Loading…

γ-Radiation Sensitivity and Risk of Glioma

Background: About 9% of human cancers are brain tumors, of which 90% are gliomas. γ-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to γ-radiation than were lymphocytes from matched co...

Full description

Saved in:
Bibliographic Details
Published in:JNCI : Journal of the National Cancer Institute 2001-10, Vol.93 (20), p.1553-1557
Main Authors: Bondy, Melissa L., Wang, Li-E., El-Zein, Randa, de Andrade, Mariza, Selvan, Mano S., Bruner, Janet M., Levin, Victor A., Alfred Yung, W. K., Adatto, Phyllis, Wei, Qingyi
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page 1557
container_issue 20
container_start_page 1553
container_title JNCI : Journal of the National Cancer Institute
container_volume 93
creator Bondy, Melissa L.
Wang, Li-E.
El-Zein, Randa
de Andrade, Mariza
Selvan, Mano S.
Bruner, Janet M.
Levin, Victor A.
Alfred Yung, W. K.
Adatto, Phyllis
Wei, Qingyi
description Background: About 9% of human cancers are brain tumors, of which 90% are gliomas. γ-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to γ-radiation than were lymphocytes from matched control subjects. In this larger case–control study, we compared the γ-radiation sensitivity of lymphocytes from glioma patients with those from control subjects and investigated the association between mutagen sensitivity and the risk for developing glioma. Methods: We used a mutagen sensitivity assay (an indirect measure of DNA repair activity) to assess chromosomal damage. We γ-irradiated (1.5 Gy) short-term lymphocyte cultures from 219 case patients with glioma and from 238 healthy control subjects frequency matched by age and sex. After irradiation, cells were cultured for 4 hours, and then Colcemid was added for 1 hour to arrest cells in mitosis. Fifty metaphases were randomly selected for each sample and scored for chromatid breaks. All statistical tests were two-sided. Results: We observed a statistically significantly higher frequency of chromatid breaks per cell from case patients with glioma (mean = 0.55; 95% confidence interval [CI] = 0.50 to 0.59) than from control subjects (mean = 0.44; 95% CI = 0.41 to 0.48) (P
doi_str_mv 10.1093/jnci/93.20.1553
format article
fullrecord <record><control><sourceid>istex_pubme</sourceid><recordid>TN_cdi_pubmed_primary_11604478</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_HXZ_Z677Q2SB_V</sourcerecordid><originalsourceid>FETCH-LOGICAL-i245t-86e2cf68c0f6533db1b081142e04924964616b3126dea01421a93b21b7cd53f63</originalsourceid><addsrcrecordid>eNo9TstKw0AUHUSxsbp2J9nLtHPnnaUWbYWC2KpIN8NMMoFpm6Rkotjv8j_8JgNV7-ZwHpxzEboEMgKSsfG6zsM4YyPacyHYEUqAS4IpEHGMEkKowlorPkBnMa5Jfxnlp2gAIAnnSifo-vsLL2wRbBeaOl36OoYufIRun9q6SBchbtKmTKfb0FT2HJ2Udhv9xS8O0cv93fNkhueP04fJzRwHykWHtfQ0L6XOSSkFY4UDRzQAp57wfj6TXIJ0DKgsvCW9DjZjjoJTeSFYKdkQXR16d--u8oXZtaGy7d78fd0H8CEQYuc__33bboxUTAkze1uZlVTqiS5vzSv7AannUeM</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>γ-Radiation Sensitivity and Risk of Glioma</title><source>Oxford Journals Online</source><creator>Bondy, Melissa L. ; Wang, Li-E. ; El-Zein, Randa ; de Andrade, Mariza ; Selvan, Mano S. ; Bruner, Janet M. ; Levin, Victor A. ; Alfred Yung, W. K. ; Adatto, Phyllis ; Wei, Qingyi</creator><creatorcontrib>Bondy, Melissa L. ; Wang, Li-E. ; El-Zein, Randa ; de Andrade, Mariza ; Selvan, Mano S. ; Bruner, Janet M. ; Levin, Victor A. ; Alfred Yung, W. K. ; Adatto, Phyllis ; Wei, Qingyi</creatorcontrib><description>Background: About 9% of human cancers are brain tumors, of which 90% are gliomas. γ-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to γ-radiation than were lymphocytes from matched control subjects. In this larger case–control study, we compared the γ-radiation sensitivity of lymphocytes from glioma patients with those from control subjects and investigated the association between mutagen sensitivity and the risk for developing glioma. Methods: We used a mutagen sensitivity assay (an indirect measure of DNA repair activity) to assess chromosomal damage. We γ-irradiated (1.5 Gy) short-term lymphocyte cultures from 219 case patients with glioma and from 238 healthy control subjects frequency matched by age and sex. After irradiation, cells were cultured for 4 hours, and then Colcemid was added for 1 hour to arrest cells in mitosis. Fifty metaphases were randomly selected for each sample and scored for chromatid breaks. All statistical tests were two-sided. Results: We observed a statistically significantly higher frequency of chromatid breaks per cell from case patients with glioma (mean = 0.55; 95% confidence interval [CI] = 0.50 to 0.59) than from control subjects (mean = 0.44; 95% CI = 0.41 to 0.48) (P&lt;.001). Using 0.40 (the median number of chromatid breaks per cell in control subjects) as the cut point for defining mutagen sensitivity and adjusting for age, sex, and smoking status, we found that mutagen sensitivity was statistically significantly associated with an increased risk for glioma (odds ratio = 2.09; 95% CI = 1.43 to 3.06). When the data were divided into tertiles, the relative risk for glioma increased from the lowest tertile to the highest tertile (trend test, P&lt;.001). Conclusion: γ-Radiation-induced mutagen sensitivity of lymphocytes may be associated with an increased risk for glioma, a result that supports our earlier preliminary findings.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/93.20.1553</identifier><identifier>PMID: 11604478</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Adult ; Animals ; Brain Neoplasms - epidemiology ; Brain Neoplasms - etiology ; Brain Neoplasms - genetics ; Case-Control Studies ; Chromatids - radiation effects ; Chromatids - ultrastructure ; Chromosome Breakage ; Demecolcine - pharmacology ; DNA - radiation effects ; DNA Damage ; DNA Repair - genetics ; DNA Repair - radiation effects ; DNA, Single-Stranded - radiation effects ; Female ; Gamma Rays - adverse effects ; Genetic Predisposition to Disease ; Glioma - epidemiology ; Glioma - etiology ; Glioma - genetics ; Humans ; Lymphocytes - pathology ; Lymphocytes - radiation effects ; Male ; Middle Aged ; Neoplasms, Radiation-Induced - epidemiology ; Neoplasms, Radiation-Induced - etiology ; Neoplasms, Radiation-Induced - genetics ; Odds Ratio ; Radiation Tolerance - genetics ; Risk ; Smoking - epidemiology</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2001-10, Vol.93 (20), p.1553-1557</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11604478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bondy, Melissa L.</creatorcontrib><creatorcontrib>Wang, Li-E.</creatorcontrib><creatorcontrib>El-Zein, Randa</creatorcontrib><creatorcontrib>de Andrade, Mariza</creatorcontrib><creatorcontrib>Selvan, Mano S.</creatorcontrib><creatorcontrib>Bruner, Janet M.</creatorcontrib><creatorcontrib>Levin, Victor A.</creatorcontrib><creatorcontrib>Alfred Yung, W. K.</creatorcontrib><creatorcontrib>Adatto, Phyllis</creatorcontrib><creatorcontrib>Wei, Qingyi</creatorcontrib><title>γ-Radiation Sensitivity and Risk of Glioma</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>JNCI J Natl Cancer Inst</addtitle><description>Background: About 9% of human cancers are brain tumors, of which 90% are gliomas. γ-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to γ-radiation than were lymphocytes from matched control subjects. In this larger case–control study, we compared the γ-radiation sensitivity of lymphocytes from glioma patients with those from control subjects and investigated the association between mutagen sensitivity and the risk for developing glioma. Methods: We used a mutagen sensitivity assay (an indirect measure of DNA repair activity) to assess chromosomal damage. We γ-irradiated (1.5 Gy) short-term lymphocyte cultures from 219 case patients with glioma and from 238 healthy control subjects frequency matched by age and sex. After irradiation, cells were cultured for 4 hours, and then Colcemid was added for 1 hour to arrest cells in mitosis. Fifty metaphases were randomly selected for each sample and scored for chromatid breaks. All statistical tests were two-sided. Results: We observed a statistically significantly higher frequency of chromatid breaks per cell from case patients with glioma (mean = 0.55; 95% confidence interval [CI] = 0.50 to 0.59) than from control subjects (mean = 0.44; 95% CI = 0.41 to 0.48) (P&lt;.001). Using 0.40 (the median number of chromatid breaks per cell in control subjects) as the cut point for defining mutagen sensitivity and adjusting for age, sex, and smoking status, we found that mutagen sensitivity was statistically significantly associated with an increased risk for glioma (odds ratio = 2.09; 95% CI = 1.43 to 3.06). When the data were divided into tertiles, the relative risk for glioma increased from the lowest tertile to the highest tertile (trend test, P&lt;.001). Conclusion: γ-Radiation-induced mutagen sensitivity of lymphocytes may be associated with an increased risk for glioma, a result that supports our earlier preliminary findings.</description><subject>Adult</subject><subject>Animals</subject><subject>Brain Neoplasms - epidemiology</subject><subject>Brain Neoplasms - etiology</subject><subject>Brain Neoplasms - genetics</subject><subject>Case-Control Studies</subject><subject>Chromatids - radiation effects</subject><subject>Chromatids - ultrastructure</subject><subject>Chromosome Breakage</subject><subject>Demecolcine - pharmacology</subject><subject>DNA - radiation effects</subject><subject>DNA Damage</subject><subject>DNA Repair - genetics</subject><subject>DNA Repair - radiation effects</subject><subject>DNA, Single-Stranded - radiation effects</subject><subject>Female</subject><subject>Gamma Rays - adverse effects</subject><subject>Genetic Predisposition to Disease</subject><subject>Glioma - epidemiology</subject><subject>Glioma - etiology</subject><subject>Glioma - genetics</subject><subject>Humans</subject><subject>Lymphocytes - pathology</subject><subject>Lymphocytes - radiation effects</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neoplasms, Radiation-Induced - epidemiology</subject><subject>Neoplasms, Radiation-Induced - etiology</subject><subject>Neoplasms, Radiation-Induced - genetics</subject><subject>Odds Ratio</subject><subject>Radiation Tolerance - genetics</subject><subject>Risk</subject><subject>Smoking - epidemiology</subject><issn>0027-8874</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNo9TstKw0AUHUSxsbp2J9nLtHPnnaUWbYWC2KpIN8NMMoFpm6Rkotjv8j_8JgNV7-ZwHpxzEboEMgKSsfG6zsM4YyPacyHYEUqAS4IpEHGMEkKowlorPkBnMa5Jfxnlp2gAIAnnSifo-vsLL2wRbBeaOl36OoYufIRun9q6SBchbtKmTKfb0FT2HJ2Udhv9xS8O0cv93fNkhueP04fJzRwHykWHtfQ0L6XOSSkFY4UDRzQAp57wfj6TXIJ0DKgsvCW9DjZjjoJTeSFYKdkQXR16d--u8oXZtaGy7d78fd0H8CEQYuc__33bboxUTAkze1uZlVTqiS5vzSv7AannUeM</recordid><startdate>20011017</startdate><enddate>20011017</enddate><creator>Bondy, Melissa L.</creator><creator>Wang, Li-E.</creator><creator>El-Zein, Randa</creator><creator>de Andrade, Mariza</creator><creator>Selvan, Mano S.</creator><creator>Bruner, Janet M.</creator><creator>Levin, Victor A.</creator><creator>Alfred Yung, W. K.</creator><creator>Adatto, Phyllis</creator><creator>Wei, Qingyi</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20011017</creationdate><title>γ-Radiation Sensitivity and Risk of Glioma</title><author>Bondy, Melissa L. ; Wang, Li-E. ; El-Zein, Randa ; de Andrade, Mariza ; Selvan, Mano S. ; Bruner, Janet M. ; Levin, Victor A. ; Alfred Yung, W. K. ; Adatto, Phyllis ; Wei, Qingyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i245t-86e2cf68c0f6533db1b081142e04924964616b3126dea01421a93b21b7cd53f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Brain Neoplasms - epidemiology</topic><topic>Brain Neoplasms - etiology</topic><topic>Brain Neoplasms - genetics</topic><topic>Case-Control Studies</topic><topic>Chromatids - radiation effects</topic><topic>Chromatids - ultrastructure</topic><topic>Chromosome Breakage</topic><topic>Demecolcine - pharmacology</topic><topic>DNA - radiation effects</topic><topic>DNA Damage</topic><topic>DNA Repair - genetics</topic><topic>DNA Repair - radiation effects</topic><topic>DNA, Single-Stranded - radiation effects</topic><topic>Female</topic><topic>Gamma Rays - adverse effects</topic><topic>Genetic Predisposition to Disease</topic><topic>Glioma - epidemiology</topic><topic>Glioma - etiology</topic><topic>Glioma - genetics</topic><topic>Humans</topic><topic>Lymphocytes - pathology</topic><topic>Lymphocytes - radiation effects</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neoplasms, Radiation-Induced - epidemiology</topic><topic>Neoplasms, Radiation-Induced - etiology</topic><topic>Neoplasms, Radiation-Induced - genetics</topic><topic>Odds Ratio</topic><topic>Radiation Tolerance - genetics</topic><topic>Risk</topic><topic>Smoking - epidemiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bondy, Melissa L.</creatorcontrib><creatorcontrib>Wang, Li-E.</creatorcontrib><creatorcontrib>El-Zein, Randa</creatorcontrib><creatorcontrib>de Andrade, Mariza</creatorcontrib><creatorcontrib>Selvan, Mano S.</creatorcontrib><creatorcontrib>Bruner, Janet M.</creatorcontrib><creatorcontrib>Levin, Victor A.</creatorcontrib><creatorcontrib>Alfred Yung, W. K.</creatorcontrib><creatorcontrib>Adatto, Phyllis</creatorcontrib><creatorcontrib>Wei, Qingyi</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bondy, Melissa L.</au><au>Wang, Li-E.</au><au>El-Zein, Randa</au><au>de Andrade, Mariza</au><au>Selvan, Mano S.</au><au>Bruner, Janet M.</au><au>Levin, Victor A.</au><au>Alfred Yung, W. K.</au><au>Adatto, Phyllis</au><au>Wei, Qingyi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>γ-Radiation Sensitivity and Risk of Glioma</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>JNCI J Natl Cancer Inst</addtitle><date>2001-10-17</date><risdate>2001</risdate><volume>93</volume><issue>20</issue><spage>1553</spage><epage>1557</epage><pages>1553-1557</pages><issn>0027-8874</issn><eissn>1460-2105</eissn><abstract>Background: About 9% of human cancers are brain tumors, of which 90% are gliomas. γ-Radiation has been identified as a risk factor for brain tumors. In a previous pilot study, we found that lymphocytes from patients with glioma were more sensitive to γ-radiation than were lymphocytes from matched control subjects. In this larger case–control study, we compared the γ-radiation sensitivity of lymphocytes from glioma patients with those from control subjects and investigated the association between mutagen sensitivity and the risk for developing glioma. Methods: We used a mutagen sensitivity assay (an indirect measure of DNA repair activity) to assess chromosomal damage. We γ-irradiated (1.5 Gy) short-term lymphocyte cultures from 219 case patients with glioma and from 238 healthy control subjects frequency matched by age and sex. After irradiation, cells were cultured for 4 hours, and then Colcemid was added for 1 hour to arrest cells in mitosis. Fifty metaphases were randomly selected for each sample and scored for chromatid breaks. All statistical tests were two-sided. Results: We observed a statistically significantly higher frequency of chromatid breaks per cell from case patients with glioma (mean = 0.55; 95% confidence interval [CI] = 0.50 to 0.59) than from control subjects (mean = 0.44; 95% CI = 0.41 to 0.48) (P&lt;.001). Using 0.40 (the median number of chromatid breaks per cell in control subjects) as the cut point for defining mutagen sensitivity and adjusting for age, sex, and smoking status, we found that mutagen sensitivity was statistically significantly associated with an increased risk for glioma (odds ratio = 2.09; 95% CI = 1.43 to 3.06). When the data were divided into tertiles, the relative risk for glioma increased from the lowest tertile to the highest tertile (trend test, P&lt;.001). Conclusion: γ-Radiation-induced mutagen sensitivity of lymphocytes may be associated with an increased risk for glioma, a result that supports our earlier preliminary findings.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>11604478</pmid><doi>10.1093/jnci/93.20.1553</doi><tpages>5</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0027-8874
ispartof JNCI : Journal of the National Cancer Institute, 2001-10, Vol.93 (20), p.1553-1557
issn 0027-8874
1460-2105
language eng
recordid cdi_pubmed_primary_11604478
source Oxford Journals Online
subjects Adult
Animals
Brain Neoplasms - epidemiology
Brain Neoplasms - etiology
Brain Neoplasms - genetics
Case-Control Studies
Chromatids - radiation effects
Chromatids - ultrastructure
Chromosome Breakage
Demecolcine - pharmacology
DNA - radiation effects
DNA Damage
DNA Repair - genetics
DNA Repair - radiation effects
DNA, Single-Stranded - radiation effects
Female
Gamma Rays - adverse effects
Genetic Predisposition to Disease
Glioma - epidemiology
Glioma - etiology
Glioma - genetics
Humans
Lymphocytes - pathology
Lymphocytes - radiation effects
Male
Middle Aged
Neoplasms, Radiation-Induced - epidemiology
Neoplasms, Radiation-Induced - etiology
Neoplasms, Radiation-Induced - genetics
Odds Ratio
Radiation Tolerance - genetics
Risk
Smoking - epidemiology
title γ-Radiation Sensitivity and Risk of Glioma
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T17%3A18%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-istex_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B3-Radiation%20Sensitivity%20and%20Risk%20of%20Glioma&rft.jtitle=JNCI%20:%20Journal%20of%20the%20National%20Cancer%20Institute&rft.au=Bondy,%20Melissa%20L.&rft.date=2001-10-17&rft.volume=93&rft.issue=20&rft.spage=1553&rft.epage=1557&rft.pages=1553-1557&rft.issn=0027-8874&rft.eissn=1460-2105&rft_id=info:doi/10.1093/jnci/93.20.1553&rft_dat=%3Cistex_pubme%3Eark_67375_HXZ_Z677Q2SB_V%3C/istex_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-i245t-86e2cf68c0f6533db1b081142e04924964616b3126dea01421a93b21b7cd53f63%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/11604478&rfr_iscdi=true