Publication: Homozygous Calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency
Homozygous Calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency
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Theocharides, A. P., Lundberg, P., Lakkaraju, A. K. K., Lysenko, V., Myburgh, R., Aguzzi, A., Skoda, R. C., & Manz, M. G. (2016). Homozygous Calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency. Blood, 127(25), 3253–3259. https://doi.org/10.1182/blood-2016-02-696310
Abstract
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The pathogenesis of acquired myeloperoxidase (MPO) deficiency, a rare phenomenon observed in patients with Philadelphia chromosome-negative myeloproliferative neoplasms (MPN), is unknown. MPO is a glycoprotein chaperoned by Calreticulin (CALR) in the endoplasmic reticulum. Mutations inCALRare frequently found in patients with myelofibrosis (MF) and essential thrombocythemia (ET) with nonmutatedJanuskinase 2(JAK2). We hypothesized that acquired MPO deficiency in MPN could be associated with the presence ofCALRmutations. A cohort of 317
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- Theocharides, Alexandre P
- Lundberg, Pontus
- Lysenko, Veronika
- Myburgh, Renier
- Skoda, Radek C
- Manz, Markus G
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Theocharides, A. P., Lundberg, P., Lakkaraju, A. K. K., Lysenko, V., Myburgh, R., Aguzzi, A., Skoda, R. C., & Manz, M. G. (2016). Homozygous Calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency. Blood, 127(25), 3253–3259. https://doi.org/10.1182/blood-2016-02-696310
