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However, there are conflicting data as to whether \u2206<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\u20132013 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\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>218) or multiplex ligation\u2010dependent probe amplification (<jats:italic>N\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>116) analyses. \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic>, found in 15%, was associated with inferior 10\u2010year probabilities of event\u2010free (60% vs. 83%; <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0\u00b7001) and overall survival (<jats:styled-content style=\"fixed-case\">pOS<\/jats:styled-content>; 73% vs. 89%; <jats:italic>P\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0\u00b7001). 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>, \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic> was the strongest independent factor for relapse and death. \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic> was present in 27% of cases with non\u2010informative cytogenetics (\u2018<jats:styled-content style=\"fixed-case\">BCP<\/jats:styled-content>\u2010other\u2019) and a poor 10\u2010year <jats:styled-content style=\"fixed-case\">pOS<\/jats:styled-content> was particularly pronounced in this group (58% vs. 90%; <jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0\u00b7001). 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 \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic>\u2010positive cases. Co\u2010occurrence 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>\u2010<jats:italic><jats:styled-content style=\"fixed-case\">CRLF<\/jats:styled-content>2<\/jats:italic>) and \u2206<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 \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic>;<jats:italic> P\u00a0<\/jats:italic>=<jats:italic>\u00a0<\/jats:italic>0\u00b7045), indicating that <jats:styled-content style=\"fixed-case\">BCP<\/jats:styled-content>\u2010other <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>\u2010<jats:italic><jats:styled-content style=\"fixed-case\">CRLF<\/jats:styled-content>2<\/jats:italic> and \u2206<jats:italic><jats:styled-content style=\"fixed-case\">IKZF<\/jats:styled-content>1<\/jats:italic> constitutes a particularly high\u2010risk group.<\/jats:p>","DOI":"10.1111\/bjh.13514","type":"journal-article","created":{"date-parts":[[2015,5,28]],"date-time":"2015-05-28T12:28:39Z","timestamp":1432816119000},"page":"847-858","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["The clinical impact of <i><scp>IKZF<\/scp>1<\/i> deletions in paediatric B\u2010cell 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"],"prefix":"10.1111","volume":"170","author":[{"given":"Linda","family":"Olsson","sequence":"first","affiliation":[{"name":"Division of Clinical Genetics Department of Laboratory Medicine Lund University Lund Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ingegerd","family":"Ivanov \u00d6fverholm","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Surgery and Centre for Molecular Medicine Karolinska Institutet Stockholm Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ulrika","family":"Nor\u00e9n\u2010Nystr\u00f6m","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences Paediatrics, Ume\u00e5 University Ume\u00e5 Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vasilios","family":"Zachariadis","sequence":"additional","affiliation":[{"name":"Department of Molecular Medicine and Surgery and Centre for Molecular Medicine Karolinska Institutet Stockholm 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