Chromatin accessibility landscape of relapsed pediatric B-lineage acute lymphoblastic leukemia
© 2023. Springer Nature Limited..
For around half of the pediatric B-lineage acute lymphoblastic leukemia (B-ALL) patients, the molecular mechanism of relapse remains unclear. To fill this gap in knowledge, here we characterize the chromatin accessibility landscape in pediatric relapsed B-ALL. We observe rewired accessible chromatin regions (ACRs) associated with transcription dysregulation in leukemia cells as compared with normal B-cell progenitors. We show that over a quarter of the ACRs in B-ALL are in quiescent regions with high heterogeneity among B-ALLs. We identify subtype-specific and allele-imbalanced chromatin accessibility by integrating multi-omics data. By characterizing the differential ACRs between diagnosis and relapse in B-ALL, we identify alterations in chromatin accessibility during drug treatment. Further analysis of ACRs associated with relapse free survival leads to the identification of a subgroup of B-ALL which show early relapse. These data provide an advanced and integrative portrait of the importance of chromatin accessibility alterations in tumorigenesis and drug responses.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:14 |
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| Enthalten in: |
Nature communications - 14(2023), 1 vom: 25. Okt., Seite 6792 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Han [VerfasserIn] |
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| Anmerkungen: |
Date Completed 27.10.2023 Date Revised 19.11.2023 published: Electronic Citation Status MEDLINE |
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| doi: |
10.1038/s41467-023-42565-z |
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| funding: |
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NLM363724281 |
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| 520 | |a For around half of the pediatric B-lineage acute lymphoblastic leukemia (B-ALL) patients, the molecular mechanism of relapse remains unclear. To fill this gap in knowledge, here we characterize the chromatin accessibility landscape in pediatric relapsed B-ALL. We observe rewired accessible chromatin regions (ACRs) associated with transcription dysregulation in leukemia cells as compared with normal B-cell progenitors. We show that over a quarter of the ACRs in B-ALL are in quiescent regions with high heterogeneity among B-ALLs. We identify subtype-specific and allele-imbalanced chromatin accessibility by integrating multi-omics data. By characterizing the differential ACRs between diagnosis and relapse in B-ALL, we identify alterations in chromatin accessibility during drug treatment. Further analysis of ACRs associated with relapse free survival leads to the identification of a subgroup of B-ALL which show early relapse. These data provide an advanced and integrative portrait of the importance of chromatin accessibility alterations in tumorigenesis and drug responses | ||
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| 700 | 1 | |a Liang, Bilin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Fang |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Fan |e verfasserin |4 aut | |
| 700 | 1 | |a Cui, Bowen |e verfasserin |4 aut | |
| 700 | 1 | |a Ding, Lixia |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Xiang |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Ronghua |e verfasserin |4 aut | |
| 700 | 1 | |a Cai, Jiaoyang |e verfasserin |4 aut | |
| 700 | 1 | |a Tang, Yanjing |e verfasserin |4 aut | |
| 700 | 1 | |a Rao, Jianan |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Wenting |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Shuang |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Wenyan |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Xiaoxiao |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Kefei |e verfasserin |4 aut | |
| 700 | 1 | |a Lai, Junchen |e verfasserin |4 aut | |
| 700 | 1 | |a Xie, Yangyang |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Benshang |e verfasserin |4 aut | |
| 700 | 1 | |a Tang, Jingyan |e verfasserin |4 aut | |
| 700 | 1 | |a Shen, Shuhong |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yu |e verfasserin |4 aut | |
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