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1 ors already being individually evaluated for chordoma.
2 ing new drug target for the rare bone cancer chordoma.
3 into the biology and treatment of skull-base chordoma.
4  efficacy of CAP in inducing cytotoxicity in chordoma.
5 11, have potent preclinical efficacy against chordoma.
6 ates with ADAR dependence and is elevated in chordoma.
7 ns in LYST, a potential novel cancer gene in chordoma.
8 ic driver landscape of 104 cases of sporadic chordoma.
9 erstone of management for chondrosarcoma and chordoma.
10 ine duplications of T that underlie familial chordoma.
11 ass, with biopsy confirming the diagnosis of chordoma.
12  in patients with unresectable or metastatic chordoma.
13  in a family with 10 individuals affected by chordoma.
14 ic target of H3K27 demethylase inhibitors in chordoma.
15 ogical and clinical insights into skull-base chordoma.
16 targets to pursue for combination therapy of chordoma.
17 ed recurrence-free survival in patients with chordomas.
18 profiles that were characteristic of primary chordomas.
19 evelopment and is expressed in most sporadic chordomas.
20 om January 2000 to May 2003, 51 patients (15 chordoma, 23 STS, 13 GIST patients) enrolled.
21  landscape of selectively essential genes in chordoma, a bone cancer with few validated targets.
22 tiplex families with at least three cases of chordoma, a cancer of presumed notochordal origin.
23 ion in a subset of common carcinomas, and in chordoma, a rare cancer showing notochordal differentiat
24                   Poorly differentiated (PD) chordoma, a rare, aggressive tumor originating from noto
25 a establish that SMARCB1 re-expression in PD chordomas alters the repertoire of SWI/SNF complexes, pe
26  an association study of 40 individuals with chordoma and 358 ancestry-matched controls, with replica
27 t molecular connection between notochord and chordoma and identified core members of a chordoma regul
28 ole in tumour growth of the rare bone cancer chordoma and is implicated in other solid tumours.
29 e control tissue limits our understanding of chordoma and its relationship to notochord.
30 his study involved a molecular comparison of chordoma and notochord to identify dysregulated cellular
31 sistency in gene expression profiles between chordoma and notochord, supporting the hypothesis that c
32                        One patient (7%) with chordoma and one patient (4%) with STS had an objective
33 f this paper is to describe a case of clival chordoma and review recent developments in diagnostic an
34  importance of the mTOR signaling pathway in chordoma and suggest it as a promising avenue for target
35 uct whole genome sequencing of 80 skull-base chordomas and identify PBRM1, a SWI/SNF (SWItch/Sucrose
36 tial new therapeutic avenue for treatment of chordomas and new chemical tools and probe compound 45 (
37 a, osteosarcoma, alveolar soft-part sarcoma, chordoma, and other sarcomas).
38 XT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kina
39 anagement, and molecular characterisation of chordomas, and discuss current research.
40       Osteosarcoma (OS), chondrosarcoma, and chordoma are characterized by multiple challenges to the
41 Here, recent advances targeting Brachyury in chordoma are discussed and how these might open doors to
42                                              Chordomas are considered insensitive to conventional che
43                                              Chordomas are rare tumors of notochordal origin, most co
44                                              Chordomas are rare tumors that can develop anywhere alon
45                                              Chordomas are thought to arise from transformed remnants
46                                              Chordomas are tumors that arise at vertebral bodies and
47                                              Chordomas are very rare bone malignant tumours that have
48 ghts into DNA binding and the context of the chordoma associated G177D variant.
49 X9, and EGFR, genes previously implicated in chordoma biology, are also recovered.
50 d epidermal growth factor receptor (EGFR) in chordoma bone cancers.
51                                              Chordomas can present a diagnostic challenge due to the
52 led through epigenetic inhibition to promote chordoma cell death.
53 lso showed synergy (CI(50) = 0.41) against a chordoma cell in vitro.
54 hibitor AZD2014, was the most potent against chordoma cell lines (IC(50) 0.35 uM U-CH1 and 0.61 uM U-
55 duction of SMARCB1, both SMARCB1-negative PD chordoma cell lines continued to proliferate.
56 ave previously demonstrated activity against chordoma cell lines in vitro.
57                      Screening of five human chordoma cell lines revealed that pharmacologic inhibiti
58                                  Eight human chordoma cell lines that we established exhibited cytolo
59 lished studies of compounds screened against chordoma cell lines were used to generate Bayesian Machi
60 and gene expression, two SMARCB1-negative PD chordoma cell lines with an inducible SMARCB1 expression
61 loss of CDKN2A (p16(INK4A)) expression in PD chordoma cell lines.
62 geting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.
63     In this study, we addressed the need for chordoma cell systems that can be used to identify thera
64                   Experimental validation in chordoma cells confirmed these findings and emphasized t
65 ic inhibition of H3K27-demethylases in human chordoma cells promotes epigenetic silencing of oncogeni
66 n vitro, finding an exquisite sensitivity of chordoma cells to CAP-mediated cytotoxicity.
67             We treated CH2, CH7 and UM-Chor1 chordoma cells with CAP, measuring resulting cell viabil
68 , which may represent a novel cancer gene in chordoma.Chordoma is a rare often incurable malignant bo
69      Our results generate an emerging map of chordoma dependencies to enable biological and therapeut
70  the discovery of therapeutically targetable chordoma dependencies via genome-scale CRISPR-Cas9 scree
71               This approach confirms a known chordoma dependency, TBXT (T; brachyury), and identifies
72 with chondrogenesis were a central driver of chordoma development.
73 nd notochord, supporting the hypothesis that chordoma develops from notochordal remnants.
74 eting on chordoma that included more than 40 chordoma experts from several disciplines and from both
75 routine for patients with chondrosarcoma and chordoma for whom surgery alone is inadequate.
76 with the contribution and sponsorship of the Chordoma Foundation, a global patient advocacy group.
77 etween EGFR and antiproliferative effects on chordoma, GAK inhibition appeared to have only a limited
78         Therefore, an unbiased comparison of chordoma, human notochord, and an atlas of normal and ca
79  brachyury transcription factor addiction in chordoma, identify a mechanism of T gene regulation that
80 ors investigate driver mutations of sporadic chordoma in 104 cases, revealing duplications in notocho
81  levels of Brachyury, a tissue biomarker for chordoma, in plasma samples.
82 ted and validated machine learning models of chordoma inhibition and screened compounds of interest i
83                              The most potent chordoma inhibitors were further characterized in a kino
84 asis samples, indicating their importance in chordoma initiation.
85                                              Chordoma is a devastating rare cancer that affects one i
86                                              Chordoma is a malignant, often incurable bone tumour sho
87                                              Chordoma is a primary bone cancer with no approved thera
88                                              Chordoma is a rare bone cancer that is aggressive, local
89                                              Chordoma is a rare bone tumor with an unknown etiology a
90                                              Chordoma is a rare malignant bone tumor that expresses t
91                                              Chordoma is a rare malignant tumor demonstrating notocho
92                                              Chordoma is a rare tumor originating from notochordal re
93                                   Skull-base chordoma is a rare, aggressive bone cancer with a high r
94                          Treatment of clival chordomas is unique from other locations with an enhance
95 ing gene expression profiling to clarify the chordoma/notochord relationship and potentially identify
96              The gold standard treatment for chordomas of the mobile spine and sacrum is en-bloc exci
97 ion-free survival rates were 47% and 33% for chordoma patients, 26% and 22% for STS patients, and 31%
98           In order to speed new medicines to chordoma patients, a drug repurposing strategy represent
99 se findings and emphasized the dependence of chordoma proliferation and survival on TGF-beta.
100 ould therefore be a useful tool in improving chordoma recurrence rates as an intraoperative adjuvant
101 nd chordoma and identified core members of a chordoma regulatory pathway involving TBXT.
102                                              Chordomas remain one of the most difficult-to-treat of s
103  the common nonsynonymous SNP rs2305089 with chordoma risk (allelic odds ratio (OR) = 6.1, 95% confid
104                         A 12-gene diagnostic chordoma signature was identified and the TBXT/transform
105 amptothecin (9-NC) in patients with advanced chordoma, soft tissue sarcoma (STS), and gastrointestina
106 MARCB1), shows strong associations with poor chordoma-specific survival (Hazard ratio [HR] = 10.55, 9
107  progression was 9.9, 8.0, and 8.3 weeks for chordoma, STS, and GIST patients, respectively.
108 all, our work offers a valuable new tool for chordoma studies including the development of novel biom
109 etwork of transcription factors critical for chordoma survival and upregulated pathways dominated by
110  also hosted a parallel consensus meeting on chordoma that included more than 40 chordoma experts fro
111 through an immunohistochemical analysis of a chordoma tissue bank of 43 patients.
112 w cell systems were highly representative of chordoma tissues.
113       These results map a locus for familial chordoma to 7q33.
114        This is the largest phase II study in chordoma to date.
115 uccessfully established organoids from seven chordoma tumor samples obtained from five patients prese
116 f clinically actionable somatic mutations in chordoma tumors(2,3).
117 phosphoproteomics analyses of 187 skull-base chordoma tumors.
118                                           In chordoma, we find that T is associated with a 1.5-Mb reg

 
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