• Media type: E-Article
  • Title: PAX5 alterations in genetically unclassified childhood Precursor B‐cell acute lymphoblastic leukaemia
  • Contributor: Stasevich, Irina; Inglott, Sarah; Austin, Nicola; Chatters, Steve; Chalker, Jane; Addy, Dilys; Dryden, Carryl; Ancliff, Philip; Ford, Anthony; Williams, Owen; Kempski, Helena
  • imprint: Wiley, 2015
  • Published in: British Journal of Haematology
  • Language: English
  • DOI: 10.1111/bjh.13543
  • ISSN: 1365-2141; 0007-1048
  • Keywords: Hematology
  • Origination:
  • Footnote:
  • Description: <jats:title>Summary</jats:title><jats:p>Here, we report a high incidence of <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> abnormalities observed in 32/68 (47%) of patients with genetically unclassified childhood precursor B‐cell acute lymphoblastic leukaemia (pre‐B <jats:styled-content style="fixed-case">ALL</jats:styled-content>). Various deletions, gains, mutations and rearrangements of <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> comprised 45%, 12%, 29% and 14%, respectively, of the abnormalities found. 28% of patients showed more than one abnormality of the gene, implying bi‐allelic impairment of <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic>. Novel <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5‐<jats:styled-content style="fixed-case">RHOXF</jats:styled-content>2</jats:italic>,<jats:italic> <jats:styled-content style="fixed-case">PAX</jats:styled-content>5‐<jats:styled-content style="fixed-case">ELK</jats:styled-content>3</jats:italic> and <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5‐<jats:styled-content style="fixed-case">CBFA</jats:styled-content>2T2</jats:italic> rearrangements, which lead to aberrant expression of <jats:styled-content style="fixed-case">PAX</jats:styled-content>5, were also identified. <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> rearrangements demonstrated a complex mechanism of formation including concurrent duplications/deletions of <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> and its partner genes. Finally, the splice variant c.1013‐2A&gt;G, seen in two patients with loss of one <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> allele, was confirmed to be germ‐line in one patient and somatic in the other. <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> alterations were also found to be clinically associated with a higher white blood cell count (<jats:italic>P</jats:italic> = 0·015). These findings contribute to the knowledge of <jats:italic><jats:styled-content style="fixed-case">PAX</jats:styled-content>5</jats:italic> alterations and their role in the pathogenesis of pre‐B <jats:styled-content style="fixed-case">ALL</jats:styled-content>.</jats:p>