{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhao K"],"funding":["NCATS NIH HHS","NCI NIH HHS"],"pagination":["1504-1511"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12784189"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["57(6)"],"pubmed_abstract":["To understand genetic evolution in cancer during metastasis, we analyzed genomic profiles of 3,732 cancer patients in whom several tumor sites were longitudinally biopsied. During distant metastasis, tumors were observed to accumulate copy number alterations (CNAs) to a much greater degree than mutations. In particular, the development of whole genome duplication was a common event during metastasis, emerging de novo in 28% of patients. Loss of 9p (including CDKN2A) developed during metastasis in 11% of patients. To a lesser degree, mutations and allelic loss in human leukocyte antigen class I and other genes associated with antigen presentation also emerged. Increasing CNA, but not increasing mutational load, was associated with immune evasion in patients treated with immunotherapy. Taken"],"journal":["Nature genetics"],"pubmed_title":["Longitudinal and multisite sampling reveals mutational and copy number evolution in tumors during metastatic dissemination."],"pmcid":["PMC12784189"],"funding_grant_id":["UL1 TR002384","P30 CA008748"],"pubmed_authors":["Jain S","Bandlamudi C","Zhou XK","Morris LGT","Muldoon D","Han CY","Lee M","Prasad M","Lee AS","Vos J","Fitzgerald C","Valero C","Lam S","Boe LA","Chan TA","Zhao K","Berger MF","Deng X"],"additional_accession":[]},"is_claimable":false,"name":"Longitudinal and multisite sampling reveals mutational and copy number evolution in tumors during metastatic dissemination.","description":"To understand genetic evolution in cancer during metastasis, we analyzed genomic profiles of 3,732 cancer patients in whom several tumor sites were longitudinally biopsied. During distant metastasis, tumors were observed to accumulate copy number alterations (CNAs) to a much greater degree than mutations. In particular, the development of whole genome duplication was a common event during metastasis, emerging de novo in 28% of patients. Loss of 9p (including CDKN2A) developed during metastasis in 11% of patients. To a lesser degree, mutations and allelic loss in human leukocyte antigen class I and other genes associated with antigen presentation also emerged. Increasing CNA, but not increasing mutational load, was associated with immune evasion in patients treated with immunotherapy. Taken","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jun","modification":"2026-06-09T03:12:37.084Z","creation":"2026-06-09T03:07:43.314Z"},"accession":"S-EPMC12784189","cross_references":{"pubmed":["40457077"],"doi":["10.1038/s41588-025-02204-3"]}}