Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study
Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in th...
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| Veröffentlicht in: | Cancers 2010-04, Vol.2 (2), p.420-435 |
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| creator | Rourke, Elizabeth A Lopez, Mirtha S Monroy, Claudia M Scheurer, Michael E Etzel, Carol J Albrecht, Thomas Bondy, Melissa L El-Zein, Randa A |
| description | Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in the presence of g-radiation; an established risk factor for gliomas. We tested the hypothesis that HCMV infection modifies the sensitivity of cells to γ-radiation-induced genetic damage. We used peripheral blood lymphocytes (PBLs) from 110 glioma patients and 100 controls to measure the level of chromosome damage and cell death. We evaluated baseline, HCMV-, γ-radiation and HCMV + γ-radiation induced genetic instability with the comprehensive Cytokinesis-Blocked Micronucleus Cytome (CBMN-CYT). HCMV, similar to radiation, induced a significant increase in aberration frequency among cases and controls. PBLs infected with HCMV prior to challenge with γ-radiation led to a significant increase in aberrations as compared to baseline, γ-radiation and HCMV alone. With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis. |
| doi_str_mv | 10.3390/cancers2020420 |
| format | Article |
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An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in the presence of g-radiation; an established risk factor for gliomas. We tested the hypothesis that HCMV infection modifies the sensitivity of cells to γ-radiation-induced genetic damage. We used peripheral blood lymphocytes (PBLs) from 110 glioma patients and 100 controls to measure the level of chromosome damage and cell death. We evaluated baseline, HCMV-, γ-radiation and HCMV + γ-radiation induced genetic instability with the comprehensive Cytokinesis-Blocked Micronucleus Cytome (CBMN-CYT). HCMV, similar to radiation, induced a significant increase in aberration frequency among cases and controls. PBLs infected with HCMV prior to challenge with γ-radiation led to a significant increase in aberrations as compared to baseline, γ-radiation and HCMV alone. With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers2020420</identifier><identifier>PMID: 24281077</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Apoptosis ; Brain cancer ; Cell death ; Cell growth ; Chromosomes ; Cytomegalovirus ; DNA damage ; Epidemiology ; Infections ; Lymphocytes ; Pathogenesis ; Radiation ; Risk factors ; Tumors</subject><ispartof>Cancers, 2010-04, Vol.2 (2), p.420-435</ispartof><rights>Copyright MDPI AG 2010</rights><rights>2010 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3330-c3e7d2406fbee3bfe2275651ee3269a8daef7de937981eb70cf5e775ee8d5d223</citedby><cites>FETCH-LOGICAL-c3330-c3e7d2406fbee3bfe2275651ee3269a8daef7de937981eb70cf5e775ee8d5d223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835085/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835085/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24281077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rourke, Elizabeth A</creatorcontrib><creatorcontrib>Lopez, Mirtha S</creatorcontrib><creatorcontrib>Monroy, Claudia M</creatorcontrib><creatorcontrib>Scheurer, Michael E</creatorcontrib><creatorcontrib>Etzel, Carol J</creatorcontrib><creatorcontrib>Albrecht, Thomas</creatorcontrib><creatorcontrib>Bondy, Melissa L</creatorcontrib><creatorcontrib>El-Zein, Randa A</creatorcontrib><title>Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. An association between HCMV infection and malignant gliomas has been reported, suggesting that HCMV may play a role in glioma pathogenesis and could facilitate an accrual of genotoxic damage in the presence of g-radiation; an established risk factor for gliomas. We tested the hypothesis that HCMV infection modifies the sensitivity of cells to γ-radiation-induced genetic damage. We used peripheral blood lymphocytes (PBLs) from 110 glioma patients and 100 controls to measure the level of chromosome damage and cell death. We evaluated baseline, HCMV-, γ-radiation and HCMV + γ-radiation induced genetic instability with the comprehensive Cytokinesis-Blocked Micronucleus Cytome (CBMN-CYT). HCMV, similar to radiation, induced a significant increase in aberration frequency among cases and controls. PBLs infected with HCMV prior to challenge with γ-radiation led to a significant increase in aberrations as compared to baseline, γ-radiation and HCMV alone. With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis.</description><subject>Apoptosis</subject><subject>Brain cancer</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Chromosomes</subject><subject>Cytomegalovirus</subject><subject>DNA damage</subject><subject>Epidemiology</subject><subject>Infections</subject><subject>Lymphocytes</subject><subject>Pathogenesis</subject><subject>Radiation</subject><subject>Risk factors</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1rFTEUxYMottRuXUrAjZup-ZgkMxvBjtoWXlG0ug2Z5E5fykzyTGaEAf_4ph-W1rvIzSW_HO7hIPSakiPOW_LemmAhZUYYqRl5hvYZUaySsq2fP7rvocOcr0gpzqmS6iXaYzVrKFFqH_09j24ZzexjwHHA343zt0N1FtxiweETCDB7iz-ZyVwC7ld82p3_wj7gb5D8bgvJjPh4jNHhzTrtttGuM2Q8pDhhg4-TKeTFMsWEO5Oh6mKYUxzxj3lx6yv0YjBjhsP7foB-fvl80Z1Wm68nZ93HTWU556ScoByriRx6AN4PwJgSUtAyMNmaxhkYlIOWq7ah0CtiBwFKCYDGCccYP0Af7nR3Sz-Bs1B2MKPeJT-ZtOpovH76EvxWX8Y_mjdckEYUgXf3Ain-XiDPevLZwjiaAHHJmtayZaRt5A369j_0Ki4pFHuaClZTIaloCnV0R9kUc04wPCxDib7JVj_Ntnx489jCA_4vSX4NYl-iAg</recordid><startdate>20100412</startdate><enddate>20100412</enddate><creator>Rourke, Elizabeth A</creator><creator>Lopez, Mirtha S</creator><creator>Monroy, Claudia M</creator><creator>Scheurer, Michael E</creator><creator>Etzel, Carol J</creator><creator>Albrecht, Thomas</creator><creator>Bondy, Melissa L</creator><creator>El-Zein, Randa A</creator><general>MDPI AG</general><general>Molecular Diversity Preservation International</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100412</creationdate><title>Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study</title><author>Rourke, Elizabeth A ; Lopez, Mirtha S ; Monroy, Claudia M ; Scheurer, Michael E ; Etzel, Carol J ; Albrecht, Thomas ; Bondy, Melissa L ; El-Zein, Randa A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3330-c3e7d2406fbee3bfe2275651ee3269a8daef7de937981eb70cf5e775ee8d5d223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Apoptosis</topic><topic>Brain cancer</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Chromosomes</topic><topic>Cytomegalovirus</topic><topic>DNA damage</topic><topic>Epidemiology</topic><topic>Infections</topic><topic>Lymphocytes</topic><topic>Pathogenesis</topic><topic>Radiation</topic><topic>Risk factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rourke, Elizabeth A</creatorcontrib><creatorcontrib>Lopez, Mirtha S</creatorcontrib><creatorcontrib>Monroy, Claudia M</creatorcontrib><creatorcontrib>Scheurer, Michael E</creatorcontrib><creatorcontrib>Etzel, Carol J</creatorcontrib><creatorcontrib>Albrecht, Thomas</creatorcontrib><creatorcontrib>Bondy, Melissa L</creatorcontrib><creatorcontrib>El-Zein, Randa A</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</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>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rourke, Elizabeth A</au><au>Lopez, Mirtha S</au><au>Monroy, Claudia M</au><au>Scheurer, Michael E</au><au>Etzel, Carol J</au><au>Albrecht, Thomas</au><au>Bondy, Melissa L</au><au>El-Zein, Randa A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study</atitle><jtitle>Cancers</jtitle><addtitle>Cancers (Basel)</addtitle><date>2010-04-12</date><risdate>2010</risdate><volume>2</volume><issue>2</issue><spage>420</spage><epage>435</epage><pages>420-435</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Human cytomegalovirus (HCMV) infection occurs early in life and viral persistence remains through life. 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With regards to apoptosis, glioma cases showed a lower percentage of induction following in vitro exposure to γ-radiation and HCMV infection as compared to controls. This strongly suggests that, HCMV infection enhances the sensitivity of PBLs to γ-radiation-induced genetic damage possibly through an increase in chromosome damage and decrease in apoptosis.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>24281077</pmid><doi>10.3390/cancers2020420</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| source | PubMed Central Open Access; MDPI - Multidisciplinary Digital Publishing Institute; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Apoptosis Brain cancer Cell death Cell growth Chromosomes Cytomegalovirus DNA damage Epidemiology Infections Lymphocytes Pathogenesis Radiation Risk factors Tumors |
| title | Modulation of Radiation-Induced Genetic Damage by HCMV in Peripheral Blood Lymphocytes from a Brain Tumor Case-Control Study |
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