ArticleAmerican journal of hematology2016
Mutant calreticulin-expressing cells induce monocyte hyperreactivity through a paracrine mechanism.
Article in American journal of hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Shaping the Future of Myeloproliferative Neoplasm Therapy: Immune-Based Strategies and Targeted Innovations.Cancers · 2024Review
- Immune-dysregulation harnessing in myeloid neoplasms.Cancer medicine · 2024Review
- Proteogenetic drug response profiling elucidates targetable vulnerabilities of myelofibrosis.Nature communications · 2023Article
- The immune landscape in BCR-ABL negative myeloproliferative neoplasms: inflammation, infections and opportunities for immunotherapy.British journal of haematology · 2022Review
- Mechanism of mutant calreticulin-mediated activation of the thrombopoietin receptor in cancers.The Journal of cell biology · 2021Article
- PPARγ agonists promote the resolution of myelofibrosis in preclinical models.The Journal of clinical investigation · 2021Article
- Impact of Calreticulin and Its Mutants on Endoplasmic Reticulum Function in Health and Disease.Progress in molecular and subcellular biology · 2021Article
- Roles of Calreticulin in Protein Folding, Immunity, Calcium Signaling and Cell Transformation.Progress in molecular and subcellular biology · 2021Article
- Surface-exposed and soluble calreticulin: conflicting biomarkers for cancer prognosis.Oncoimmunology · 2020Article
- Cancer Immune Therapy for Philadelphia Chromosome-Negative Chronic Myeloproliferative Neoplasms.Cancers · 2020Review
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- Overview of the Mutational Landscape in Primary Myelofibrosis and Advances in Novel Therapeutics.Asian Pacific journal of cancer prevention : APJCP · 2019Review
- Diallyl disulfide down-regulates calreticulin and promotes C/EBPα expression in differentiation of human leukaemia cells.Journal of cellular and molecular medicine · 2019Article
- Tumor-associated calreticulin variants functionally compromise the peptide loading complex and impair its recruitment of MHC-I.The Journal of biological chemistry · 2018Article
- Recent advances in the genomics and therapy of BCR/ABL1-positive and -negative chronic myeloproliferative neoplasms.Leukemia research · 2018Review
- Multiple Roles of Glycans in Hematological Malignancies.Frontiers in oncology · 2018Review
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- Calreticulin-mutant proteins induce megakaryocytic signaling to transform hematopoietic cells and undergo accelerated degradation and Golgi-mediated secretion.Journal of hematology & oncology · 2016Article
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the calreticulin gene (CALR) were recently identified in approximately 70-80% of patients with JAK2-V617F-negative essential thrombocytosis and primary myelofibrosis. All frameshift mutations generate a recurring novel C-terminus. Here we provide evidence that mutant calreticulin does not accumulate efficiently in cells and is abnormally enriched in the nucleus and extracellular space compared to wildtype calreticulin. The main determinant of these findings is the loss of the calcium-binding and KDEL domains. Expression of type I mutant CALR in Ba/F3 cells confers minimal IL-3-independent growth. Interestingly, expression of type I and type II mutant CALR in a nonhematopoietic cell line does not directly activate JAK/STAT signaling compared to wildtype CALR and JAK2-V617F expression. These results led us to investigate paracrine mechanisms of JAK/STAT activation. Here we show that conditioned media from cells expressing type I mutant CALR exaggerate cytokine production from normal monocytes with or without treatment with a toll-like receptor agonist. These effects are not dependent on the novel C-terminus. These studies offer novel insights into the mechanism of JAK/STAT activation in patients with JAK2-V617F-negative essential thrombocytosis and primary myelofibrosis.
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Registered trials
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