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Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft
A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1...
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Published in: | Cancer research (Chicago, Ill.) Ill.), 1997-07, Vol.57 (14), p.2933-2936 |
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creator | FRIEDMAN, H. S JOHNSON, S. P GERMAIN, G DRUMMOND, J. T KEIR, S MARCELLI, S BIGNER, D. D MODRICH, P DONG, Q SCHOLD, S. C AHMED RASHEED, B. K BIGNER, S. H ALI-OSMAN, F DOLAN, E COLVIN, O. M HOUGHTON, P |
description | A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2. |
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S ; JOHNSON, S. P ; GERMAIN, G ; DRUMMOND, J. T ; KEIR, S ; MARCELLI, S ; BIGNER, D. D ; MODRICH, P ; DONG, Q ; SCHOLD, S. C ; AHMED RASHEED, B. K ; BIGNER, S. H ; ALI-OSMAN, F ; DOLAN, E ; COLVIN, O. M ; HOUGHTON, P</creator><creatorcontrib>FRIEDMAN, H. S ; JOHNSON, S. P ; GERMAIN, G ; DRUMMOND, J. T ; KEIR, S ; MARCELLI, S ; BIGNER, D. D ; MODRICH, P ; DONG, Q ; SCHOLD, S. C ; AHMED RASHEED, B. K ; BIGNER, S. H ; ALI-OSMAN, F ; DOLAN, E ; COLVIN, O. M ; HOUGHTON, P</creatorcontrib><description>A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9230204</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; DNA Methylation ; DNA Repair ; Drug Resistance ; General aspects ; Glioblastoma - drug therapy ; Glioblastoma - genetics ; Humans ; Medical sciences ; Melanocyte-Stimulating Hormones - analysis ; Methyltransferases - metabolism ; Mice ; Mice, Inbred BALB C ; Microsatellite Repeats ; Neoplasm Transplantation ; O-Methylguanine-DNA Methyltransferase ; Pharmacology. Drug treatments ; Transplantation, Heterologous ; Tumor Cells, Cultured</subject><ispartof>Cancer research (Chicago, Ill.), 1997-07, Vol.57 (14), p.2933-2936</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2771710$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9230204$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FRIEDMAN, H. S</creatorcontrib><creatorcontrib>JOHNSON, S. P</creatorcontrib><creatorcontrib>GERMAIN, G</creatorcontrib><creatorcontrib>DRUMMOND, J. T</creatorcontrib><creatorcontrib>KEIR, S</creatorcontrib><creatorcontrib>MARCELLI, S</creatorcontrib><creatorcontrib>BIGNER, D. D</creatorcontrib><creatorcontrib>MODRICH, P</creatorcontrib><creatorcontrib>DONG, Q</creatorcontrib><creatorcontrib>SCHOLD, S. C</creatorcontrib><creatorcontrib>AHMED RASHEED, B. K</creatorcontrib><creatorcontrib>BIGNER, S. H</creatorcontrib><creatorcontrib>ALI-OSMAN, F</creatorcontrib><creatorcontrib>DOLAN, E</creatorcontrib><creatorcontrib>COLVIN, O. M</creatorcontrib><creatorcontrib>HOUGHTON, P</creatorcontrib><title>Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>DNA Methylation</subject><subject>DNA Repair</subject><subject>Drug Resistance</subject><subject>General aspects</subject><subject>Glioblastoma - drug therapy</subject><subject>Glioblastoma - genetics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Melanocyte-Stimulating Hormones - analysis</subject><subject>Methyltransferases - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microsatellite Repeats</subject><subject>Neoplasm Transplantation</subject><subject>O-Methylguanine-DNA Methyltransferase</subject><subject>Pharmacology. Drug treatments</subject><subject>Transplantation, Heterologous</subject><subject>Tumor Cells, Cultured</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><recordid>eNo9kE1LxDAQhoMo67r6E4QcxFshaZImPcriF6x42XuZppPdSD_WJAX77w24eBqG52V45r0ga66EKbSU6pKsGWOmUFKX1-Qmxq-8Ks7UiqzqUrCSyTWxH5iOSw9pCjRg9DHBaJEO2HlI2NF2oYOPAyR7zPwEPtAOnbceR7tQP1Kgh95PbQ8xTQPQYe6Td1MYkP7gOB0CuHRLrhz0Ee_Oc0P2L8_77Vux-3x93z7timNZ1anAqs16lag011oCUwwYZ3XplNCGKydsxZnFDqVpDYJhGlgnnEHpJPBSbMjj39lTmL5njKnJ5hb7Hkac5tjomsuqUiYH78_Buc2PNqfgBwhLcy4l84czh2ihdyFX4uN_rNRZkDPxCxuWbHY</recordid><startdate>19970715</startdate><enddate>19970715</enddate><creator>FRIEDMAN, H. S</creator><creator>JOHNSON, S. P</creator><creator>GERMAIN, G</creator><creator>DRUMMOND, J. T</creator><creator>KEIR, S</creator><creator>MARCELLI, S</creator><creator>BIGNER, D. 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Drug treatments</topic><topic>Transplantation, Heterologous</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FRIEDMAN, H. S</creatorcontrib><creatorcontrib>JOHNSON, S. P</creatorcontrib><creatorcontrib>GERMAIN, G</creatorcontrib><creatorcontrib>DRUMMOND, J. T</creatorcontrib><creatorcontrib>KEIR, S</creatorcontrib><creatorcontrib>MARCELLI, S</creatorcontrib><creatorcontrib>BIGNER, D. D</creatorcontrib><creatorcontrib>MODRICH, P</creatorcontrib><creatorcontrib>DONG, Q</creatorcontrib><creatorcontrib>SCHOLD, S. C</creatorcontrib><creatorcontrib>AHMED RASHEED, B. K</creatorcontrib><creatorcontrib>BIGNER, S. H</creatorcontrib><creatorcontrib>ALI-OSMAN, F</creatorcontrib><creatorcontrib>DOLAN, E</creatorcontrib><creatorcontrib>COLVIN, O. M</creatorcontrib><creatorcontrib>HOUGHTON, P</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FRIEDMAN, H. S</au><au>JOHNSON, S. P</au><au>GERMAIN, G</au><au>DRUMMOND, J. T</au><au>KEIR, S</au><au>MARCELLI, S</au><au>BIGNER, D. D</au><au>MODRICH, P</au><au>DONG, Q</au><au>SCHOLD, S. C</au><au>AHMED RASHEED, B. K</au><au>BIGNER, S. H</au><au>ALI-OSMAN, F</au><au>DOLAN, E</au><au>COLVIN, O. M</au><au>HOUGHTON, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1997-07-15</date><risdate>1997</risdate><volume>57</volume><issue>14</issue><spage>2933</spage><epage>2936</epage><pages>2933-2936</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>A methylator-resistant human glioblastoma multiforme xenograft, D-245 MG (PR), in athymic nude mice was established by serially treating the parent xenograft D-245 MG with procarbazine. D-245 MG xenografts were sensitive to procarbazine, temozolomide, N-methyl-N-nitrosourea, 1,3-bis(2-chloroethyl)-1-nitrosourea, 9-aminocamptothecin, topotecan, CPT-11, cyclophosphamide, and busulfan. D-245 MG (PR) xenografts were resistant to procarbazine, temozolomide, N-methyl-N-nitrosourea, and busulfan, but they were sensitive to the other agents. Both D-245 MG and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathione and glutathione-S-transferase were similar. D-245 MG xenografts expressed the human mismatch repair proteins hMSH2 and hMLH1, whereas D-245 MG (PR) expressed hMLH1 but not hMSH2.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9230204</pmid><tpages>4</tpages></addata></record> |
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subjects | Animals Antineoplastic agents Biological and medical sciences DNA Methylation DNA Repair Drug Resistance General aspects Glioblastoma - drug therapy Glioblastoma - genetics Humans Medical sciences Melanocyte-Stimulating Hormones - analysis Methyltransferases - metabolism Mice Mice, Inbred BALB C Microsatellite Repeats Neoplasm Transplantation O-Methylguanine-DNA Methyltransferase Pharmacology. Drug treatments Transplantation, Heterologous Tumor Cells, Cultured |
title | Methylator resistance mediated by mismatch repair deficiency in a glioblastoma multiforme xenograft |
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