Akt-regulated pathways in prostate cancer
Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate c...
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| Veröffentlicht in: | Oncogene 2005-11, Vol.24 (50), p.7465-7474 |
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| creator | Majumder, Pradip K Sellers, William R |
| description | Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development. |
| doi_str_mv | 10.1038/sj.onc.1209096 |
| format | Article |
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Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1209096</identifier><identifier>PMID: 16288293</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Apoptosis ; Cell Biology ; Gene deletion ; Genes ; Hsp90 protein ; Human Genetics ; Humans ; Internal Medicine ; Kinases ; Male ; Medicine ; Medicine & Public Health ; Metastases ; Metastasis ; Mutation ; Oncology ; Phosphatase ; Phosphatidylinositol 3-Kinases - genetics ; Phosphatidylinositol 3-Kinases - metabolism ; Point mutation ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - physiopathology ; Protein Kinases - genetics ; Protein Kinases - physiology ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - physiology ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - physiology ; PTEN protein ; Radiation therapy ; review ; Signal Transduction ; TOR protein ; TOR Serine-Threonine Kinases ; Tumors</subject><ispartof>Oncogene, 2005-11, Vol.24 (50), p.7465-7474</ispartof><rights>Springer Nature Limited 2005</rights><rights>COPYRIGHT 2005 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Nov 14, 2005</rights><rights>Nature Publishing Group 2005.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-73c086cae4679b89a7fa73957ff8ce3e9e10731213de8aa52f9633c5e444cf1e3</citedby><cites>FETCH-LOGICAL-c480t-73c086cae4679b89a7fa73957ff8ce3e9e10731213de8aa52f9633c5e444cf1e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2727,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16288293$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Majumder, Pradip K</creatorcontrib><creatorcontrib>Sellers, William R</creatorcontrib><title>Akt-regulated pathways in prostate cancer</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Cell Biology</subject><subject>Gene deletion</subject><subject>Genes</subject><subject>Hsp90 protein</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mutation</subject><subject>Oncology</subject><subject>Phosphatase</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Point mutation</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - physiopathology</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - physiology</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - physiology</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - physiology</subject><subject>PTEN protein</subject><subject>Radiation therapy</subject><subject>review</subject><subject>Signal Transduction</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases</subject><subject>Tumors</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</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>eNqFkUtLAzEUhYMoWh9bd0pREFxMzWvyWJbiCwQ3ug5pelOnTjM1mUH67410oCAUySJw73du7slB6JzgEcFM3aXFqAluRCjWWIs9NCBciqIsNd9HA6xLXGjK6BE6TmmBMZYa00N0RARVimo2QLfjz7aIMO9q28JsuLLtx7ddp2EVhqvYpDZXh84GB_EUHXhbJzjr7xP0_nD_NnkqXl4fnyfjl8JxhdtCMoeVcBa4kHqqtJXeSqZL6b1ywEADwZIRStgMlLUl9Vow5krgnDtPgJ2gm83c_P5XB6k1yyo5qGsboOmSEUphyTn9FyRaMpoNZ_D6D7houhiyCUMFJ6zUjOlMXe2kqGTZDv-FRhtobmswVfBNG63LZwbLyjUBfJXrY6I0FlyWfCtw-TdTBG9WsVrauDYEm98ETVqYnKDpE8yCy36NbrqE2RbvI8vA3QZIuRXmELd77hx5sVEE23YRtiP7_g91Hq3N</recordid><startdate>20051114</startdate><enddate>20051114</enddate><creator>Majumder, Pradip K</creator><creator>Sellers, William R</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>20051114</creationdate><title>Akt-regulated pathways in prostate cancer</title><author>Majumder, Pradip K ; Sellers, William R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-73c086cae4679b89a7fa73957ff8ce3e9e10731213de8aa52f9633c5e444cf1e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Cell Biology</topic><topic>Gene deletion</topic><topic>Genes</topic><topic>Hsp90 protein</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Oncology</topic><topic>Phosphatase</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Point mutation</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - physiopathology</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - physiology</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - physiology</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - physiology</topic><topic>PTEN protein</topic><topic>Radiation therapy</topic><topic>review</topic><topic>Signal Transduction</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Majumder, Pradip K</creatorcontrib><creatorcontrib>Sellers, William R</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>Majumder, Pradip K</au><au>Sellers, William R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Akt-regulated pathways in prostate cancer</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2005-11-14</date><risdate>2005</risdate><volume>24</volume><issue>50</issue><spage>7465</spage><epage>7474</epage><pages>7465-7474</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>16288293</pmid><doi>10.1038/sj.onc.1209096</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0950-9232 |
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| source | MEDLINE; Nature; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Apoptosis Cell Biology Gene deletion Genes Hsp90 protein Human Genetics Humans Internal Medicine Kinases Male Medicine Medicine & Public Health Metastases Metastasis Mutation Oncology Phosphatase Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Point mutation Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - physiopathology Protein Kinases - genetics Protein Kinases - physiology Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - physiology PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - physiology PTEN protein Radiation therapy review Signal Transduction TOR protein TOR Serine-Threonine Kinases Tumors |
| title | Akt-regulated pathways in prostate cancer |
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