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Clonal origins of relapse in ETV6-RUNX1 acute lymphoblastic leukemia
FW. van Delft, S. Horsley, S. Colman, K. Anderson, C. Bateman, H. Kempski, J. Zuna, C. Eckert, V. Saha, L. Kearney, A. Ford, M. Greaves,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NS10004
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Free Medical Journals
od 1946 do Před 1 rokem
Freely Accessible Science Journals
od 1946 do Před 1 rokem
Open Access Digital Library
od 1946-01-01
Open Access Digital Library
od 1946-01-01
Elsevier Open Access Journals
od 1946-01-01 do 2023-06-22
ROAD: Directory of Open Access Scholarly Resources
Elsevier Open Archive Journals
od 1946 do Před 1 rokem
- MeSH
- akutní lymfatická leukemie genetika metabolismus mortalita terapie MeSH
- cyklin C MeSH
- dítě MeSH
- fúzní onkogenní proteiny genetika metabolismus MeSH
- inhibitor p15 cyklin-dependentní kinasy genetika metabolismus MeSH
- inhibitor p16 cyklin-dependentní kinasy genetika metabolismus MeSH
- lidé MeSH
- lidské chromozomy, pár 16 genetika metabolismus MeSH
- lidské chromozomy, pár 6 genetika metabolismus MeSH
- předškolní dítě MeSH
- protein PEBP2A2 MeSH
- recidiva MeSH
- sekvenční delece * MeSH
- translokace genetická * MeSH
- Check Tag
- dítě MeSH
- lidé MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (TEL-AML1) fusion has an overall good prognosis, but relapses occur, usually after cessation of treatment and occasionally many years later. We have investigated the clonal origins of relapse by comparing the profiles of genomewide copy number alterations at presentation in 21 patients with those in matched relapse (12-119 months). We identified, in total, 159 copy number alterations at presentation and 231 at relapse (excluding Ig/TCR). Deletions of CDKN2A/B or CCNC (6q16.2-3) or both increased from 38% at presentation to 76% in relapse, suggesting that cell-cycle deregulation contributed to emergence of relapse. A novel observation was recurrent gain of chromosome 16 (2 patients at presentation, 4 at relapse) and deletion of plasmocytoma variant translocation 1 in 3 patients. The data indicate that, irrespective of time to relapse, the relapse clone was derived from either a major or minor clone at presentation. Backtracking analysis by FISH identified a minor subclone at diagnosis whose genotype matched that observed in relapse ∼ 10 years later. These data indicate subclonal diversity at diagnosis, providing a variable basis for intraclonal origins of relapse and extended periods (years) of dormancy, possibly by quiescence, for stem cells in ETV6-RUNX1(+) acute lymphoblastic leukemia.
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- $a B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (TEL-AML1) fusion has an overall good prognosis, but relapses occur, usually after cessation of treatment and occasionally many years later. We have investigated the clonal origins of relapse by comparing the profiles of genomewide copy number alterations at presentation in 21 patients with those in matched relapse (12-119 months). We identified, in total, 159 copy number alterations at presentation and 231 at relapse (excluding Ig/TCR). Deletions of CDKN2A/B or CCNC (6q16.2-3) or both increased from 38% at presentation to 76% in relapse, suggesting that cell-cycle deregulation contributed to emergence of relapse. A novel observation was recurrent gain of chromosome 16 (2 patients at presentation, 4 at relapse) and deletion of plasmocytoma variant translocation 1 in 3 patients. The data indicate that, irrespective of time to relapse, the relapse clone was derived from either a major or minor clone at presentation. Backtracking analysis by FISH identified a minor subclone at diagnosis whose genotype matched that observed in relapse ∼ 10 years later. These data indicate subclonal diversity at diagnosis, providing a variable basis for intraclonal origins of relapse and extended periods (years) of dormancy, possibly by quiescence, for stem cells in ETV6-RUNX1(+) acute lymphoblastic leukemia.
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