{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Baker TM"],"funding":["UCLH Biomedical Research Centre (UCL)","Stand Up To Cancer","Cancer Research UK","UCLH Biomedical Research Centre","Stand Up To Cancer (SU2C)","Cancer Prevention and Research Institute of Texas (CPRIT)","Fonds De La Recherche Scientifique - FNRS (FNRS)","Sarcoma UK (SUK)","Bone Cancer Research Trust (BCRT)","Fonds De La Recherche Scientifique - FNRS","Rosetrees Trust (Rosetrees)","Royal Society","Royal Society (The Royal Society)","Boehringer Ingelheim Fonds (BIF)","Cancer Prevention and Research Institute of Texas","Breast Cancer Research Foundation (BCRF)","Sarcoma UK","Breast Cancer Research Foundation","Rosetrees Trust","European Research Council","Medical Research Council","Bone Cancer Research Trust","Wellcome Trust","Boehringer Ingelheim Fonds"],"pagination":["1810-1822"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7616501"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(10)"],"pubmed_abstract":["Tumors frequently display high chromosomal instability and contain multiple copies of genomic regions. Here, we describe Gain Route Identification and Timing In Cancer (GRITIC), a generic method for timing genomic gains leading to complex copy number states, using single-sample bulk whole-genome sequencing data. By applying GRITIC to 6,091 tumors, we found that non-parsimonious evolution is frequent in the formation of complex copy number states in genome-doubled tumors. We measured chromosomal instability before and after genome duplication in human tumors and found that late genome doubling was followed by an increase in the rate of copy number gain. Copy number gains often accumulate as punctuated bursts, commonly after genome doubling. We infer that genome duplications typically affect"],"journal":["Cancer discovery"],"pubmed_title":["The History of Chromosomal Instability in Genome-Doubled Tumors."],"pmcid":["PMC7616501"],"funding_grant_id":["835297","RCCCEA-Nov23/100003","Chromavision 665233","SUKG01.2018","CC2041","TRACERx","18387","665233","RP210028","617844","BCRF 20-157","FP7-THESEUS-617844","RP150154","SU2C-AACR-DT23-17","RP/EA/180007","607722","FP7-PloidyNet 607722","CC2008","C11496/A17786","C11496/A30025","PROTEUS 835297","RR210006"],"pubmed_authors":["Swanton C","Ogilvie HA","Spellman PT","Baker TM","Dentro S","Bowes AL","Van Loo P","Verfaillie A","Lynch AR","Pillay N","Lesluyes T","Tarabichi M","Flanagan AM","Lai S","Yan H"],"additional_accession":[]},"is_claimable":false,"name":"The History of Chromosomal Instability in Genome-Doubled Tumors.","description":"Tumors frequently display high chromosomal instability and contain multiple copies of genomic regions. Here, we describe Gain Route Identification and Timing In Cancer (GRITIC), a generic method for timing genomic gains leading to complex copy number states, using single-sample bulk whole-genome sequencing data. By applying GRITIC to 6,091 tumors, we found that non-parsimonious evolution is frequent in the formation of complex copy number states in genome-doubled tumors. We measured chromosomal instability before and after genome duplication in human tumors and found that late genome doubling was followed by an increase in the rate of copy number gain. Copy number gains often accumulate as punctuated bursts, commonly after genome doubling. We infer that genome duplications typically affect","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-06T23:08:56.314Z","creation":"2025-04-04T01:20:37.231Z"},"accession":"S-EPMC7616501","cross_references":{"pubmed":["38943574"],"doi":["10.1158/2159-8290.CD-23-1249"]}}