Multiple Drug Resistance in Cancer Revisited: The Cancer Stem Cell Hypothesis
The failure to eradicate cancer may be as fundamental as a misidentification of the target. Current therapies succeed at eliminating bulky disease but often miss a tumor reservoir that is the source of disease recurrence and metastasis. Recent advances in the understanding of tissue development and...
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| Veröffentlicht in: | Journal of clinical pharmacology 2005-08, Vol.45 (8), p.872-877 |
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| container_title | Journal of clinical pharmacology |
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| creator | Donnenberg, Vera S. Donnenberg, Albert D. |
| description | The failure to eradicate cancer may be as fundamental as a misidentification of the target. Current therapies succeed at eliminating bulky disease but often miss a tumor reservoir that is the source of disease recurrence and metastasis. Recent advances in the understanding of tissue development and repair cause us to revisit the process of drug resistance as it applies to oncogenesis and tumor heterogeneity. The cancer stem cell hypothesis states that the cancer‐initiating cell is a transformed tissue stem cell, which retains the essential property of self‐protection through the activity of multiple drug resistance (MDR) transporters. This resting constitutively drug‐resistant cell remains at low frequency among a heterogeneous tumor mass. In the context of this hypothesis, the authors review the discovery of MDR transporters in cancer and normal stem cells and the failure of MDR reversal agents to increase the therapeutic index of substrate antineoplastic agents. |
| doi_str_mv | 10.1177/0091270005276905 |
| format | Article |
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Current therapies succeed at eliminating bulky disease but often miss a tumor reservoir that is the source of disease recurrence and metastasis. Recent advances in the understanding of tissue development and repair cause us to revisit the process of drug resistance as it applies to oncogenesis and tumor heterogeneity. The cancer stem cell hypothesis states that the cancer‐initiating cell is a transformed tissue stem cell, which retains the essential property of self‐protection through the activity of multiple drug resistance (MDR) transporters. This resting constitutively drug‐resistant cell remains at low frequency among a heterogeneous tumor mass. 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Current therapies succeed at eliminating bulky disease but often miss a tumor reservoir that is the source of disease recurrence and metastasis. Recent advances in the understanding of tissue development and repair cause us to revisit the process of drug resistance as it applies to oncogenesis and tumor heterogeneity. The cancer stem cell hypothesis states that the cancer‐initiating cell is a transformed tissue stem cell, which retains the essential property of self‐protection through the activity of multiple drug resistance (MDR) transporters. This resting constitutively drug‐resistant cell remains at low frequency among a heterogeneous tumor mass. In the context of this hypothesis, the authors review the discovery of MDR transporters in cancer and normal stem cells and the failure of MDR reversal agents to increase the therapeutic index of substrate antineoplastic agents.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>ATP Binding Cassette Transporter, Subfamily B - antagonists & inhibitors</subject><subject>ATP Binding Cassette Transporter, Subfamily B - metabolism</subject><subject>ATP Binding Cassette Transporter, Subfamily B, Member 1 - antagonists & inhibitors</subject><subject>ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism</subject><subject>ATP Binding Cassette Transporter, Subfamily G, Member 2</subject><subject>ATP-Binding Cassette Sub-Family B Member 4</subject><subject>ATP-Binding Cassette Transporters - antagonists & inhibitors</subject><subject>ATP-Binding Cassette Transporters - metabolism</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer stem cell</subject><subject>Chemotherapy</subject><subject>Drug resistance</subject><subject>Drug Resistance, Multiple</subject><subject>Drug Resistance, Neoplasm</subject><subject>Health aspects</subject><subject>Humans</subject><subject>multiple drug resistance</subject><subject>Neoplasm Proteins - antagonists & inhibitors</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - pathology</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>oncogenesis</subject><subject>Risk factors</subject><issn>0091-2700</issn><issn>1552-4604</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EosuWOyeUP5B2_J1wqwJ0qVo-2iK4WV5n0jX1blZ2tmX_PY6ygMQF-WDPO_O8Gr0m5BWFE0q1PgWoKdMAIJlWNcgnZEalZKVQIJ6S2dgux_4ReZHSDwCqhKTPyRFVwDSv9YxcXe3C4LcBi7dxd1dcY_JpsBuHhd8UzfiIWXzwyQ_YviluV_hbvRlwXTQYQrHYb_thNZLH5FlnQ8KXh3tOvr5_d9ssystP5x-as8vSSS14SZdO69bRCrq20ktXCZSIijNZ1xoo6_SyUk5ZbK2WLTDBlOCaY-esVoy2fE5OJt87G9D4TdcP0bp8Wlx712-w81k_owIqpipBMwAT4GKfUsTObKNf27g3FMwYpfk3yoy8npDtbrnG9i9wyC4PiGngsQ8DxnQfdo8YzQptGFbZD0Bkv5JlS6hyVY4Sz5g6YHnH_X_3MBfN54WscmxzUk5g_iH8-Qe08d4ozbU03z6eG339hVH2fWEu-C9q_Jqb</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Donnenberg, Vera S.</creator><creator>Donnenberg, Albert D.</creator><general>Blackwell Publishing Ltd</general><general>SAGE Publications</general><general>Sage Publications, Inc</general><scope>BSCLL</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></search><sort><creationdate>200508</creationdate><title>Multiple Drug Resistance in Cancer Revisited: The Cancer Stem Cell Hypothesis</title><author>Donnenberg, Vera S. ; Donnenberg, Albert D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5743-1bc77dc180fd87bc84e5ee6325997012f7b86c6aeda75d024264373efca7621d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>ATP Binding Cassette Transporter, Subfamily B - antagonists & inhibitors</topic><topic>ATP Binding Cassette Transporter, Subfamily B - metabolism</topic><topic>ATP Binding Cassette Transporter, Subfamily B, Member 1 - antagonists & inhibitors</topic><topic>ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism</topic><topic>ATP Binding Cassette Transporter, Subfamily G, Member 2</topic><topic>ATP-Binding Cassette Sub-Family B Member 4</topic><topic>ATP-Binding Cassette Transporters - antagonists & inhibitors</topic><topic>ATP-Binding Cassette Transporters - metabolism</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer stem cell</topic><topic>Chemotherapy</topic><topic>Drug resistance</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Resistance, Neoplasm</topic><topic>Health aspects</topic><topic>Humans</topic><topic>multiple drug resistance</topic><topic>Neoplasm Proteins - antagonists & inhibitors</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - pathology</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>oncogenesis</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Donnenberg, Vera S.</creatorcontrib><creatorcontrib>Donnenberg, Albert D.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of clinical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Donnenberg, Vera S.</au><au>Donnenberg, Albert D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multiple Drug Resistance in Cancer Revisited: The Cancer Stem Cell Hypothesis</atitle><jtitle>Journal of clinical pharmacology</jtitle><addtitle>J Clin Pharmacol</addtitle><date>2005-08</date><risdate>2005</risdate><volume>45</volume><issue>8</issue><spage>872</spage><epage>877</epage><pages>872-877</pages><issn>0091-2700</issn><eissn>1552-4604</eissn><abstract>The failure to eradicate cancer may be as fundamental as a misidentification of the target. 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| identifier | ISSN: 0091-2700 |
| ispartof | Journal of clinical pharmacology, 2005-08, Vol.45 (8), p.872-877 |
| issn | 0091-2700 1552-4604 |
| language | eng |
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| source | MEDLINE; Wiley Journals |
| subjects | Animals Antineoplastic Agents - pharmacology ATP Binding Cassette Transporter, Subfamily B - antagonists & inhibitors ATP Binding Cassette Transporter, Subfamily B - metabolism ATP Binding Cassette Transporter, Subfamily B, Member 1 - antagonists & inhibitors ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism ATP Binding Cassette Transporter, Subfamily G, Member 2 ATP-Binding Cassette Sub-Family B Member 4 ATP-Binding Cassette Transporters - antagonists & inhibitors ATP-Binding Cassette Transporters - metabolism Cancer Cancer cells Cancer stem cell Chemotherapy Drug resistance Drug Resistance, Multiple Drug Resistance, Neoplasm Health aspects Humans multiple drug resistance Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - metabolism Neoplasms - drug therapy Neoplasms - pathology Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism oncogenesis Risk factors |
| title | Multiple Drug Resistance in Cancer Revisited: The Cancer Stem Cell Hypothesis |
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