[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-368843-105":59,"doc-detail-368843-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","myc-as-a-target-for-cancer-treatment-from-undruggable-to-druggable","MYC as a Target for Cancer Treatment - from Undruggable to Druggable?","","MYC is among the most frequently altered cancer genes, with an estimated 70% prevalence of deregulation. Deregulated MYC drives tumor formation and progression through multiple mechanisms, including effects within tumor cells, remodeling of the tumor microenvironment, and promotion of host immune suppression. Although MYC is an attractive anticancer target, conventional drug discovery has been hampered because MYC lacks an obvious druggable pocket and is mainly localized in the nucleus. Recent advances include anti-MYC agents such as Omomyc and MYCi975, which show anti-cancer activity in animal models, improve immune responsiveness, and are being evaluated in clinical trials; early phase I data with OMO-103 indicate tolerability and target inhibition via reduced expression of MYC-regulated genes.",{"@graph":69,"@context":123},[70,84,106],{"@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":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/myc-as-a-target-for-cancer-treatment-from-undruggable-to-druggable/368843/",{"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/myc-as-a-target-for-cancer-treatment-from-undruggable-to-druggable/368843.png","ImageObject",300,407,{"name":92,"@type":93},"Franzy","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-01","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",13,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"Why has MYC been difficult to target with standard anticancer drugs?","Question",{"text":113,"@type":114},"MYC has not presented an obvious druggable pocket for low-molecular-weight inhibitors and is predominantly localized in the cell nucleus, making conventional pharmacological approaches challenging.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"What anti-MYC compounds are highlighted as promising options?",{"text":118,"@type":114},"Omomyc and MYCi975 are described as promising anti-MYC compounds with anti-cancer activity in multiple animal models and apparently little short-term toxicity.",{"name":120,"@type":111,"acceptedAnswer":121},"How do Omomyc or MYCi975 influence the tumor-immune response?",{"text":122,"@type":114},"They are shown to increase uptake of anti-tumor lymphocytes and enhance response to immunotherapy, consistent with MYC’s role in promoting a pro-tumor microenvironment and inducing immune evasion.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},368843,1790278451,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146},2336478945519,"https://ap-avatar.wpscdn.com/davatar_085a072bc5b1113ac321206ff7593b45","Targeted Oncology (2025) 20:791–801  \n[https://doi.org/10.1007/s1](https://doi.org/10.1007/s1) 1523-025-01169-x  \nMYC as a Target for Cancer Treatment: from Undruggable to Druggable?  \nMichael J. Duffy1,2 · Minhong Tang1 · John Crown3  \nAccepted: 29 July 2025 / Published online: 15 August 2025 © The Author(s) 2025  \nAbstract  \nMYC is one of the most frequently altered genes in cancer with an estimated 70% prevalence of deregulation. Deregulated MYC is believed to promote cancer formation/progression via multiple mechanisms including tumour cell intrinsic mechanisms, altering the tumour microenvironment and promoting host immune suppression. Owing to the high prevalence of alterations and its causative role in tumorigenesis, MYC is a highly attractive target for new anticancer therapies. However, as MYC lacks a readily identifiably pocket for potential low molecular weight inhibitors and is predominantly located in the cell nucleus, it has proved difficult to target using standard pharmacological approaches. Recently, however, these problems appear to have been successfully resolved, with the discovery of promising anti-MYC compounds such as Omomycor MYCi975 . Both Omomyc and MYCi975 exhibit anti-cancer activity in several different animal models, with apparently little short-term toxicity. Furthermore, consistent with the ability of MYC to promote a pro-tumour microenvironment and induce immune evasion, treatment with Omomyc or MYCi975 was shown to increase uptake of anti-tumour lymphocytes and enhance response to immunotherapy. Currently, at least five anti-MYC compounds are being evaluated for potential anti-cancer activity in clinical trials. Results from a phase I trial with OMO-103 (a form of Omomyc) suggest that the inhibitor is well tolerated, with most of its adverse effects being at grade 1 level. Evidence of target inhibition was the finding of decreased expression of multiple MYC regulated genes.  \nPublisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.  \n* Michael J. Duffy [michael.j.duffy@ucd.ie](michael.j.duffy@ucd.ie)  \n1 UCD School of Medicine, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland  \n2 UCD Clinical Research Centre, St. Vincent’s University Hospital, Dublin, Ireland  \n3 Department of Medical Oncology, St Vincent’s University Hospital, Dublin, Ireland  \n1 Introduction  \nThe MYC family of genes that comprise C-MYC, N-MYC and L-MYC, are amongst the most frequently altered genes inhuman cancer [1–5] . Of these three paralogs, C-MYC (hereafter referred to as MYC) is the most frequently deregulated and is the best studied. Unlike most cancer-causing genes that tend to be altered by a single mechanism, such as mutation or amplification, MYC can be deregulated by diverse processes. These include amplification (mostly occur in epithelial tumours), translocation (mostly in leukaemia’s/lymphomas), increased oncogenic signalling which increases MYC expression and/or stability (most cancer types), enhancer activation, viral insertion (HPV in cervical cancer) and post-translational mechanisms such as loss of E3 ubiquitin ligases [3–6] . In contrast to many oncogenes/tumour suppressor genes, the protein coding sequence of MYC is rarely mutated in cancer, although such alterations have been detected in small numbers of specimens (\u003C 1%) [7] . MYC mutations, however, have been found in up to 40% of Burkitt’s lymphoma [8] . Overall, MYC is believed to altered/ deregulated, by one of the above mechanisms, in approximately 70% of all human malignancies [9] .  \nBecause of its high prevalence of deregulation, MYC is an attractive target for the new drugs to treat cancer. Development of effective anti-MYC therapies with clinical efficacy, however, has historically been difficult. The difficulties, however, appear to have been successfully addressed, as recently several compounds targeting MYC-de","cbCaiaiYbsHOKWvU","https://ap.wps.com/l/cbCaiaiYbsHOKWvU","pdf",1088638,11,"English","# Abstract\n# Introduction\n# Role of MYC in Cancer Formation\n## MYC regulation of gene expression","[{\"question\":\"Why has MYC been difficult to target with standard anticancer drugs?\",\"answer\":\"MYC has not presented an obvious druggable pocket for low-molecular-weight inhibitors and is predominantly localized in the cell nucleus, making conventional pharmacological approaches challenging.\"},{\"question\":\"What anti-MYC compounds are highlighted as promising options?\",\"answer\":\"Omomyc and MYCi975 are described as promising anti-MYC compounds with anti-cancer activity in multiple animal models and apparently little short-term toxicity.\"},{\"question\":\"How do Omomyc or MYCi975 influence the tumor-immune response?\",\"answer\":\"They are shown to increase uptake of anti-tumor lymphocytes and enhance response to immunotherapy, consistent with MYC’s role in promoting a pro-tumor microenvironment and inducing immune evasion.\"}]","MYC as a Target for Cancer Treatment - from Undruggable to Druggable? | PDF",1790178907,28]