetics</topic><topic>Lymphoma, B-Cell, Marginal Zone - pathology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Stomach Neoplasms - complications</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Min, Ki Ouk</creatorcontrib><creatorcontrib>Seo, Eun Joo</creatorcontrib><creatorcontrib>Kwon, Hi Jeong</creatorcontrib><creatorcontrib>Lee, Eui Jin</creatorcontrib><creatorcontrib>Kim, Won Il</creatorcontrib><creatorcontrib>Kang, Chang Suk</creatorcontrib><creatorcontrib>Kim, Kyoung-Mee</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Modern pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Min, Ki Ouk</au><au>Seo, Eun Joo</au><au>Kwon, Hi Jeong</au><au>Lee, Eui Jin</au><au>Kim, Won Il</au><au>Kang, Chang Suk</au><au>Kim, Kyoung-Mee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas</atitle><jtitle>Modern pathology</jtitle><addtitle>Mod Pathol</addtitle><date>2006-01</date><risdate>2006</risdate><volume>19</volume><issue>1</issue><spage>141</spage><epage>148</epage><pages>141-148</pages><issn>0893-3952</issn><abstract>p16(INK4A) and p57(KIP2) are inhibitors of cyclin-dependent kinases and their inactivation by methylation has been reported as a major tumorigenic mechanism in tumors. To examine whether methylation of p16(INK4A) and p57(KIP2) is involved in the development and progression of gastric MALT lymphomas, 24 gastric low-grade lymphomas of MALT, 11 diffuse large B-cell lymphomas, and 10 each case of gastric lymphoid follicles with and without Helicobacter pylori infection were studied. H. pylori infection was positive in 85.7% of the gastric lymphomas. In the gastric lymphoid follicles positive for H. pylori, methylation of p16(INK4A) was detected in 10% of cases, while methylation of p57(KIP2) was not detected. In low-grade MALT lymphomas, p16(INK4A) and p57(KIP2) were methylated in 41.7 and 29.2% of the cases, respectively. In diffuse large B-cell lymphomas, methylation of p16(INK4A) and p57(KIP2) was found in 72.7 and 36.4% of the cases, respectively. All but one case with p16(INK4A) and p57(KIP2) methylation was H. pylori positive and most of them were stage I. Our results indicate that methylation of p16(INK4A) followed by p57(KIP2) methylation involves during the tumorigenesis of gastric MALT lymphomas associated with H. pylori infection. As methylation of these two genes was more frequent in the higher grade (P<0.05), it may contribute to the malignant progression of gastric MALT lymphomas.</abstract><cop>United States</cop><pmid>16357845</pmid><doi>10.1038/modpathol.3800505</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0893-3952 |
| ispartof | Modern pathology, 2006-01, Vol.19 (1), p.141-148 |
| issn | 0893-3952 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67573306 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p57 - genetics Disease Progression DNA Methylation Female Helicobacter Infections - complications Humans Lymphoma, B-Cell, Marginal Zone - complications Lymphoma, B-Cell, Marginal Zone - genetics Lymphoma, B-Cell, Marginal Zone - pathology Male Middle Aged Polymerase Chain Reaction - methods Stomach Neoplasms - complications Stomach Neoplasms - genetics Stomach Neoplasms - pathology |
| title | Methylation of p16(INK4A) and p57(KIP2) are involved in the development and progression of gastric MALT lymphomas |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T19%3A13%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Methylation%20of%20p16(INK4A)%20and%20p57(KIP2)%20are%20involved%20in%20the%20development%20and%20progression%20of%20gastric%20MALT%20lymphomas&rft.jtitle=Modern%20pathology&rft.au=Min,%20Ki%20Ouk&rft.date=2006-01&rft.volume=19&rft.issue=1&rft.spage=141&rft.epage=148&rft.pages=141-148&rft.issn=0893-3952&rft_id=info:doi/10.1038/modpathol.3800505&rft_dat=%3Cproquest_pubme%3E67573306%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67573306&rft_id=info:pmid/16357845&rfr_iscdi=true |