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Molecular profiling is expanding biomarker-guided and targeted treatment options. A literature review using PubMed and the Cochrane Library through July 2026, supplemented by major oncology conference materials, summarizes current and emerging targeted therapies. Precision approaches include PARP inhibition, immune checkpoint blockade, TRK inhibition, and KRAS/RAS-directed strategies, while resistance, toxicity, and access to comprehensive testing remain major challenges.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/targeted-therapy-in-pancreatic-ductal-adenocarcinoma-current-advances-and-challenges/354660/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/targeted-therapy-in-pancreatic-ductal-adenocarcinoma-current-advances-and-challenges/354660.png","ImageObject",300,407,{"name":92,"@type":93},"LangkahRina","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-23","2026-09-22",true,{"@type":102,"interactionType":103,"userInteractionCount":8},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why is PDAC difficult to treat with standard systemic therapies?","Question",{"text":112,"@type":113},"PDAC is often diagnosed at an advanced stage and shows aggressive tumor biology with limited responsiveness to conventional systemic therapy, leading to poor survival outcomes.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Which established targeted therapies are highlighted for specific genetic alterations?",{"text":117,"@type":113},"The review describes PARP inhibitors for patients with BRCA1, BRCA2, or PALB2 pathogenic variants, immune checkpoint inhibition for mismatch repair-deficient or microsatellite instability-high tumors, and TRK inhibitors for tumors with NTRK gene fusions.",{"name":119,"@type":110,"acceptedAnswer":120},"What progress is discussed for KRAS and RAS-targeted therapy?",{"text":121,"@type":113},"Direct KRAS/RAS inhibition is presented as a major breakthrough. Evidence includes KRAS G12C inhibitor proof of concept and RASolute 302 results showing daraxonrasib improved survival versus chemotherapy in previously treated RAS-mutant metastatic PDAC, with further activity for KRAS G12D-mutant strategies under study.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},354660,1790168343,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":8,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},962090893776,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Review  \nTargeted Therapy in Pancreatic Ductal Adenocarcinoma: Current Advances and Challenges  \nRamy Habib 1, Erika Arnold 1, Tasin Obi 2, Franco J. Vizeacoumar 2,3 and Shahid Ahmed 2,3, *  \nReceived: 20 June 2026  \nRevised: 25 July 2026  \nAccepted: 27 July 2026  \nPublished: 28 July 2026  \nCopyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 School of Medicine, University of Limerick, Limerick V94 T9PX, Munster, Ireland; [23316373@studentmail.ul.ie](23316373@studentmail.ul.ie) (R.H.); [erika.arnold@mail.mcgill.ca](erika.arnold@mail.mcgill.ca) (E.A.)  \n2 Department of Oncology, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada; [bnv137@mail.usask.ca](bnv137@mail.usask.ca) (T.O.); [franco.vizeacoumar@usask.ca](franco.vizeacoumar@usask.ca) (F.J.V.)  \n3 Saskatchewan Cancer Agency, Regina, SK S4W 0G3, Canada  \n* Correspondence: shahid.ahmed@saskcancer.ca; Tel.: +1-(306)-655-2710; Fax: +1-(306)-655-0633  \nSimple Summary  \nPancreatic ductal adenocarcinoma (PDAC) is one of the deadliest forms of cancer and remains difficult to treat because it is often diagnosed at an advanced stage and responds poorly to standard treatments. Recent advances in genetic and molecular testing have improved our understanding of the biological changes that drive pancreatic cancer and have created new opportunities for more personalized treatment approaches. This review summarizes current and emerging targeted therapies for PDAC. Established treatments include PARP inhibitors for patients with BRCA1, BRCA2, or PALB2 pathogenic variants, immunotherapy for rare tumors with mismatch repair deficiency, and TRK inhibitors for cancers with NTRK gene fusions. New therapies that directly target KRAS and RAS, key cancer-driving proteins found in most pancreatic cancers, represent a major breakthrough and are showing promising results. A randomized phase III trial demonstrated that daraxonrasib improved survival compared with chemotherapy in previously treated RASmutant metastatic PDAC, providing strong clinical evidence that RAS can be successfully targeted. Other KRAS-directed agents, including therapies for the common KRAS G12D mutation, are also advancing in clinical trials. Continued advances in molecular testing and targeted therapies may help expand treatment options and improve outcomes for patients with pancreatic cancer.  \nAbstract  \nBackground: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid malignancies, with poor survival driven by late presentation, aggressive tumor biology, and limited responsiveness to conventional systemic therapy. Advances in molecular profiling have expanded opportunities for biomarker-guided and targeted therapeutic approaches. Methods: A literature review was conducted using PubMed and the Cochrane Library through July 2026, supplemented by abstracts and proceedings from major international oncology conferences. Results: Pancreatic cancer is driven mainly by somatic changes in KRAS, TP53, CDKN2A, and SMAD4 . Established precision approaches include maintenance olaparib for selected platinum-sensitive tumors with germline BRCA1 or BRCA2 pathogenic variants, immune checkpoint inhibition for mismatch repair-deficient or microsatellite instability-high tumors, and tropomyosin receptor kinase inhibition for cancers with neurotrophic tyrosine receptor kinase gene fusions. Direct inhibition of KRASand RAS represents a major therapeutic breakthrough. KRAS G12C inhibitors established proof of concept, while agents targeting the more common KRAS G12D mutation are showing encouraging early activity. In the randomized phase III RASolute 302 trial, the  \nmultiselective RAS inhibitor daraxonrasib improved survival compared with chemotherapy in previously treated metastatic disease with oncogenic RAS mutations. Early studies of zoldo","cbCaic2mWOBtcA2K","https://ap.wps.com/l/cbCaic2mWOBtcA2K","pdf",507455,29,"English","# Simple Summary\n# Abstract\n# Keywords\n# Introduction","[{\"question\":\"Why is PDAC difficult to treat with standard systemic therapies?\",\"answer\":\"PDAC is often diagnosed at an advanced stage and shows aggressive tumor biology with limited responsiveness to conventional systemic therapy, leading to poor survival outcomes.\"},{\"question\":\"Which established targeted therapies are highlighted for specific genetic alterations?\",\"answer\":\"The review describes PARP inhibitors for patients with BRCA1, BRCA2, or PALB2 pathogenic variants, immune checkpoint inhibition for mismatch repair-deficient or microsatellite instability-high tumors, and TRK inhibitors for tumors with NTRK gene fusions.\"},{\"question\":\"What progress is discussed for KRAS and RAS-targeted therapy?\",\"answer\":\"Direct KRAS/RAS inhibition is presented as a major breakthrough. Evidence includes KRAS G12C inhibitor proof of concept and RASolute 302 results showing daraxonrasib improved survival versus chemotherapy in previously treated RAS-mutant metastatic PDAC, with further activity for KRAS G12D-mutant strategies under study.\"}]","Targeted Therapy in Pancreatic Ductal Adenocarcinoma - Current Advances and Challenges | PDF",1790112812,73]