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| 005 | 20240229112555.0 | ||
| 024 | 7 | _ | |a 10.1038/s41467-019-09633-9 |2 doi |
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| 100 | 1 | _ | |a Gröschel, Stefan |0 P:(DE-He78)5120a331b1c28045c8ca6a8b1c73c95f |b 0 |e First author |
| 245 | _ | _ | |a Defective homologous recombination DNA repair as therapeutic target in advanced chordoma. |
| 260 | _ | _ | |a [London] |c 2019 |b Nature Publishing Group UK |
| 336 | 7 | _ | |a article |2 DRIVER |
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| 520 | _ | _ | |a Chordomas are rare bone tumors with few therapeutic options. Here we show, using whole-exome and genome sequencing within a precision oncology program, that advanced chordomas (n = 11) may be characterized by genomic patterns indicative of defective homologous recombination (HR) DNA repair and alterations affecting HR-related genes, including, for example, deletions and pathogenic germline variants of BRCA2, NBN, and CHEK2. A mutational signature associated with HR deficiency was significantly enriched in 72.7% of samples and co-occurred with genomic instability. The poly(ADP-ribose) polymerase (PARP) inhibitor olaparib, which is preferentially toxic to HR-incompetent cells, led to prolonged clinical benefit in a patient with refractory chordoma, and whole-genome analysis at progression revealed a PARP1 p.T910A mutation predicted to disrupt the autoinhibitory PARP1 helical domain. These findings uncover a therapeutic opportunity in chordoma that warrants further exploration, and provide insight into the mechanisms underlying PARP inhibitor resistance. |
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| 773 | _ | _ | |a 10.1038/s41467-019-09633-9 |g Vol. 10, no. 1, p. 1635 |0 PERI:(DE-600)2553671-0 |n 1 |p 1635 |t Nature Communications |v 10 |y 2019 |x 2041-1723 |
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