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| 001 | 179973 | ||
| 005 | 20240229145601.0 | ||
| 024 | 7 | _ | |a 10.1038/s41375-022-01587-0 |2 doi |
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| 037 | _ | _ | |a DKFZ-2022-01013 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Richter-Pechańska, Paulina |b 0 |
| 245 | _ | _ | |a Pediatric T-ALL type-1 and type-2 relapses develop along distinct pathways of clonal evolution. |
| 260 | _ | _ | |a London |c 2022 |b Springer Nature |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1663058680_5887 |2 PUB:(DE-HGF) |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a #LA:B062# / 2022 Jul;36(7):1759-1768 |
| 520 | _ | _ | |a The mechanisms underlying T-ALL relapse remain essentially unknown. Multilevel-omics in 38 matched pairs of initial and relapsed T-ALL revealed 18 (47%) type-1 (defined by being derived from the major ancestral clone) and 20 (53%) type-2 relapses (derived from a minor ancestral clone). In both types of relapse, we observed known and novel drivers of multidrug resistance including MDR1 and MVP, NT5C2 and JAK-STAT activators. Patients with type-1 relapses were specifically characterized by IL7R upregulation. In remarkable contrast, type-2 relapses demonstrated (1) enrichment of constitutional cancer predisposition gene mutations, (2) divergent genetic and epigenetic remodeling, and (3) enrichment of somatic hypermutator phenotypes, related to BLM, BUB1B/PMS2 and TP53 mutations. T-ALLs that later progressed to type-2 relapses exhibited a complex subclonal architecture, unexpectedly, already at the time of initial diagnosis. Deconvolution analysis of ATAC-Seq profiles showed that T-ALLs later developing into type-1 relapses resembled a predominant immature thymic T-cell population, whereas T-ALLs developing into type-2 relapses resembled a mixture of normal T-cell precursors. In sum, our analyses revealed fundamentally different mechanisms driving either type-1 or type-2 T-ALL relapse and indicate that differential capacities of disease evolution are already inherent to the molecular setup of the initial leukemia. |
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| 700 | 1 | _ | |a Kunz, Joachim B |b 1 |
| 700 | 1 | _ | |a Rausch, Tobias |0 0000-0001-5773-5620 |b 2 |
| 700 | 1 | _ | |a Erarslan-Uysal, Büşra |b 3 |
| 700 | 1 | _ | |a Bornhauser, Beat |0 0000-0003-2890-3191 |b 4 |
| 700 | 1 | _ | |a Frismantas, Viktoras |b 5 |
| 700 | 1 | _ | |a Assenov, Yassen |0 P:(DE-He78)45a6854ecf41ba2e65ca3ba0d560f14c |b 6 |
| 700 | 1 | _ | |a Zimmermann, Martin |b 7 |
| 700 | 1 | _ | |a Happich, Margit |b 8 |
| 700 | 1 | _ | |a von Knebel-Doeberitz, Caroline |b 9 |
| 700 | 1 | _ | |a von Neuhoff, Nils |b 10 |
| 700 | 1 | _ | |a Köhler, Rolf |b 11 |
| 700 | 1 | _ | |a Stanulla, Martin |0 0000-0002-3834-0727 |b 12 |
| 700 | 1 | _ | |a Schrappe, Martin |b 13 |
| 700 | 1 | _ | |a Cario, Gunnar |b 14 |
| 700 | 1 | _ | |a Escherich, Gabriele |b 15 |
| 700 | 1 | _ | |a Kirschner-Schwabe, Renate |0 0000-0001-6335-3274 |b 16 |
| 700 | 1 | _ | |a Eckert, Cornelia |0 P:(DE-He78)fd9d6272a48791a31f40a854585db572 |b 17 |u dkfz |
| 700 | 1 | _ | |a Avigad, Smadar |b 18 |
| 700 | 1 | _ | |a Pfister, Stefan M |0 P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9 |b 19 |u dkfz |
| 700 | 1 | _ | |a Muckenthaler, Martina U |b 20 |
| 700 | 1 | _ | |a Bourquin, Jean-Pierre |b 21 |
| 700 | 1 | _ | |a Korbel, Jan O |b 22 |
| 700 | 1 | _ | |a Kulozik, Andreas |0 P:(DE-He78)ca062b8db1ee864e03f0a92897728df3 |b 23 |e Last author |u dkfz |
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