A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan
We hypothesized that the genomic response to folate deficiency might be different between breast cancer cases and healthy subjects. To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes f...
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| Veröffentlicht in: | Mutagenesis 2006-01, Vol.21 (1), p.41-47 |
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| creator | Wang, Xu Wu, Xiayu Liang, Ziqing Huang, Yunchao Fenech, Michael Xue, Jinglun |
| description | We hypothesized that the genomic response to folate deficiency might be different between breast cancer cases and healthy subjects. To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes from 19 breast cancer patients and 20 age-matched healthy females from Yunnan, China using the cytokinesis-block micronucleus assay. Lymphocytes from the volunteers were cultured in RPMI1640 medium containing 30, 120 or 240 nM FA for 9 days. The results showed that 30 nM FA was associated with increased frequencies of micronucleated binucleated cell (MNed BNC), nucleoplasmic bridges (NPB), nuclear buds (BUD), apoptosis (APO) and necrosis (NEC) relative to 120 and 240 nM FA (P < 0.001) in lymphocytes of case and control groups in vitro, however there were no significant differences between the 120 and 240 nM FA within each sampling group. The case group showed significantly higher frequencies of MNed BNC than control at 120 and 240 nM FA (P < 0.05–0.001) but not at 30 nM FA (P = 0.052). NEC was significantly higher in breast cancer group than control at all concentrations of FA (P < 0.005). FA concentration explained 60, 39, 39, 52 and 71% of the variance of MNed BNC, NPB, BUD, APO and NEC, respectively compared with breast cancer status which only explained 6 and 7% of the variance of MNed BNC and NEC(Two way ANOVA, P < 0.0001). Difference of difference analysis showed that breast cancer cases were not abnormally sensitive to the genome-damaging effect of folate deficiency. We concluded that (i) increased concentrations of FA abolished the genome-damaging effect of FA deficiency in lymphocytes of both breast cancer patients and controls to a similar extent and (ii) FA concentration is much more important than breast cancer status in determining genomic instability and cell death. |
| doi_str_mv | 10.1093/mutage/gei069 |
| format | Article |
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To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes from 19 breast cancer patients and 20 age-matched healthy females from Yunnan, China using the cytokinesis-block micronucleus assay. Lymphocytes from the volunteers were cultured in RPMI1640 medium containing 30, 120 or 240 nM FA for 9 days. The results showed that 30 nM FA was associated with increased frequencies of micronucleated binucleated cell (MNed BNC), nucleoplasmic bridges (NPB), nuclear buds (BUD), apoptosis (APO) and necrosis (NEC) relative to 120 and 240 nM FA (P < 0.001) in lymphocytes of case and control groups in vitro, however there were no significant differences between the 120 and 240 nM FA within each sampling group. The case group showed significantly higher frequencies of MNed BNC than control at 120 and 240 nM FA (P < 0.05–0.001) but not at 30 nM FA (P = 0.052). NEC was significantly higher in breast cancer group than control at all concentrations of FA (P < 0.005). FA concentration explained 60, 39, 39, 52 and 71% of the variance of MNed BNC, NPB, BUD, APO and NEC, respectively compared with breast cancer status which only explained 6 and 7% of the variance of MNed BNC and NEC(Two way ANOVA, P < 0.0001). Difference of difference analysis showed that breast cancer cases were not abnormally sensitive to the genome-damaging effect of folate deficiency. We concluded that (i) increased concentrations of FA abolished the genome-damaging effect of FA deficiency in lymphocytes of both breast cancer patients and controls to a similar extent and (ii) FA concentration is much more important than breast cancer status in determining genomic instability and cell death.</description><identifier>ISSN: 0267-8357</identifier><identifier>EISSN: 1464-3804</identifier><identifier>DOI: 10.1093/mutage/gei069</identifier><identifier>PMID: 16339195</identifier><identifier>CODEN: MUTAEX</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aged ; Apoptosis - drug effects ; Biological and medical sciences ; Breast - metabolism ; Breast - pathology ; Breast Neoplasms - epidemiology ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Case-Control Studies ; China - epidemiology ; Cytokinesis - drug effects ; Female ; Folic Acid - pharmacology ; Folic Acid Deficiency - metabolism ; Fundamental and applied biological sciences. Psychology ; Genomic Instability ; Humans ; Lymphocytes - drug effects ; Micronuclei, Chromosome-Defective ; Micronucleus Tests ; Middle Aged ; Molecular and cellular biology ; Molecular genetics ; Mutagenesis. Repair ; Necrosis ; Population Groups</subject><ispartof>Mutagenesis, 2006-01, Vol.21 (1), p.41-47</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jan 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-2d09885b4e138f66ed0f06e5554a46de3e2c364415938d2dab2572739c1c86763</citedby><cites>FETCH-LOGICAL-c456t-2d09885b4e138f66ed0f06e5554a46de3e2c364415938d2dab2572739c1c86763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17548938$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16339195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xu</creatorcontrib><creatorcontrib>Wu, Xiayu</creatorcontrib><creatorcontrib>Liang, Ziqing</creatorcontrib><creatorcontrib>Huang, Yunchao</creatorcontrib><creatorcontrib>Fenech, Michael</creatorcontrib><creatorcontrib>Xue, Jinglun</creatorcontrib><title>A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan</title><title>Mutagenesis</title><addtitle>Mutagenesis</addtitle><description>We hypothesized that the genomic response to folate deficiency might be different between breast cancer cases and healthy subjects. To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes from 19 breast cancer patients and 20 age-matched healthy females from Yunnan, China using the cytokinesis-block micronucleus assay. Lymphocytes from the volunteers were cultured in RPMI1640 medium containing 30, 120 or 240 nM FA for 9 days. The results showed that 30 nM FA was associated with increased frequencies of micronucleated binucleated cell (MNed BNC), nucleoplasmic bridges (NPB), nuclear buds (BUD), apoptosis (APO) and necrosis (NEC) relative to 120 and 240 nM FA (P < 0.001) in lymphocytes of case and control groups in vitro, however there were no significant differences between the 120 and 240 nM FA within each sampling group. The case group showed significantly higher frequencies of MNed BNC than control at 120 and 240 nM FA (P < 0.05–0.001) but not at 30 nM FA (P = 0.052). NEC was significantly higher in breast cancer group than control at all concentrations of FA (P < 0.005). FA concentration explained 60, 39, 39, 52 and 71% of the variance of MNed BNC, NPB, BUD, APO and NEC, respectively compared with breast cancer status which only explained 6 and 7% of the variance of MNed BNC and NEC(Two way ANOVA, P < 0.0001). Difference of difference analysis showed that breast cancer cases were not abnormally sensitive to the genome-damaging effect of folate deficiency. We concluded that (i) increased concentrations of FA abolished the genome-damaging effect of FA deficiency in lymphocytes of both breast cancer patients and controls to a similar extent and (ii) FA concentration is much more important than breast cancer status in determining genomic instability and cell death.</description><subject>Adult</subject><subject>Aged</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Breast - metabolism</subject><subject>Breast - pathology</subject><subject>Breast Neoplasms - epidemiology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Case-Control Studies</subject><subject>China - epidemiology</subject><subject>Cytokinesis - drug effects</subject><subject>Female</subject><subject>Folic Acid - pharmacology</subject><subject>Folic Acid Deficiency - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genomic Instability</subject><subject>Humans</subject><subject>Lymphocytes - drug effects</subject><subject>Micronuclei, Chromosome-Defective</subject><subject>Micronucleus Tests</subject><subject>Middle Aged</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutagenesis. Repair</subject><subject>Necrosis</subject><subject>Population Groups</subject><issn>0267-8357</issn><issn>1464-3804</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU2LFDEQhhtR3HH16FWCoLd2k85X93EZP1YYEWEV3UvIJNWzWbuTNkmD_aP8j2aZxgFPVfA-9VYlb1U9J_gNwR29GOesD3BxAIdF96DaECZYTVvMHlYb3AhZt5TLs-pJSncYE9kI_Lg6I4LSjnR8U_25RCaMk44uBY9Cj_owOIO0cRZZ6J1x4M1SO29nAxYdwIex6M6nrPducHkpPRqWcboNZsmQ7j32EXTKyGhvIKJJ52KSE9LeIh_iqIdSfL3KJvgcw5BQH8OINNreOg8J0BSmeSij5ayy4cfsvfZPq0e9HhI8W-t59fX9u-vtVb37_OHj9nJXG8ZFrhuLu7blewaEtr0QYHGPBXDOmWbCAoXGUMEY4R1tbWP1vuGykbQzxLRCCnpevT76TjH8miFlNbpkYBi0hzAnRbqOMUZZAV_-B96FOfpym2qIbDlvJS5QfYRMDClF6NUU3ajjoghW9yGqY4jqGGLhX6ym834Ee6LX1ArwagV0MnroY_lJl06c5KwtLzstdinD73-6jj-VkFRydfX9Rl3fvBVfdt-k-kT_Ak39uSs</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>Wang, Xu</creator><creator>Wu, Xiayu</creator><creator>Liang, Ziqing</creator><creator>Huang, Yunchao</creator><creator>Fenech, Michael</creator><creator>Xue, Jinglun</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>200601</creationdate><title>A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan</title><author>Wang, Xu ; Wu, Xiayu ; Liang, Ziqing ; Huang, Yunchao ; Fenech, Michael ; Xue, Jinglun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-2d09885b4e138f66ed0f06e5554a46de3e2c364415938d2dab2572739c1c86763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Breast - metabolism</topic><topic>Breast - pathology</topic><topic>Breast Neoplasms - epidemiology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Case-Control Studies</topic><topic>China - epidemiology</topic><topic>Cytokinesis - drug effects</topic><topic>Female</topic><topic>Folic Acid - pharmacology</topic><topic>Folic Acid Deficiency - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genomic Instability</topic><topic>Humans</topic><topic>Lymphocytes - drug effects</topic><topic>Micronuclei, Chromosome-Defective</topic><topic>Micronucleus Tests</topic><topic>Middle Aged</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutagenesis. Repair</topic><topic>Necrosis</topic><topic>Population Groups</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xu</creatorcontrib><creatorcontrib>Wu, Xiayu</creatorcontrib><creatorcontrib>Liang, Ziqing</creatorcontrib><creatorcontrib>Huang, Yunchao</creatorcontrib><creatorcontrib>Fenech, Michael</creatorcontrib><creatorcontrib>Xue, Jinglun</creatorcontrib><collection>Istex</collection><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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Mutagenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xu</au><au>Wu, Xiayu</au><au>Liang, Ziqing</au><au>Huang, Yunchao</au><au>Fenech, Michael</au><au>Xue, Jinglun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan</atitle><jtitle>Mutagenesis</jtitle><addtitle>Mutagenesis</addtitle><date>2006-01</date><risdate>2006</risdate><volume>21</volume><issue>1</issue><spage>41</spage><epage>47</epage><pages>41-47</pages><issn>0267-8357</issn><eissn>1464-3804</eissn><coden>MUTAEX</coden><abstract>We hypothesized that the genomic response to folate deficiency might be different between breast cancer cases and healthy subjects. To test this hypothesis, we performed a comprehensive study on the genotoxic and cytotoxic effects of in vitro folic acid (FA) deficiency on primary human lymphocytes from 19 breast cancer patients and 20 age-matched healthy females from Yunnan, China using the cytokinesis-block micronucleus assay. Lymphocytes from the volunteers were cultured in RPMI1640 medium containing 30, 120 or 240 nM FA for 9 days. The results showed that 30 nM FA was associated with increased frequencies of micronucleated binucleated cell (MNed BNC), nucleoplasmic bridges (NPB), nuclear buds (BUD), apoptosis (APO) and necrosis (NEC) relative to 120 and 240 nM FA (P < 0.001) in lymphocytes of case and control groups in vitro, however there were no significant differences between the 120 and 240 nM FA within each sampling group. The case group showed significantly higher frequencies of MNed BNC than control at 120 and 240 nM FA (P < 0.05–0.001) but not at 30 nM FA (P = 0.052). NEC was significantly higher in breast cancer group than control at all concentrations of FA (P < 0.005). FA concentration explained 60, 39, 39, 52 and 71% of the variance of MNed BNC, NPB, BUD, APO and NEC, respectively compared with breast cancer status which only explained 6 and 7% of the variance of MNed BNC and NEC(Two way ANOVA, P < 0.0001). Difference of difference analysis showed that breast cancer cases were not abnormally sensitive to the genome-damaging effect of folate deficiency. We concluded that (i) increased concentrations of FA abolished the genome-damaging effect of FA deficiency in lymphocytes of both breast cancer patients and controls to a similar extent and (ii) FA concentration is much more important than breast cancer status in determining genomic instability and cell death.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>16339195</pmid><doi>10.1093/mutage/gei069</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Apoptosis - drug effects Biological and medical sciences Breast - metabolism Breast - pathology Breast Neoplasms - epidemiology Breast Neoplasms - genetics Breast Neoplasms - metabolism Case-Control Studies China - epidemiology Cytokinesis - drug effects Female Folic Acid - pharmacology Folic Acid Deficiency - metabolism Fundamental and applied biological sciences. Psychology Genomic Instability Humans Lymphocytes - drug effects Micronuclei, Chromosome-Defective Micronucleus Tests Middle Aged Molecular and cellular biology Molecular genetics Mutagenesis. Repair Necrosis Population Groups |
| title | A comparison of folic acid deficiency-induced genomic instability in lymphocytes of breast cancer patients and normal non-cancer controls from a Chinese population in Yunnan |
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