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Olsson, Linda;
Ivanov Öfverholm, Ingegerd;
Norén‐Nyström, Ulrika;
Zachariadis, Vasilios;
Nordlund, Jessica;
Sjögren, Helene;
Golovleva, Irina;
Nordgren, Ann;
Paulsson, Kajsa;
Heyman, Mats;
Barbany, Gisela;
Johansson, Bertil
The clinical impact of IKZF1 deletions in paediatric B‐cell precursor acute lymphoblastic leukaemia is independent of minimal residual disease stratification in Nordic Society for Paediatric Haematology and Oncology treatment protocols used between 1992 and 2013
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- Medientyp: E-Artikel
- Titel: The clinical impact of IKZF1 deletions in paediatric B‐cell precursor acute lymphoblastic leukaemia is independent of minimal residual disease stratification in Nordic Society for Paediatric Haematology and Oncology treatment protocols used between 1992 and 2013
- Beteiligte: Olsson, Linda; Ivanov Öfverholm, Ingegerd; Norén‐Nyström, Ulrika; Zachariadis, Vasilios; Nordlund, Jessica; Sjögren, Helene; Golovleva, Irina; Nordgren, Ann; Paulsson, Kajsa; Heyman, Mats; Barbany, Gisela; Johansson, Bertil
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Erschienen:
Wiley, 2015
- Erschienen in: British Journal of Haematology
- Sprache: Englisch
- DOI: 10.1111/bjh.13514
- ISSN: 0007-1048; 1365-2141
- Entstehung:
- Anmerkungen:
- Beschreibung: <jats:title>Summary</jats:title><jats:p>Paediatric B‐cell precursor acute lymphoblastic leukaemias (<jats:styled-content style="fixed-case">BCP ALL</jats:styled-content>) with <jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> deletions (∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic>) are associated with a poor outcome. However, there are conflicting data as to whether ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> is an independent risk factor if minimal residual disease (<jats:styled-content style="fixed-case">MRD</jats:styled-content>) and other copy number alterations also are taken into account. We investigated 334 paediatric <jats:styled-content style="fixed-case">BCP ALL</jats:styled-content>, diagnosed 1992–2013 and treated according to Nordic Society for Paediatric Haematology and Oncology <jats:styled-content style="fixed-case">ALL</jats:styled-content> protocols, with known <jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> status based on either single nucleotide polymorphism array (<jats:italic>N </jats:italic>=<jats:italic> </jats:italic>218) or multiplex ligation‐dependent probe amplification (<jats:italic>N </jats:italic>=<jats:italic> </jats:italic>116) analyses. ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic>, found in 15%, was associated with inferior 10‐year probabilities of event‐free (60% vs. 83%; <jats:italic>P </jats:italic><<jats:italic> </jats:italic>0·001) and overall survival (<jats:styled-content style="fixed-case">pOS</jats:styled-content>; 73% vs. 89%; <jats:italic>P </jats:italic>=<jats:italic> </jats:italic>0·001). Adjusting for known risk factors, including white blood cell (<jats:styled-content style="fixed-case">WBC</jats:styled-content>) count and <jats:styled-content style="fixed-case">MRD</jats:styled-content>, ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> was the strongest independent factor for relapse and death. ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> was present in 27% of cases with non‐informative cytogenetics (‘<jats:styled-content style="fixed-case">BCP</jats:styled-content>‐other’) and a poor 10‐year <jats:styled-content style="fixed-case">pOS</jats:styled-content> was particularly pronounced in this group (58% vs. 90%; <jats:italic>P </jats:italic><<jats:italic> </jats:italic>0·001). Importantly, neither <jats:styled-content style="fixed-case">MRD</jats:styled-content> nor <jats:styled-content style="fixed-case">WBC</jats:styled-content> count predicted events in the ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic>‐positive cases. Co‐occurrence of pseudoautosomal region 1 (<jats:styled-content style="fixed-case">PAR</jats:styled-content>1) deletions in Xp22.33/Yp11.32 (<jats:italic>P2<jats:styled-content style="fixed-case">RY</jats:styled-content>8</jats:italic>‐<jats:italic><jats:styled-content style="fixed-case">CRLF</jats:styled-content>2</jats:italic>) and ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> increased the risk of relapse (75% vs. 30% for cases with only ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic>;<jats:italic> P </jats:italic>=<jats:italic> </jats:italic>0·045), indicating that <jats:styled-content style="fixed-case">BCP</jats:styled-content>‐other <jats:styled-content style="fixed-case">ALL</jats:styled-content> with both <jats:italic>P2<jats:styled-content style="fixed-case">RY</jats:styled-content>8</jats:italic>‐<jats:italic><jats:styled-content style="fixed-case">CRLF</jats:styled-content>2</jats:italic> and ∆<jats:italic><jats:styled-content style="fixed-case">IKZF</jats:styled-content>1</jats:italic> constitutes a particularly high‐risk group.</jats:p>