ReviewInternational journal of hematology2020
The role of calreticulin mutations in myeloproliferative neoplasms.
Review in International journal of hematology, 2020. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Molecular Profile of BCR-ABL1 Negative Myeloproliferative Neoplasm in a Moroccan Population.Asian Pacific journal of cancer prevention : APJCP · 2024Article
- The Role of Mutated Calreticulin in the Pathogenesis ofInternational journal of molecular sciences · 2024Article
- Effects of calreticulin mutations on cell transformation and immunity.Journal of cellular and molecular medicine · 2023Review
- Structural and Dynamic Differences between Calreticulin Mutants Associated with Essential Thrombocythemia.Biomolecules · 2023Article
- Transcriptomic Analysis Reveals JAK2/MPL-Independent Effects of Calreticulin Mutations in aCells · 2023Article
- The Oncolytic herpes simplex virus type-1 (HSV-1) vaccine strain VC2 causes intratumor infiltration of functionally active T cells and inhibition of tumor metastasis and pro-tumor genes VEGF and PDL1 expression in the 4T1/Balb/c mouse model of stage four breast cancer.Frontiers in molecular biosciences · 2023Article
- A Broad Overview of Signaling inCancers · 2021Review
- Megakaryocytes, erythropoietic and granulopoietic cells express CAL2 antibody in myeloproliferative neoplasms carrying CALR gene mutations.International journal of experimental pathology · 2021Article
- Fedratinib, a newly approved treatment for patients with myeloproliferative neoplasm-associated myelofibrosis.Leukemia · 2021Review
- Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR-ABL-Negative Myeloproliferative Neoplasm.Antioxidants (Basel, Switzerland) · 2020Review
- JAK2, CALR, and MPL Mutation Profiles in Colombian patients with BCR-ABL Negative Myeloproliferative Neoplasms.Colombia medica (Cali, Colombia)Article
- Genetic and Clinical Characteristics of Patients with Philadelphia-Negative Myeloproliferative Neoplasm Carrying Concurrent Mutations inTechnology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Unique frameshift mutations in the calreticulin (CALR) gene, which encodes an endoplasmic reticulum (ER)-localized molecular chaperone, have been identified in patients with essential thrombocythemia (ET) and primary myelofibrosis (PMF), which are subgroups of myeloproliferative neoplasms (MPNs). In this review, we discuss the current understanding of the consequences of these mutations with regard to tumorigenesis and/or signal transduction. Expression of mutant CALR induces thrombocytosis in animal models, producing the phenotype of ET. Mutant CALR preferentially interacts with and activates the thrombopoietin receptor MPL, resulting in MPL-dependent cellular transformation. A novel carboxyl-terminal sequence generated by a frameshift mutation in CALR mediates intermolecular interactions to form homomultimers and induces structural changes required for MPL binding and activation. The homomultimerized mutant CALR behaves similarly to a cytokine, stabilizing homodimerized MPL by binding to immature MPL N-glycans. Mutant CALR may engage with MPL in the ER, but fails to dissociate, conveying MPL to the cell surface where MPL activation is likely to occur. Collectively, cell-autonomous and constitutive activation of MPL is a cause of MPNs that are mediated by mutant CALR. Novel therapeutic strategies for treating MPNs that target these mechanisms should, therefore, be developed.
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