[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-376418-105":59,"doc-detail-376418-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","telomere-maintenance-and-oncogenesis-research-overview","Telomere Maintenance and Oncogenesis - Research Overview","","An overwhelming majority of cancers show telomere shortening and differentiation-associated markers consistent with a post-stem cell origin. While telomere damage can protect cells from malignant transformation by triggering apoptosis, cancer development may increase when apoptotic regulators such as p53 are absent. Proposed mechanisms link telomere shortening to telomeric chromatin architecture changes and to tumor maintenance. Signaling pathways may release Rap1 from telomeres, where interaction with Zscan4 supports immortalization and malignant transformation.",{"@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/telomere-maintenance-and-oncogenesis-research-overview/376418/",{"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/telomere-maintenance-and-oncogenesis-research-overview/376418.png","ImageObject",300,407,{"name":92,"@type":93},"kopisore","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-25","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",11,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What relationship does the article describe between most cancers and telomere changes?","Question",{"text":113,"@type":114},"Most cancers show telomere length reduction together with differentiation markers, supporting a post-stem cell of origin in the article’s framing.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How can telomere shortening simultaneously protect against and promote cancer?",{"text":118,"@type":114},"Telomere shortening/damage can induce apoptosis and senescence to protect cells, but reduced apoptotic factors (e.g., p53 loss) and telomere dysfunction can facilitate carcinogenesis.",{"name":120,"@type":111,"acceptedAnswer":121},"What mechanism does the article propose involving Rap1 and Zscan4?",{"text":122,"@type":114},"It proposes that signaling pathways, together with telomere shortening/damage, may release Rap1 from telomeres, and that Rap1 interaction with Zscan4 may support immortalization and malignant transformation.","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},376418,1790711657,{"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":41,"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},962090880963,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","Review  \nTelomere Maintenance and Oncogenesis  \nAntonio Torres-Montaner †,‡  \nAcademic Editor: Amelia Casamassimi  \nReceived: 10 September 2025  \nRevised: 6 November 2025  \nAccepted: 10 November 2025  \nPublished: 12 November 2025  \nCitation: Torres-Montaner, A. Telomere Maintenance and Oncogenesis. Int. J. Mol. Sci. 2025, 26, 10941. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ijms262210941  \nCopyright: © 2025 by the author. 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 ([https://creativecommons.org/](https://creativecommons.org/)[ ](https://creativecommons.org/)[licenses/by/4.0/](licenses/by/4.0/)) .  \nIndependent Researcher, 22400 Monzon, Spain; [atorresmontaner@gmail.com](atorresmontaner@gmail.com)  \n† Former affiliation: Department of Pathology, Queen’s Hospital, Rom Valley Way, Romford, London RM7 OAG, UK.  \n‡ Former affiliation: Departamento de Bioquimica y Biologia Molecular, Universidad de Cádiz, Puerto Real, 11510 Cadiz, Spain.  \nAbstract  \nAn overwhelming majority of cancers exhibit telomere length reduction and differentiation markers consistent with a post-stem cell of origin. On the other hand, telomere shortening/damage is believed to protect cells from malignant transformation through induction of apoptosis. However, increased cancer incidence in the absence of apoptotic factors like p53 may suggest a favorable role of telomere shortening/damage in cancer development. Some findings suggest that telomere shortening may induce architectural changes in telomeric chromatin, such as those underlying the telomere position effect that support telomere maintenance of some tumors Here, we propose that several signaling pathways, in conjunction with telomere shortening/damage, may result in the release of Rap1 from telomeres. Its subsequent interaction with the embryonic stem cell marker Zscan4 may support immortalization and malignant transformation of the target cell.  \nKeywords: telomeres; Rap1; Zscan4; PI3K/AKT pathway  \n1. Introduction  \nIn the quest to understand the nature of cancer, a point of departure is provided by one of the most fundamental aspects of living organisms: the capacity for regeneration and self-renewal, which is also a hallmark of cancer. This property is compartmentalized within organisms and linked to germinal structures or cells endowed with embryonic features that maintain a capacity for regeneration. This idea led Conheim [1] to propose that cancer originates in embryonic remnants that persist into adult life, disconnected from their original sources, and later undergo aberrant growth. Later, histological research established that specialized somatic cells present in every tissue, initially known as reserve cells and later as normal stem cells, are responsible for replenishing the population of tissue cells, which are continually lost to wear and tear or shed after multiple rounds of proliferation and differentiation. The ability to indefinitely self-renew, which is shared by the so-called reserve cells and cancer cells, with its dual physiological and pathological functions, led to the assumption that cancer growth arises from a failure of tissue stem cells to respond to tissue regulatory signals that maintain normal tissue architecture. In other words, cancer originates directly from tissue stem cells. The modern concept of cancer stem cells assumes this hierarchical organization, ascribing embryonic/stem features to these cells and generally disregarding the concept of an origin in embryonic rests. However, this feature is often interpreted to preclude an origin of cancer in committed cells.  \nRegeneration potential is lost as soon as cells leave the stem cell compartment. This was first confirmed in the hematopoietic system. Even in the transition from long-term hematopoietic stem cells (LT-HSCs) to short-term hematopoietic stem ce","cbCaibzB6xxeCY85","https://ap.wps.com/l/cbCaibzB6xxeCY85","pdf",1238159,"English","# Abstract\n# Keywords\n# Introduction","[{\"question\":\"What relationship does the article describe between most cancers and telomere changes?\",\"answer\":\"Most cancers show telomere length reduction together with differentiation markers, supporting a post-stem cell of origin in the article’s framing.\"},{\"question\":\"How can telomere shortening simultaneously protect against and promote cancer?\",\"answer\":\"Telomere shortening/damage can induce apoptosis and senescence to protect cells, but reduced apoptotic factors (e.g., p53 loss) and telomere dysfunction can facilitate carcinogenesis.\"},{\"question\":\"What mechanism does the article propose involving Rap1 and Zscan4?\",\"answer\":\"It proposes that signaling pathways, together with telomere shortening/damage, may release Rap1 from telomeres, and that Rap1 interaction with Zscan4 may support immortalization and malignant transformation.\"}]","Telomere Maintenance and Oncogenesis - Research Overview | PDF",1790219061,76]