ArticleBlood cancer journal2016
Expression of CALR mutants causes mpl-dependent thrombocytosis in zebrafish.
Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023Review
- Transcriptomic Analysis Reveals JAK2/MPL-Independent Effects of Calreticulin Mutations in aCells · 2023Article
- Learning from Zebrafish Hematopoiesis.Advances in experimental medicine and biology · 2023Review
- Interacting Effects of Sea Louse (Frontiers in immunology · 2022Article
- Calreticulin and cancer.Cell research · 2021Review
- Editorial: Novel Treatment Strategies for Myeloproliferative Neoplasms.Frontiers in oncology · 2021Article
- Zebrafish for thrombocytopoiesis- and hemostasis-related researches and disorders.Blood science (Baltimore, Md.) · 2020Review
- The role of calreticulin mutations in myeloproliferative neoplasms.International journal of hematology · 2020Review
- Mutant Calreticulin in the Myeloproliferative Neoplasms.HemaSphere · 2020Review
- Review
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Peering through zebrafish to understand inherited bone marrow failure syndromes.Haematologica · 2019Review
- Increased B cell activation is present in JAK2V617F-mutated, CALR-mutated and triple-negative essential thrombocythemia.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CALR mutations are identified in about 30% of JAK2/MPL-unmutated myeloproliferative neoplasms (MPNs) including essential thrombocythemia (ET) and primary myelofibrosis. Although the molecular pathogenesis of CALR mutations leading to MPNs has been studied using in vitro cell lines models, how mutant CALR may affect developmental hematopoiesis remains unknown. Here we took advantage of the zebrafish model to examine the effects of mutant CALR on early hematopoiesis and model human CALR-mutated MPNs. We identified three zebrafish genes orthologous to human CALR, referred to as calr, calr3a and calr3b. The expression of CALR-del52 and CALR-ins5 mutants caused an increase in the hematopoietic stem/progenitor cells followed by thrombocytosis without affecting normal angiogenesis. The expression of CALR mutants also perturbed early developmental hematopoiesis in zebrafish. Importantly, morpholino knockdown of mpl but not epor or csf3r could significantly attenuate the effects of mutant CALR. Furthermore, the expression of mutant CALR caused jak-stat signaling activation in zebrafish that could be blocked by JAK inhibitors (ruxolitinib and fedratinib). These findings showed that mutant CALR activates jak-stat signaling through an mpl-dependent mechanism to mediate pathogenic thrombopoiesis in zebrafish, and illustrated that the signaling machinery related to mutant CALR tumorigenesis are conserved between human and zebrafish.
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