ArticleOncogene2020
Different impact of calreticulin mutations on human hematopoiesis in myeloproliferative neoplasms.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Effects of Calreticulin Mutations on HLA Class I Expression in Myeloproliferative Neoplasms.bioRxiv : the preprint server for biology · 2025Article
- New approaches to standard of care in early-phase myeloproliferative neoplasms: can interferon-α alter the natural history of the disease?Haematologica · 2025Review
- Type 1 CALR mutation allele frequency correlates with CD34/CXCR4 expression in myelofibrosis-type megakaryocyte dysplasia: A mechanism of disease progression?Blood cancer journal · 2024Article
- Proteogenetic drug response profiling elucidates targetable vulnerabilities of myelofibrosis.Nature communications · 2023Article
- Leukemic conversion involvingFrontiers in oncology · 2023Article
- Inferring the initiation and development of myeloproliferative neoplasms.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Observational
- CALR frameshift mutations in MPN patient-derived iPSCs accelerate maturation of megakaryocytes.Stem cell reports · 2021Article
- Induced Pluripotent Stem Cells Enable Disease Modeling and Drug Screening in Calreticulin del52 and ins5 Myeloproliferative Neoplasms.HemaSphere · 2021Article
Corrections and comments
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Authors and funding
24 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of calreticulin (CALRm) define a subtype of myeloproliferative neoplasms (MPN). We studied the biological and genetic features of CALR-mutated essential thrombocythemia and myelofibrosis patients. In most cases, CALRm were found in granulocytes, monocytes, B and NK cells, but also in T cells. However, the type 1 CALRm spreads more easily than the type 2 CALRm in lymphoid cells. The CALRm were also associated with an early clonal dominance at the level of hematopoietic stem and progenitor cells (HSPC) with no significant increase during granulo/monocytic differentiation in most cases. Moreover, we found that half of type 2 CALRm patients harbors some homozygous progenitors. Those patients were associated with a higher clonal dominance during granulo/monocytic differentiation than patients with only heterozygous type 2 CALRm progenitors. When associated mutations were present, CALRm were the first genetic event suggesting that they are both the initiating and phenotypic event. In blood, type 1 CALRm led to a greater increased number of all types of progenitors compared with the type 2 CALRm. However, both types of CALRm induced an increase in megakaryocytic progenitors associated with a ruxolitinib-sensitive independent growth and with a mild constitutive signaling in megakaryocytes. At the transcriptional level, type 1 CALRm seems to deregulate more pathways than the type 2 CALRm in megakaryocytes. Altogether, our results show that CALRm modify both the HSPC and megakaryocyte biology with a stronger effect for type 1 than for type 2 CALRm.
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