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• W3108968950 abstract "We thank Quintino G D'Alessandris and colleagues for their comments on our Article on apatinib in advanced chordoma. 1 Liu C Jia Q Wei H et al. Apatinib in patients with advanced chordoma: a single-arm, single-centre, phase 2 study. Lancet Oncol. 2020; 21: 1244-1252 Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar We acknowledge that molecular selection of patients through immunohistochemistry was technically limited by decalcification in our study, 1 Liu C Jia Q Wei H et al. Apatinib in patients with advanced chordoma: a single-arm, single-centre, phase 2 study. Lancet Oncol. 2020; 21: 1244-1252 Summary Full Text Full Text PDF PubMed Scopus (22) Google Scholar as well as in a previous study. 2 Stacchiotti S Longhi A Ferraresi V et al. Phase II study of imatinib in advanced chordoma. J Clin Oncol. 2012; 30: 914-920 Crossref PubMed Scopus (182) Google Scholar Although next-generation sequencing or high-throughput sequencing has made it possible to profile tumours on a molecular basis, thus facilitating diagnosis, identification of unsuspected germline mutations, and detection of potentially targetable mutations, 3 Nikiforova MN Wald AI Melan MA et al. Targeted next-generation sequencing panel (GlioSeq) provides comprehensive genetic profiling of central nervous system tumors. Neuro Oncol. 2016; 18: 379-387 Crossref PubMed Scopus (80) Google Scholar chordomas show low mutation load and no recurrent oncogene mutations. 4 Wang L Zehir A Nafa K et al. Genomic aberrations frequently alter chromatin regulatory genes in chordoma. Genes Chromosomes Cancer. 2016; 55: 591-600 Crossref PubMed Scopus (35) Google Scholar Comprehensive genomic evaluation of 104 chordomas 5 Tarpey PS Behjati S Young MD et al. The driver landscape of sporadic chordoma. Nat Commun. 2017; 8: 890 Crossref PubMed Scopus (55) Google Scholar found recurrent somatic brachyury duplication (27%), alterations in chromatin modelling genes, including ARID1A, PBRM1, and SETD2 (17%), as well as alterations in PI3K signalling genes (16%). Recurrent alterations in LYST (10%) were also identified as a novel cancer gene in chordomas. Although these results help to better understand the tumour biology of chordomas, about 45% of tumours did not have a single plausible driver variant, 5 Tarpey PS Behjati S Young MD et al. The driver landscape of sporadic chordoma. Nat Commun. 2017; 8: 890 Crossref PubMed Scopus (55) Google Scholar suggesting that some other alterations could support chordoma oncogenesis. At our centre (Changzheng Hospital, Shanghai, China), systematically derived signatures of functional alterations with clinically significant relevance, including tumour mutation burden, microsatellite instability, and homologous recombination deficiency score, have been estimated in 114 pairs of samples, with the aim of identifying genomic traits of tumour development and opportunities to design new therapeutic options. Shifting from targeted therapies to personalised treatment in chordomaWe read with great interest the Article by Chao Liu and colleagues1 on apatinib in advanced chordoma. The strength of the work is that apatinib, a tyrosine-kinase inhibitor of VEGFR2, improves the overall survival of patients with advanced chordoma (9-month overall survival of 88%) with manageable toxicity. Full-Text PDF Apatinib in patients with advanced chordoma: a single-arm, single-centre, phase 2 studyTo our knowledge, this is the first trial of apatinib for the treatment of advanced chordoma. Apatinib shows promising activity and manageable toxicity and thus might be an option for the treatment of advanced chordoma. Full-Text PDF" @default.
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• W3108968950 date "2020-12-01" @default.
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• W3108968950 title "Shifting from targeted therapies to personalised treatment in chordoma – Authors' reply" @default.
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• W3108968950 doi "https://doi.org/10.1016/s1470-2045(20)30696-3" @default.
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