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Clonal evolution of glioblastoma under therapy
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, Jiguang | - |
dc.contributor.author | Cazzato, Emanuela | - |
dc.contributor.author | Ladewig, Erik | - |
dc.contributor.author | Frattini, Veronique | - |
dc.contributor.author | Rosenbloom, Daniel I. S. | - |
dc.contributor.author | Zairis, Sakellarios | - |
dc.contributor.author | Abate, Francesco | - |
dc.contributor.author | Liu, Zhaoqi | - |
dc.contributor.author | Elliott, Oliver | - |
dc.contributor.author | Shin, Yong-Jae | - |
dc.contributor.author | Lee, Jin-Ku | - |
dc.contributor.author | Lee, In-Hee | - |
dc.contributor.author | Park, Woong-Yang | - |
dc.contributor.author | Eoli, Marica | - |
dc.contributor.author | Blumberg, Andrew J. | - |
dc.contributor.author | Lasorella, Anna | - |
dc.contributor.author | Nam, Do-Hyun | - |
dc.contributor.author | Finocchiaro, Gaetano | - |
dc.contributor.author | Iavarone, Antonio | - |
dc.contributor.author | Rabadan, Raul | - |
dc.date.accessioned | 2023-04-26T05:06:59Z | - |
dc.date.available | 2023-04-26T05:06:59Z | - |
dc.date.created | 2023-04-26 | - |
dc.date.created | 2023-04-26 | - |
dc.date.created | 2023-04-26 | - |
dc.date.issued | 2016-07 | - |
dc.identifier.citation | Nature Genetics, Vol.48 No.7, pp.768-776 | - |
dc.identifier.issn | 1061-4036 | - |
dc.identifier.uri | https://hdl.handle.net/10371/191550 | - |
dc.description.abstract | Glioblastoma (GBM) is the most common and aggressive primary brain tumor. To better understand how GBM evolves, we analyzed longitudinal genomic and transcriptomic data from 114 patients. The analysis shows a highly branched evolutionary pattern in which 63% of patients experience expression-based subtype changes. The branching pattern, together with estimates of evolutionary rate, suggests that relapse-associated clones typically existed years before diagnosis. Fifteen percent of tumors present hypermutation at relapse in highly expressed genes, with a clear mutational signature. We find that 11% of recurrence tumors harbor mutations in LTBP4, which encodes a protein binding to TGF-beta. Silencing LTBP4 in GBM cells leads to suppression of TGF-beta activity and decreased cell proliferation. In recurrent GBM with wild-type IDH1, high LTBP4 expression is associated with worse prognosis, highlighting the TGF-b pathway as a potential therapeutic target in GBM. | - |
dc.language | 영어 | - |
dc.publisher | Nature Publishing Group | - |
dc.title | Clonal evolution of glioblastoma under therapy | - |
dc.type | Article | - |
dc.identifier.doi | 10.1038/ng.3590 | - |
dc.citation.journaltitle | Nature Genetics | - |
dc.identifier.wosid | 000378840100014 | - |
dc.identifier.scopusid | 2-s2.0-84976318961 | - |
dc.citation.endpage | 776 | - |
dc.citation.number | 7 | - |
dc.citation.startpage | 768 | - |
dc.citation.volume | 48 | - |
dc.description.isOpenAccess | Y | - |
dc.contributor.affiliatedAuthor | Lee, Jin-Ku | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | TGF-BETA | - |
dc.subject.keywordPlus | GENOMIC ALTERATIONS | - |
dc.subject.keywordPlus | SEQUENCING DATA | - |
dc.subject.keywordPlus | BRAIN-TUMORS | - |
dc.subject.keywordPlus | CANCER GENOMICS | - |
dc.subject.keywordPlus | MSH6 MUTATIONS | - |
dc.subject.keywordPlus | GENE FUSIONS | - |
dc.subject.keywordPlus | GLIOMA | - |
dc.subject.keywordPlus | TEMOZOLOMIDE | - |
dc.subject.keywordPlus | LANDSCAPE | - |
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