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Eickhardt‐Dalbøge, Christina Schjellerup; Nielsen, Henrik V.; Fuursted, Kurt; Stensvold, Christen Rune; Andersen, Lee O' Brien; Lilje, Berit; Larsen, Morten Kranker; Kjær, Lasse; Christensen, Sarah Friis; Knudsen, Trine Alma; Skov, Vibe; Sørensen, Anders Lindholm; Ellervik, Christina; Olsen, Lars Rønn; Christensen, Jens Jørgen Elmer; Nielsen, Xiaohui Chen; Hasselbalch, Hans Carl; Ingham, Anna Cäcilia

JAK2V617F drives gut microbiota differences in patients with myeloproliferative neoplasms

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  • Media type: E-Article
  • Title: JAK2V617F drives gut microbiota differences in patients with myeloproliferative neoplasms
  • Contributor: Eickhardt‐Dalbøge, Christina Schjellerup; Nielsen, Henrik V.; Fuursted, Kurt; Stensvold, Christen Rune; Andersen, Lee O' Brien; Lilje, Berit; Larsen, Morten Kranker; Kjær, Lasse; Christensen, Sarah Friis; Knudsen, Trine Alma; Skov, Vibe; Sørensen, Anders Lindholm; Ellervik, Christina; Olsen, Lars Rønn; Christensen, Jens Jørgen Elmer; Nielsen, Xiaohui Chen; Hasselbalch, Hans Carl; Ingham, Anna Cäcilia
  • imprint: Wiley, 2024
  • Published in: European Journal of Haematology
  • Language: English
  • DOI: 10.1111/ejh.14169
  • ISSN: 1600-0609; 0902-4441
  • Keywords: Hematology ; General Medicine
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (MF) are myeloproliferative neoplasms (MPN). Inflammation is involved in the initiation, progression, and symptomology of the diseases. The gut microbiota impacts the immune system, infection control, and steady‐state hematopoiesis.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We analyzed the gut microbiota of 227 MPN patients and healthy controls (HCs) using next‐generation sequencing. We expanded our previous results in PV and ET patients with additional PV, pre‐MF, and MF patients which allowed us to compare MPN patients collectively, MPN sub‐diagnoses, and MPN mutations (separately and combined) vs. HCs (<jats:italic>N</jats:italic> = 42) and compare within MPN sub‐diagnoses and MPN mutation.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>MPN patients had a higher observed richness (median, 245 [range, 49–659]) compared with HCs (191.5 [range, 111–300; <jats:italic>p</jats:italic> = .003]) and a lower relative abundance of taxa within the <jats:italic>Firmicutes</jats:italic> phylum; for example, <jats:italic>Faecalibacterium</jats:italic> (6% vs. 14%, <jats:italic>p</jats:italic> &lt; .001). The microbiota of <jats:italic>CALR</jats:italic>‐positive patients (<jats:italic>N</jats:italic> = 30) resembled that of HCs more than that of patients with <jats:italic>JAK2V617F</jats:italic> (<jats:italic>N</jats:italic> = 177). In <jats:italic>JAK2V617F</jats:italic>‐positive patients, only minor differences in the gut microbiota were observed between MPN sub‐diagnoses, illustrating the importance of this mutation.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>The gut microbiota in MPN patients differs from HCs and is driven by <jats:italic>JAK2V617F</jats:italic>, whereas the gut microbiota in <jats:italic>CALR</jats:italic> patients resembles HCs more.</jats:p></jats:sec>