Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines
Previous work identified TK6 and WTK1 as human lymphoblast cell lines from one donor that have different capacities to catalyze recombination and that vary significantly in their response to ionizing radiation. WTK1 cells are more resistant to the toxic effects of X-rays yet more sensitive to induce...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1995-01, Vol.55 (1), p.12-15 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | FEN XIA XI WANG YI-HAN WANG NGAN-MING TSANG YANDELL, D. W KELSEY, K. T LIBER, H. L |
| description | Previous work identified TK6 and WTK1 as human lymphoblast cell lines from one donor that have different capacities to catalyze recombination and that vary significantly in their response to ionizing radiation. WTK1 cells are more resistant to the toxic effects of X-rays yet more sensitive to induced mutation. We demonstrate here that although both cell lines contain equal levels of p53 mRNA, baseline protein levels are 4 times higher in WTK1. Irradiation leads to higher levels of p53 protein in both lines but to a greater extent in TK6. TK6 contains a wild-type p53 sequence, while WTK1 has a homozygous mutation in codon 237 of exon 7. We also observed a significant difference in the kinetics but not the overall degree of apoptosis induced by X-rays in these cells; apoptotic death is delayed for 3 days in WTK1. We hypothesize that this p53 mutation is responsible for the difference in apoptosis as well as for the differences in mutability and mutational spectra reported previously. |
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W ; KELSEY, K. T ; LIBER, H. L</creator><creatorcontrib>FEN XIA ; XI WANG ; YI-HAN WANG ; NGAN-MING TSANG ; YANDELL, D. W ; KELSEY, K. T ; LIBER, H. L</creatorcontrib><description>Previous work identified TK6 and WTK1 as human lymphoblast cell lines from one donor that have different capacities to catalyze recombination and that vary significantly in their response to ionizing radiation. WTK1 cells are more resistant to the toxic effects of X-rays yet more sensitive to induced mutation. We demonstrate here that although both cell lines contain equal levels of p53 mRNA, baseline protein levels are 4 times higher in WTK1. Irradiation leads to higher levels of p53 protein in both lines but to a greater extent in TK6. TK6 contains a wild-type p53 sequence, while WTK1 has a homozygous mutation in codon 237 of exon 7. We also observed a significant difference in the kinetics but not the overall degree of apoptosis induced by X-rays in these cells; apoptotic death is delayed for 3 days in WTK1. We hypothesize that this p53 mutation is responsible for the difference in apoptosis as well as for the differences in mutability and mutational spectra reported previously.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 7805021</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Apoptosis ; Biological and medical sciences ; Genes, p53 ; genomic instability ; Humans ; lymphoblastoid cell lines ; man ; Medical sciences ; Mutation ; p53 protein ; Radiation therapy and radiosensitizing agent ; radiosensitivity ; RNA, Messenger - analysis ; Treatment with physical agents ; Treatment. General aspects ; Tumor Cells, Cultured - radiation effects ; Tumor Suppressor Protein p53 - genetics ; Tumors ; X radiation</subject><ispartof>Cancer research (Chicago, Ill.), 1995-01, Vol.55 (1), p.12-15</ispartof><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3379564$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7805021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FEN XIA</creatorcontrib><creatorcontrib>XI WANG</creatorcontrib><creatorcontrib>YI-HAN WANG</creatorcontrib><creatorcontrib>NGAN-MING TSANG</creatorcontrib><creatorcontrib>YANDELL, D. W</creatorcontrib><creatorcontrib>KELSEY, K. T</creatorcontrib><creatorcontrib>LIBER, H. L</creatorcontrib><title>Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Previous work identified TK6 and WTK1 as human lymphoblast cell lines from one donor that have different capacities to catalyze recombination and that vary significantly in their response to ionizing radiation. WTK1 cells are more resistant to the toxic effects of X-rays yet more sensitive to induced mutation. We demonstrate here that although both cell lines contain equal levels of p53 mRNA, baseline protein levels are 4 times higher in WTK1. Irradiation leads to higher levels of p53 protein in both lines but to a greater extent in TK6. TK6 contains a wild-type p53 sequence, while WTK1 has a homozygous mutation in codon 237 of exon 7. We also observed a significant difference in the kinetics but not the overall degree of apoptosis induced by X-rays in these cells; apoptotic death is delayed for 3 days in WTK1. We hypothesize that this p53 mutation is responsible for the difference in apoptosis as well as for the differences in mutability and mutational spectra reported previously.</description><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Genes, p53</subject><subject>genomic instability</subject><subject>Humans</subject><subject>lymphoblastoid cell lines</subject><subject>man</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>p53 protein</subject><subject>Radiation therapy and radiosensitizing agent</subject><subject>radiosensitivity</subject><subject>RNA, Messenger - analysis</subject><subject>Treatment with physical agents</subject><subject>Treatment. General aspects</subject><subject>Tumor Cells, Cultured - radiation effects</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumors</subject><subject>X radiation</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE9LAzEQxRdRaq1-BCEH8baQ3STd9FiK_6DgRc9lkszSSDZZd7KWfhM_rosWT8O895v3YM6KeaWELhsp1Xkx55zrUsmmviyuiD6mVVVczYpZo7nidTUvvtch44CO9UowypBHYjYNAwbISOzg854537YTE-0k-MgII_nsv3w-spzYAM5D9imWPrrRTlHdmH8FBtEx6FOfE_nf03xIzIZEGI7sr8Kx_dhBZOHY9ftkAlBmwUek6-KihUB4c5qL4v3x4W3zXG5fn1426225r6s6l447ro12ugFjhDDIEYzmQhtUrdWcW8dlZQyXAmrd1AbcCmWzamtUaJZGLIr7v9x-SJ8jUt51niyGABHTSLtq2UglBZ_A2xM4mg7drh98B8Nxd3rl5N-dfCALoR0gWk__mBDNSi2l-AEB_oJ0</recordid><startdate>19950101</startdate><enddate>19950101</enddate><creator>FEN XIA</creator><creator>XI WANG</creator><creator>YI-HAN WANG</creator><creator>NGAN-MING TSANG</creator><creator>YANDELL, D. W</creator><creator>KELSEY, K. T</creator><creator>LIBER, H. L</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T3</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope></search><sort><creationdate>19950101</creationdate><title>Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines</title><author>FEN XIA ; XI WANG ; YI-HAN WANG ; NGAN-MING TSANG ; YANDELL, D. W ; KELSEY, K. T ; LIBER, H. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h212t-d0d08b8d87abb33be0eab8038be5fc800cd041bb043a2872bad9e479f2e5eb6b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Genes, p53</topic><topic>genomic instability</topic><topic>Humans</topic><topic>lymphoblastoid cell lines</topic><topic>man</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>p53 protein</topic><topic>Radiation therapy and radiosensitizing agent</topic><topic>radiosensitivity</topic><topic>RNA, Messenger - analysis</topic><topic>Treatment with physical agents</topic><topic>Treatment. General aspects</topic><topic>Tumor Cells, Cultured - radiation effects</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumors</topic><topic>X radiation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FEN XIA</creatorcontrib><creatorcontrib>XI WANG</creatorcontrib><creatorcontrib>YI-HAN WANG</creatorcontrib><creatorcontrib>NGAN-MING TSANG</creatorcontrib><creatorcontrib>YANDELL, D. W</creatorcontrib><creatorcontrib>KELSEY, K. T</creatorcontrib><creatorcontrib>LIBER, H. 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L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1995-01-01</date><risdate>1995</risdate><volume>55</volume><issue>1</issue><spage>12</spage><epage>15</epage><pages>12-15</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Previous work identified TK6 and WTK1 as human lymphoblast cell lines from one donor that have different capacities to catalyze recombination and that vary significantly in their response to ionizing radiation. WTK1 cells are more resistant to the toxic effects of X-rays yet more sensitive to induced mutation. We demonstrate here that although both cell lines contain equal levels of p53 mRNA, baseline protein levels are 4 times higher in WTK1. Irradiation leads to higher levels of p53 protein in both lines but to a greater extent in TK6. TK6 contains a wild-type p53 sequence, while WTK1 has a homozygous mutation in codon 237 of exon 7. We also observed a significant difference in the kinetics but not the overall degree of apoptosis induced by X-rays in these cells; apoptotic death is delayed for 3 days in WTK1. We hypothesize that this p53 mutation is responsible for the difference in apoptosis as well as for the differences in mutability and mutational spectra reported previously.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>7805021</pmid><tpages>4</tpages></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 1995-01, Vol.55 (1), p.12-15 |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Apoptosis Biological and medical sciences Genes, p53 genomic instability Humans lymphoblastoid cell lines man Medical sciences Mutation p53 protein Radiation therapy and radiosensitizing agent radiosensitivity RNA, Messenger - analysis Treatment with physical agents Treatment. General aspects Tumor Cells, Cultured - radiation effects Tumor Suppressor Protein p53 - genetics Tumors X radiation |
| title | Altered p53 status correlates with differences in sensitivity to radiation-induced mutation and apoptosis in two closely related human lymphoblast lines |
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