[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-detail-326675-en":3,"doc-seo-326675-105":31,"detail-sidebar-cat-0-en-105":99},{"code":4,"msg":5,"data":6},0,"success",{"doc_id":7,"user_id":8,"nickname":9,"user_avatar":10,"doc_module":4,"category_id":11,"category_name":12,"doc_title":13,"doc_description":14,"doc_content":15,"file_id":16,"file_url":17,"file_type":18,"file_size":19,"view_count":20,"is_deleted":4,"is_public":21,"is_downloadable":21,"audit_status":21,"page_count":22,"language":23,"language_code":24,"site_id":25,"html_lang":24,"table_of_contents":26,"faqs":27,"seo_title":28,"seo_description":14,"update_tm":29,"read_time":30,"preview_page_count":4},326675,1099513958607,"Jiven","https://ap-avatar.wpscdn.com/avatar/100002390cf8733938c?x-image-process=image/resize,m_fixed,w_180,h_180&k=1778829742770036399",8,"Research & Report","Transcriptional signals of transformation in human cancer","Malignant transformation reshapes cell identity as normal cells evolve into cancers, shifting transcriptomic programs toward stem-like, more primordial, foetal, or embryonic states. The resulting final-state transcriptomic profile can reflect cancer origin and relationships to corresponding normal cell counterparts. Using single-cell atlases and bulk transcriptomes across adult and childhood cancers, the study interrogates links between cancer and normal cell state programs and validates findings with organ-specific single-cell cancer datasets.","Kildisiute et al. Genome Medicine (2024) 16:8 [https://doi.org/10.1186/s13073-023-01279-z](https://doi.org/10.1186/s13073-023-01279-z)  \nGenome Medicine  \n RESEARCH Open Access  \nTranscriptional signals of transformation in human cancer  \nGerda Kildisiute 1†, Maria Kalyva2†, Rasa Elmentaite 1, Stijn van Dongen 1, Christine Thevanesan3,  \nAlice Piapi3, Kirsty Ambridge1, Elena Prigmore 1, Muzlifah Haniffa 1,4, Sarah A. Teichmann 1,5, Karin Straathof3, Isidro Cortés‑Ciriano2*, Sam Behjati1,6,7* and Matthew D. Young 1*  \nAbstract  \nBackground As normal cells transform into cancers, their cell state changes, which may drive cancer cells  \ninto a stem‑like or more primordial, foetal, or embryonic cell state. The transcriptomic profile of this final state may encode information about cancer’s origin and how cancers relate to their normal cell counterparts.  \nMethods Here, we used single‑cell atlases to study cancer transformation in transcriptional terms. We utilised bulk transcriptomes across a wide spectrum of adult and childhood cancers, using a previously established method to interrogate their relationship to normal cell states. We extend and validate these findings using single‑cell cancer transcriptomes and organ‑specific atlases of colorectal and liver cancer.  \nResults Our bulk transcriptomic data reveals that adult cancers rarely return to an embryonic state, but that a foetal state is a near‑universal feature of childhood cancers. This finding was confirmed with single‑cell cancer transcriptomes.  \nConclusions Our findings provide a nuanced picture of transformation in human cancer, indicating cancer‑specific rather than universal patterns of transformation pervade adult epithelial cancers.  \n†Gerda Kildisiute and Maria Kalyva contributed equally.  \n*Correspondence: Isidro Cortés‑Ciriano[icortes@ebi.ac.uk](icortes@ebi.ac.uk)[ ](icortes@ebi.ac.uk)Sam Behjati [sb31@sanger.ac.uk](sb31@sanger.ac.uk)[ ](sb31@sanger.ac.uk)Matthew D. Young [my4@sanger.ac.uk](my4@sanger.ac.uk)  \n1 Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1SA, UK  \n2 EMBL‑EBI, Wellcome Genome Campus, Hinxton, Cambridge, UK  \n3 University College London Cancer Institute and Great Ormond Street Biomedical Research Centre, London, UK  \n4 Biosciences Institute and Newcastle NIHR‑BRC Dermatology, Newcastle University, Newcastle Upon Tyne, UK  \n5 Cavendish Laboratory, University of Cambridge, JJ Thomson Ave, Cambridge, UK  \n6 Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK  \n7 Department of Paediatrics, University of Cambridge, Cambridge, UK  \nBackground  \nMalignant transformation is underpinned by changes in the cell state towards a less differentiated or stem-like cell state. Consequently, cancers may broadly retain the cell state of origin or transform to resemble a more primitive cell type, of tissue-specific foetal or primordial embryonic cells. Which cell state—primordial or otherwise—cancer assumes is a fundamental question of cancer biology as it provides a net readout of the consequences of cancer formation.  \nThe cancer cell state can be studied using transcriptional readouts that represent cellular phenotypes and differentiation states. The key challenge in such an analysis is defining cellular states, such as stemness, embryonicness, foetalness, etc., in quantitative molecular terms. One approach is to use appropriate mRNA signals, identified using unsupervised  \n© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material","cbCaif65EKWwci4U","https://ap.wps.com/l/cbCaif65EKWwci4U","pdf",3444044,7,1,10,"English","en",105,"# Abstract\n## Background\n## Methods\n## Results\n## Conclusions\n# Background\n## Defining cellular states via transcriptional readouts\n# References and licensing notes","[{\"question\":\"What biological question does the study address about cancer transformation?\",\"answer\":\"It asks how malignant transformation changes cell state and which developmental programs—primordial, foetal, or embryonic—cancers adopt as a consequence of cancer formation.\"},{\"question\":\"How did the authors investigate transcriptional transformation in cancers?\",\"answer\":\"They used single-cell atlases to analyze transcriptional terms and employed bulk transcriptomes across a spectrum of adult and childhood cancers, then extended and validated results with single-cell cancer transcriptomes and organ-specific atlases.\"},{\"question\":\"What key finding differentiates adult and childhood cancers in this work?\",\"answer\":\"Adult cancers rarely return to an embryonic state, whereas a foetal state is described as a near-universal feature of childhood cancers, confirmed using single-cell cancer transcriptomes.\"}]","Transcriptional signals of transformation in human cancer | 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biological question does the study address about cancer transformation?","Question",{"text":82,"@type":83},"It asks how malignant transformation changes cell state and which developmental programs—primordial, foetal, or embryonic—cancers adopt as a consequence of cancer formation.","Answer",{"name":85,"@type":80,"acceptedAnswer":86},"How did the authors investigate transcriptional transformation in cancers?",{"text":87,"@type":83},"They used single-cell atlases to analyze transcriptional terms and employed bulk transcriptomes across a spectrum of adult and childhood cancers, then extended and validated results with single-cell cancer transcriptomes and organ-specific atlases.",{"name":89,"@type":80,"acceptedAnswer":90},"What key finding differentiates adult and childhood cancers in this work?",{"text":91,"@type":83},"Adult cancers rarely return to an embryonic state, whereas a foetal state is described as a near-universal feature of childhood cancers, confirmed using single-cell cancer 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