Concepts to Target MYC in Pancreatic Cancer
Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to esta...
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Veröffentlicht in: | Molecular cancer therapeutics 2016-08, Vol.15 (8), p.1792-1798 |
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container_title | Molecular cancer therapeutics |
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creator | Wirth, Matthias Mahboobi, Siavosh Krämer, Oliver H Schneider, Günter |
description | Current data suggest that MYC is an important signaling hub and driver in pancreatic ductal adenocarcinoma (PDAC), a tumor entity with a strikingly poor prognosis. No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792-8. ©2016 AACR. |
doi_str_mv | 10.1158/1535-7163.MCT-16-0050 |
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No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. 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No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792-8. ©2016 AACR.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carrier Proteins</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Regulatory Networks</subject><subject>Genetic Variation</subject><subject>Humans</subject><subject>Molecular Targeted Therapy</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Protein Binding</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Proto-Oncogene Proteins c-myc - antagonists & inhibitors</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Signal Transduction - drug effects</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LAzEQhoMotlZ_grJHQbZmkubrKItf0KKHevAUknQiK-1uTbYH_727tnqal-F5Z-Ah5BLoFEDoWxBclAokny6qZQmypFTQIzLu97rUAmbHv3nPjMhZzp-UgjYMTsmIqRmVRssxuanaJuC2y0XXFkuXPrArFu9VUTfFq2tCQtfVoaj6iOmcnES3znhxmBPy9nC_rJ7K-cvjc3U3LwNXoiuF8c4xDwGM98xEGlZeUs5c1BF9BJAaFIsKmBNM-RmnGDGG6OSKa6OQT8j1_u42tV87zJ3d1Dngeu0abHfZgqZGUsmA96jYoyG1OSeMdpvqjUvfFqgdPNnBgR0c2N6TBWkHT33v6vBi5ze4-m_9ieE_pXViPQ</recordid><startdate>201608</startdate><enddate>201608</enddate><creator>Wirth, Matthias</creator><creator>Mahboobi, Siavosh</creator><creator>Krämer, Oliver H</creator><creator>Schneider, Günter</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></search><sort><creationdate>201608</creationdate><title>Concepts to Target MYC in Pancreatic Cancer</title><author>Wirth, Matthias ; 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No targeted therapies with a meaningful clinical impact were successfully developed against PDAC so far. This points to the need to establish novel concepts targeting the relevant drivers of PDAC, like KRAS or MYC. Here, we discuss recent developments of direct or indirect MYC inhibitors and their potential mode of action in PDAC. Mol Cancer Ther; 15(8); 1792-8. ©2016 AACR.</abstract><cop>United States</cop><pmid>27406986</pmid><doi>10.1158/1535-7163.MCT-16-0050</doi><tpages>7</tpages></addata></record> |
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source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research |
subjects | Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Carrier Proteins Gene Expression Regulation, Neoplastic - drug effects Gene Regulatory Networks Genetic Variation Humans Molecular Targeted Therapy Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Protein Binding Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Proto-Oncogene Proteins c-myc - antagonists & inhibitors Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism Signal Transduction - drug effects |
title | Concepts to Target MYC in Pancreatic Cancer |
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