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Molecular pathways: translational and therapeutic implications of the Notch signaling pathway in cancer
Over 100 years have passed since the first observation of the notched wing phenotype in Drosophila melanogaster, and significant progress has been made to characterize the role of the Notch receptor, its ligands, downstream targets, and cross-talk with other signaling pathways. The canonical Notch p...
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Published in: | Clinical cancer research 2015-03, Vol.21 (5), p.955-961 |
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container_title | Clinical cancer research |
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creator | Previs, Rebecca A Coleman, Robert L Harris, Adrian L Sood, Anil K |
description | Over 100 years have passed since the first observation of the notched wing phenotype in Drosophila melanogaster, and significant progress has been made to characterize the role of the Notch receptor, its ligands, downstream targets, and cross-talk with other signaling pathways. The canonical Notch pathway with four Notch receptors (Notch1-4) and five ligands (DLL1, 3-4, Jagged 1-2) is an evolutionarily conserved cell signaling pathway that plays critical roles in cell-fate determination, differentiation, development, tissue patterning, cell proliferation, and death. In cancer, these roles have a critical impact on tumor behavior and response to therapy. Because the role of Notch remains tissue and context dependent, alterations within this pathway may lead to tumor suppressive or oncogenic phenotypes. Although no FDA-approved therapies currently exist for the Notch pathway, multiple therapeutics (e.g., demcizumab, tarextumab, GSI MK-0752, R04929097, and PF63084014) have been developed to target different aspects of this pathway for both hematologic and solid malignancies. Understanding the context-specific effects of the Notch pathway will be important for individualized therapies targeting this pathway. |
doi_str_mv | 10.1158/1078-0432.ccr-14-0809 |
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The canonical Notch pathway with four Notch receptors (Notch1-4) and five ligands (DLL1, 3-4, Jagged 1-2) is an evolutionarily conserved cell signaling pathway that plays critical roles in cell-fate determination, differentiation, development, tissue patterning, cell proliferation, and death. In cancer, these roles have a critical impact on tumor behavior and response to therapy. Because the role of Notch remains tissue and context dependent, alterations within this pathway may lead to tumor suppressive or oncogenic phenotypes. Although no FDA-approved therapies currently exist for the Notch pathway, multiple therapeutics (e.g., demcizumab, tarextumab, GSI MK-0752, R04929097, and PF63084014) have been developed to target different aspects of this pathway for both hematologic and solid malignancies. Understanding the context-specific effects of the Notch pathway will be important for individualized therapies targeting this pathway.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Drug Discovery</subject><subject>Humans</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Oncogene Proteins - metabolism</subject><subject>Patient Selection</subject><subject>Receptors, Notch - antagonists & inhibitors</subject><subject>Receptors, Notch - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Translational Research, Biomedical</subject><subject>Tumor Suppressor Proteins - metabolism</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNpVkUtP3DAQx60KVB7tR2jlI5eAJ37E2wMSWrWAxENC7dlyZp1dV147tRMQ356ksKg9jaX_Y8b6EfIF2CmA1GfAGl0xwetTxFyBqJhmiw_kEKRsKl4ruTe9d54DclTKb8ZAABMfyUEtudag-CFZ36bgcAw2094Omyf7XL7RIdtYgh18ijZQG1d02LhsezcOHqnf9sHjX7XQ1M0avUsDbmjx6yng43rXRX2kaCO6_InsdzYU9_ltHpNfP77_XF5VN_eX18uLmwplvRiqTjAtddcy3mpphZItolDNSiI00KyQodSubhnUjeStbReiA6EsIqiaC93yY3L-2tuP7dat0MXpM8H02W9tfjbJevO_Ev3GrNOjEZzzmqmp4OStIKc_oyuD2fqCLgQbXRqLAaWYklIvYLLKVyvmVEp23fsaYGaGZGYAZgZglssHA8LMkKbc139vfE_tqPAXg72Qvg</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Previs, Rebecca A</creator><creator>Coleman, Robert L</creator><creator>Harris, Adrian L</creator><creator>Sood, Anil K</creator><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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150301</creationdate><title>Molecular pathways: translational and therapeutic implications of the Notch signaling pathway in cancer</title><author>Previs, Rebecca A ; Coleman, Robert L ; Harris, Adrian L ; Sood, Anil K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-f40858fb03b85a465bcc467d5c1717dc0c58e2b012753bab94f146acc162348b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Drug Discovery</topic><topic>Humans</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Oncogene Proteins - metabolism</topic><topic>Patient Selection</topic><topic>Receptors, Notch - antagonists & inhibitors</topic><topic>Receptors, Notch - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Translational Research, Biomedical</topic><topic>Tumor Suppressor Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Previs, Rebecca A</creatorcontrib><creatorcontrib>Coleman, Robert L</creatorcontrib><creatorcontrib>Harris, Adrian L</creatorcontrib><creatorcontrib>Sood, Anil K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Previs, Rebecca A</au><au>Coleman, Robert L</au><au>Harris, Adrian L</au><au>Sood, Anil K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular pathways: translational and therapeutic implications of the Notch signaling pathway in cancer</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>21</volume><issue>5</issue><spage>955</spage><epage>961</epage><pages>955-961</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Over 100 years have passed since the first observation of the notched wing phenotype in Drosophila melanogaster, and significant progress has been made to characterize the role of the Notch receptor, its ligands, downstream targets, and cross-talk with other signaling pathways. 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source | Freely Accessible Science Journals at publisher websites |
subjects | Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Antineoplastic Combined Chemotherapy Protocols - therapeutic use Drug Discovery Humans Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - metabolism Oncogene Proteins - metabolism Patient Selection Receptors, Notch - antagonists & inhibitors Receptors, Notch - metabolism Signal Transduction - drug effects Translational Research, Biomedical Tumor Suppressor Proteins - metabolism |
title | Molecular pathways: translational and therapeutic implications of the Notch signaling pathway in cancer |
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