Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks
Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should the...
Gespeichert in:
| Veröffentlicht in: | Oncogene 2004-04, Vol.23 (16), p.2934-2949 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2949 |
|---|---|
| container_issue | 16 |
| container_start_page | 2934 |
| container_title | Oncogene |
| container_volume | 23 |
| creator | Pommier, Yves Sordet, Olivier Antony, Smitha Hayward, Richard L Kohn, Kurt W |
| description | Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-
κ
B) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and I
κ
B/NF-
κ
B networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the ‘permissive apoptosis-resistance’ model for the selection of multidrug-resistant cells. |
| doi_str_mv | 10.1038/sj.onc.1207515 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_71819287</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A189162874</galeid><sourcerecordid>A189162874</sourcerecordid><originalsourceid>FETCH-LOGICAL-c590t-c218c08786243ce82673f8329efaebd5625b29ac3f1e06087939d94af594b21e3</originalsourceid><addsrcrecordid>eNqFks9LHDEUx0Op1K3ttccyVOht1vyYTBJvi7RVELxoryGbedHZziRjkkH8782yCwtFkRwC-X7e970Xvgh9I3hJMJNnabMM3i4JxYIT_gEtSCPamnPVfEQLrDiuFWX0GH1OaYMxFgrTT-iYcCwE4XyB_q6mMOWQ-lR14MDmVBnfVfYBxpAfIJrpuYpQ5Gy8hfNqDAPYeTCx6n0uss198NVopl2dh_wU4r_0BR05MyT4ur9P0N3vX7cXl_X1zZ-ri9V1bbnCubaUSIulkC1tmAVJW8GcZFSBM7DueEv5mipjmSOA2wIqpjrVGFf2W1MC7AT93PlOMTzOkLIe-2RhGIyHMCctiCSKSvEuSITiAnNewNP_wE2Yoy9LaNo2hDEheVOoH29SVLBWUC4PVvdmAN17F3L5sG1fvSJSkbYMtrVavkKV08HY2-DB9eX9tQIbQ0oRnJ5iP5r4rAnW21DotNElFHofilLwfT_svB6hO-D7FBTgbAekIvl7iIdt3rB8ASLQwIc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>227367258</pqid></control><display><type>article</type><title>Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Springer Nature - Complete Springer Journals</source><source>Nature Journals Online</source><creator>Pommier, Yves ; Sordet, Olivier ; Antony, Smitha ; Hayward, Richard L ; Kohn, Kurt W</creator><creatorcontrib>Pommier, Yves ; Sordet, Olivier ; Antony, Smitha ; Hayward, Richard L ; Kohn, Kurt W</creatorcontrib><description>Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-
κ
B) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and I
κ
B/NF-
κ
B networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the ‘permissive apoptosis-resistance’ model for the selection of multidrug-resistant cells.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1207515</identifier><identifier>PMID: 15077155</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>AKT protein ; Animals ; Apaf-1 protein ; Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Bcl-2 protein ; Cancer therapies ; Cell Biology ; Cell cycle ; Cell death ; Chemoresistance ; Chemotherapy ; Drug metabolism ; Drug resistance ; Drug Resistance, Neoplasm ; Human Genetics ; Humans ; Internal Medicine ; Medical research ; Medicine ; Medicine & Public Health ; Metabolism ; Multidrug resistance ; Multidrug resistant organisms ; Mutation ; Neoplasms - drug therapy ; Neoplasms - pathology ; NF-kappa B - metabolism ; NF-κB protein ; Oncology ; Protein-Serine-Threonine Kinases ; Proteins - physiology ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2 - physiology ; review ; Tumors</subject><ispartof>Oncogene, 2004-04, Vol.23 (16), p.2934-2949</ispartof><rights>Springer Nature Limited 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 12, 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-c218c08786243ce82673f8329efaebd5625b29ac3f1e06087939d94af594b21e3</citedby><cites>FETCH-LOGICAL-c590t-c218c08786243ce82673f8329efaebd5625b29ac3f1e06087939d94af594b21e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1207515$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1207515$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15077155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pommier, Yves</creatorcontrib><creatorcontrib>Sordet, Olivier</creatorcontrib><creatorcontrib>Antony, Smitha</creatorcontrib><creatorcontrib>Hayward, Richard L</creatorcontrib><creatorcontrib>Kohn, Kurt W</creatorcontrib><title>Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-
κ
B) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and I
κ
B/NF-
κ
B networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the ‘permissive apoptosis-resistance’ model for the selection of multidrug-resistant cells.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Apaf-1 protein</subject><subject>Apoptosis</subject><subject>Apoptotic Protease-Activating Factor 1</subject><subject>Bcl-2 protein</subject><subject>Cancer therapies</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Chemoresistance</subject><subject>Chemotherapy</subject><subject>Drug metabolism</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolism</subject><subject>Multidrug resistance</subject><subject>Multidrug resistant organisms</subject><subject>Mutation</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - pathology</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oncology</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Proteins - physiology</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Proto-Oncogene Proteins c-bcl-2 - physiology</subject><subject>review</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFks9LHDEUx0Op1K3ttccyVOht1vyYTBJvi7RVELxoryGbedHZziRjkkH8782yCwtFkRwC-X7e970Xvgh9I3hJMJNnabMM3i4JxYIT_gEtSCPamnPVfEQLrDiuFWX0GH1OaYMxFgrTT-iYcCwE4XyB_q6mMOWQ-lR14MDmVBnfVfYBxpAfIJrpuYpQ5Gy8hfNqDAPYeTCx6n0uss198NVopl2dh_wU4r_0BR05MyT4ur9P0N3vX7cXl_X1zZ-ri9V1bbnCubaUSIulkC1tmAVJW8GcZFSBM7DueEv5mipjmSOA2wIqpjrVGFf2W1MC7AT93PlOMTzOkLIe-2RhGIyHMCctiCSKSvEuSITiAnNewNP_wE2Yoy9LaNo2hDEheVOoH29SVLBWUC4PVvdmAN17F3L5sG1fvSJSkbYMtrVavkKV08HY2-DB9eX9tQIbQ0oRnJ5iP5r4rAnW21DotNElFHofilLwfT_svB6hO-D7FBTgbAekIvl7iIdt3rB8ASLQwIc</recordid><startdate>20040412</startdate><enddate>20040412</enddate><creator>Pommier, Yves</creator><creator>Sordet, Olivier</creator><creator>Antony, Smitha</creator><creator>Hayward, Richard L</creator><creator>Kohn, Kurt W</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20040412</creationdate><title>Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks</title><author>Pommier, Yves ; Sordet, Olivier ; Antony, Smitha ; Hayward, Richard L ; Kohn, Kurt W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-c218c08786243ce82673f8329efaebd5625b29ac3f1e06087939d94af594b21e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Apaf-1 protein</topic><topic>Apoptosis</topic><topic>Apoptotic Protease-Activating Factor 1</topic><topic>Bcl-2 protein</topic><topic>Cancer therapies</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Chemoresistance</topic><topic>Chemotherapy</topic><topic>Drug metabolism</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolism</topic><topic>Multidrug resistance</topic><topic>Multidrug resistant organisms</topic><topic>Mutation</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - pathology</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oncology</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Proteins - physiology</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Proto-Oncogene Proteins c-bcl-2 - physiology</topic><topic>review</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pommier, Yves</creatorcontrib><creatorcontrib>Sordet, Olivier</creatorcontrib><creatorcontrib>Antony, Smitha</creatorcontrib><creatorcontrib>Hayward, Richard L</creatorcontrib><creatorcontrib>Kohn, Kurt W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pommier, Yves</au><au>Sordet, Olivier</au><au>Antony, Smitha</au><au>Hayward, Richard L</au><au>Kohn, Kurt W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2004-04-12</date><risdate>2004</risdate><volume>23</volume><issue>16</issue><spage>2934</spage><epage>2949</epage><pages>2934-2949</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-
κ
B) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and I
κ
B/NF-
κ
B networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the ‘permissive apoptosis-resistance’ model for the selection of multidrug-resistant cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15077155</pmid><doi>10.1038/sj.onc.1207515</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
| ispartof | Oncogene, 2004-04, Vol.23 (16), p.2934-2949 |
| issn | 0950-9232 1476-5594 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71819287 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature - Complete Springer Journals; Nature Journals Online |
| subjects | AKT protein Animals Apaf-1 protein Apoptosis Apoptotic Protease-Activating Factor 1 Bcl-2 protein Cancer therapies Cell Biology Cell cycle Cell death Chemoresistance Chemotherapy Drug metabolism Drug resistance Drug Resistance, Neoplasm Human Genetics Humans Internal Medicine Medical research Medicine Medicine & Public Health Metabolism Multidrug resistance Multidrug resistant organisms Mutation Neoplasms - drug therapy Neoplasms - pathology NF-kappa B - metabolism NF-κB protein Oncology Protein-Serine-Threonine Kinases Proteins - physiology Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-bcl-2 - physiology review Tumors |
| title | Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T17%3A53%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Apoptosis%20defects%20and%20chemotherapy%20resistance:%20molecular%20interaction%20maps%20and%20networks&rft.jtitle=Oncogene&rft.au=Pommier,%20Yves&rft.date=2004-04-12&rft.volume=23&rft.issue=16&rft.spage=2934&rft.epage=2949&rft.pages=2934-2949&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/sj.onc.1207515&rft_dat=%3Cgale_proqu%3EA189162874%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=227367258&rft_id=info:pmid/15077155&rft_galeid=A189162874&rfr_iscdi=true |