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Sensitivity of camptothecin-resistant human leukemia cells and tumors to anticancer drugs with diverse mechanisms of action
Human leukemia U-937 cell clones resistant to 9-nitrocamptothecin (9NC) appear after exposure to increase 9NC-concentrations. Drug resistance is irreversible, regardless of whether the 9NC-resistant (U-937/CR150) cells grow in media with or without 9NC. U-937/ CR150 cells are more sensitive than wil...
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| Published in: | Leukemia research 1995, Vol.19 (1), p.43-55 |
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| Main Authors: | , , , , , , |
| Format: | Article |
| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c417t-60a57a6bcc6ff0ecab64e26d91f4e36bcf582976cbc5393281b2fd56126ce1c3 |
| container_end_page | 55 |
| container_issue | 1 |
| container_start_page | 43 |
| container_title | Leukemia research |
| container_volume | 19 |
| creator | Pantazis, Panayotis Vardeman, Dana Mendoza, John Early, Janet Kozielski, Anthony DeJesus, Albert Giovanella, Beppino |
| description | Human leukemia U-937 cell clones resistant to 9-nitrocamptothecin (9NC) appear after exposure to increase 9NC-concentrations. Drug resistance is irreversible, regardless of whether the 9NC-resistant (U-937/CR150) cells grow in media with or without 9NC. U-937/ CR150 cells are more sensitive than wild type U-937 (U-937/wt) cells to topoisomerase II-directed drugs, amsacrine, daunorubicin, and etoposide. The mitotic inhibitor, vincristine, induces hyperdiploidy in U-937/wt, but not in U-937/CR150 cells, whereas the antimetabolites, cytarabine and methotrexate, and the nitrosourea, carmustine, elicit similar responses in both U-937/wt and U-937/CR150 cells. U-937/CR150-generated tumors in nude mice are sensitive to etoposide. The clinical implications of increased sensitivity of 9NC-resistant tumors to some anticancer drugs are discussed. |
| doi_str_mv | 10.1016/0145-2126(94)00060-N |
| format | article |
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Drug resistance is irreversible, regardless of whether the 9NC-resistant (U-937/CR150) cells grow in media with or without 9NC. U-937/ CR150 cells are more sensitive than wild type U-937 (U-937/wt) cells to topoisomerase II-directed drugs, amsacrine, daunorubicin, and etoposide. The mitotic inhibitor, vincristine, induces hyperdiploidy in U-937/wt, but not in U-937/CR150 cells, whereas the antimetabolites, cytarabine and methotrexate, and the nitrosourea, carmustine, elicit similar responses in both U-937/wt and U-937/CR150 cells. U-937/CR150-generated tumors in nude mice are sensitive to etoposide. The clinical implications of increased sensitivity of 9NC-resistant tumors to some anticancer drugs are discussed.</description><identifier>ISSN: 0145-2126</identifier><identifier>EISSN: 1873-5835</identifier><identifier>DOI: 10.1016/0145-2126(94)00060-N</identifier><identifier>PMID: 7837817</identifier><identifier>CODEN: LEREDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Antineoplastic agents ; Antineoplastic Agents - pharmacology ; apoptosis ; Apoptosis - physiology ; Biological and medical sciences ; Camptothecin - analogs & derivatives ; Camptothecin - pharmacology ; cell cycle ; Cell Cycle - drug effects ; Cell Division - drug effects ; Chemotherapy ; DNA, Neoplasm - analysis ; Drug Resistance ; Drug Screening Assays, Antitumor ; Flow Cytometry ; Humans ; Leukemia - drug therapy ; Leukemia - pathology ; Male ; Medical sciences ; Mice ; Mice, Nude ; nude mouse ; Pharmacology. Drug treatments ; Topoisomerase ; Topoisomerase II Inhibitors</subject><ispartof>Leukemia research, 1995, Vol.19 (1), p.43-55</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-60a57a6bcc6ff0ecab64e26d91f4e36bcf582976cbc5393281b2fd56126ce1c3</citedby><cites>FETCH-LOGICAL-c417t-60a57a6bcc6ff0ecab64e26d91f4e36bcf582976cbc5393281b2fd56126ce1c3</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=3426608$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7837817$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pantazis, Panayotis</creatorcontrib><creatorcontrib>Vardeman, Dana</creatorcontrib><creatorcontrib>Mendoza, John</creatorcontrib><creatorcontrib>Early, Janet</creatorcontrib><creatorcontrib>Kozielski, Anthony</creatorcontrib><creatorcontrib>DeJesus, Albert</creatorcontrib><creatorcontrib>Giovanella, Beppino</creatorcontrib><title>Sensitivity of camptothecin-resistant human leukemia cells and tumors to anticancer drugs with diverse mechanisms of action</title><title>Leukemia research</title><addtitle>Leuk Res</addtitle><description>Human leukemia U-937 cell clones resistant to 9-nitrocamptothecin (9NC) appear after exposure to increase 9NC-concentrations. Drug resistance is irreversible, regardless of whether the 9NC-resistant (U-937/CR150) cells grow in media with or without 9NC. U-937/ CR150 cells are more sensitive than wild type U-937 (U-937/wt) cells to topoisomerase II-directed drugs, amsacrine, daunorubicin, and etoposide. The mitotic inhibitor, vincristine, induces hyperdiploidy in U-937/wt, but not in U-937/CR150 cells, whereas the antimetabolites, cytarabine and methotrexate, and the nitrosourea, carmustine, elicit similar responses in both U-937/wt and U-937/CR150 cells. U-937/CR150-generated tumors in nude mice are sensitive to etoposide. The clinical implications of increased sensitivity of 9NC-resistant tumors to some anticancer drugs are discussed.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Camptothecin - analogs & derivatives</subject><subject>Camptothecin - pharmacology</subject><subject>cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Division - drug effects</subject><subject>Chemotherapy</subject><subject>DNA, Neoplasm - analysis</subject><subject>Drug Resistance</subject><subject>Drug Screening Assays, Antitumor</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Leukemia - drug therapy</subject><subject>Leukemia - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>nude mouse</subject><subject>Pharmacology. 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Drug treatments</topic><topic>Topoisomerase</topic><topic>Topoisomerase II Inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pantazis, Panayotis</creatorcontrib><creatorcontrib>Vardeman, Dana</creatorcontrib><creatorcontrib>Mendoza, John</creatorcontrib><creatorcontrib>Early, Janet</creatorcontrib><creatorcontrib>Kozielski, Anthony</creatorcontrib><creatorcontrib>DeJesus, Albert</creatorcontrib><creatorcontrib>Giovanella, Beppino</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>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Leukemia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pantazis, Panayotis</au><au>Vardeman, Dana</au><au>Mendoza, John</au><au>Early, Janet</au><au>Kozielski, Anthony</au><au>DeJesus, Albert</au><au>Giovanella, Beppino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sensitivity of camptothecin-resistant human leukemia cells and tumors to anticancer drugs with diverse mechanisms of action</atitle><jtitle>Leukemia research</jtitle><addtitle>Leuk Res</addtitle><date>1995</date><risdate>1995</risdate><volume>19</volume><issue>1</issue><spage>43</spage><epage>55</epage><pages>43-55</pages><issn>0145-2126</issn><eissn>1873-5835</eissn><coden>LEREDD</coden><abstract>Human leukemia U-937 cell clones resistant to 9-nitrocamptothecin (9NC) appear after exposure to increase 9NC-concentrations. Drug resistance is irreversible, regardless of whether the 9NC-resistant (U-937/CR150) cells grow in media with or without 9NC. U-937/ CR150 cells are more sensitive than wild type U-937 (U-937/wt) cells to topoisomerase II-directed drugs, amsacrine, daunorubicin, and etoposide. The mitotic inhibitor, vincristine, induces hyperdiploidy in U-937/wt, but not in U-937/CR150 cells, whereas the antimetabolites, cytarabine and methotrexate, and the nitrosourea, carmustine, elicit similar responses in both U-937/wt and U-937/CR150 cells. U-937/CR150-generated tumors in nude mice are sensitive to etoposide. The clinical implications of increased sensitivity of 9NC-resistant tumors to some anticancer drugs are discussed.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>7837817</pmid><doi>10.1016/0145-2126(94)00060-N</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0145-2126 |
| ispartof | Leukemia research, 1995, Vol.19 (1), p.43-55 |
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| language | eng |
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| source | Elsevier |
| subjects | Animals Antineoplastic agents Antineoplastic Agents - pharmacology apoptosis Apoptosis - physiology Biological and medical sciences Camptothecin - analogs & derivatives Camptothecin - pharmacology cell cycle Cell Cycle - drug effects Cell Division - drug effects Chemotherapy DNA, Neoplasm - analysis Drug Resistance Drug Screening Assays, Antitumor Flow Cytometry Humans Leukemia - drug therapy Leukemia - pathology Male Medical sciences Mice Mice, Nude nude mouse Pharmacology. Drug treatments Topoisomerase Topoisomerase II Inhibitors |
| title | Sensitivity of camptothecin-resistant human leukemia cells and tumors to anticancer drugs with diverse mechanisms of action |
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