ArticleHaematologica2014
Distinct clinical characteristics of myeloproliferative neoplasms with calreticulin mutations.
Article in Haematologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05401864 (Characteristics of Patients With Philadelphia Negative Myeloproliferative Neoplasms at Assiut University Hospital), which is not on this map. Cited by 33 papers, 2 of them syntheses that pooled it.
What it found
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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.
The trial behind it
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.
Characteristics of Patients With Philadelphia Negative Myeloproliferative Neoplasms at Assiut University Hospital
Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 98 citations in OpenAlex.
- Estimation of diagnosis and prognosis in ET by assessment of CALR and JAK2Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2017Pooled it
- A meta-analysis comparing clinical characteristics and outcomes in CALR-mutated and JAK2V617F essential thrombocythaemia.International journal of hematology · 2015Pooled it
- JAK2 V617F, MPL, and CALR mutations in essential thrombocythaemia and major thrombotic complications: a single-institute retrospective analysis.Pathology oncology research : POR · 2015Trial
- CALR-mutant myeloproliferative neoplasms: insights from next-generation sequencing.Journal of applied genetics · 2026Article
- Analysis of CALR-mutated essential thrombocythemia as a distinct disease entity compared with JAK2 V617F-mutated and triple-negative patients.Turkish journal of medical sciences · 2026Article
- The Role of Mutated Calreticulin in the Pathogenesis ofInternational journal of molecular sciences · 2024Article
- Molecular Genetics of Thrombotic Myeloproliferative Neoplasms: Implications in Precision Oncology.Diagnostics (Basel, Switzerland) · 2023Review
- Case Report: First longitudinal study of a patient with CALR positive clonal hematopoiesis of indeterminate potential developing into pre-fibrotic myelofibrosis.Frontiers in oncology · 2023Article
- Effects ofDiagnostics (Basel, Switzerland) · 2022Article
- Myeloproliferative neoplasms complicated with β-thalassemia: Two case report.World journal of clinical cases · 2022Article
- Article
- The Genetic Basis of Primary Myelofibrosis and Its Clinical Relevance.International journal of molecular sciences · 2020Review
- Review
- Different impact of calreticulin mutations on human hematopoiesis in myeloproliferative neoplasms.Oncogene · 2020Article
- A distinct molecular mutational profile and its clinical impact in essential thrombocythemia and primary myelofibrosis patients.BMC cancer · 2020Observational
- Article
- Guideline on myeloproliferative neoplasms: Associacão Brasileira de Hematologia, Hemoterapia e Terapia Cellular: Project guidelines: Associação Médica Brasileira - 2019.Hematology, transfusion and cell therapy · 2019Article
- High frequencies of circulating memory T cells specific for calreticulin exon 9 mutations in healthy individuals.Blood cancer journal · 2019Article
- Comparison of the Mutational Profiles of Primary Myelofibrosis, Polycythemia Vera, and Essential Thrombocytosis.American journal of clinical pathology · 2017Article
- The Mutation Profile of Calreticulin in Patients with Myeloproliferative Neoplasms and Acute Leukemia.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic insertions/deletions in the calreticulin gene have recently been discovered to be causative alterations in myeloproliferative neoplasms. A combination of qualitative and quantitative allele-specific polymerase chain reaction, fragment-sizing, high resolution melting and Sanger-sequencing was applied for the detection of three driver mutations (in Janus kinase 2, calreticulin and myeloproliferative leukemia virus oncogene genes) in 289 cases of essential thrombocythemia and 99 cases of primary myelofibrosis. In essential thrombocythemia, 154 (53%) Janus kinase 2 V617F, 96 (33%) calreticulin, 9 (3%) myeloproliferative leukemia virus oncogene gene mutation-positive and 30 triple-negative (11%) cases were identified, while in primary myelofibrosis 56 (57%) Janus kinase 2 V617F, 25 (25%) calreticulin, 7 (7%) myeloproliferative leukemia virus oncogene gene mutation-positive and 11 (11%) triple-negative cases were identified. Patients positive for the calreticulin mutation were younger and had higher platelet counts compared to Janus kinase 2 mutation-positive counterparts. Calreticulin mutation-positive patients with essential thrombocythemia showed a lower risk of developing venous thrombosis, but no difference in overall survival. Calreticulin mutation-positive patients with primary myelofibrosis had a better overall survival compared to that of the Janus kinase 2 mutation-positive (P=0.04) or triple-negative cases (P=0.01). Type 2 calreticulin mutation occurred more frequently in essential thrombocythemia than in primary myelofibrosis (P=0.049). In essential thrombocythemia, the calreticulin mutational load was higher than the Janus kinase 2 mutational load (P<0.001), and increased gradually in advanced stages. Calreticulin mutational load influenced blood counts even at the time point of diagnosis in essential thrombocythemia. We confirm that calreticulin mutation is associated with distinct clinical characteristics and explored relationships between mutation type, load and clinical outcome.
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