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The S505A MPL mutation is associated with childhood hereditary thrombocytosis and essential thrombocythemia.
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Frameshift mutation in the MPL gene is associated with congenital amegakaryocytic thrombocytopenia.
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positive CD110 expression in PDAC was associated with poor prognosis and liver metastasis of human PDAC samples
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MPL, CALR and JAK2 are considered driver mutations in myeloproliferative neoplasms.The occurrence of two driver mutations in the same patient was determined and the clinical presentation and disease progression were compared with those in patients with only one driver mutation. Co-occurrence of 2 driver mutations affects the presentation or evolution of MPN, especially essential thrombocythemia.
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JAK2, CALR, MPL and ASXL1 mutational status correlates with distinct histological features in Philadelphia chromosome-negative myeloproliferative neoplasms
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Insights into the mechanism of the pathogenic mutant CALR-MPL interaction in myeloproliferative neoplasms.
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This study explored the relationship between mutations in the Janus kinase 2 gene ( JAK2), MPL, and the calreticulin gene ( CALR) in Uygur and Han Chinese patients with BCR-ABL fusion gene-negative myeloproliferative neoplasms.
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JAK2V617F mutation was found in 37 (61.7%) patients with ET. Among 23 patients without JAK2V617F mutation, 7 (11.7%) had CALR mutation and 1 (1.7%) had MPL mutation. Fifteen (25.0%) patients were negative for all 3 mutations: JAK2V617F(-), CALR(-), and MPL(-).
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Comprehensive genomic characterization identified distinct genetic subgroups and provided a classification of myeloproliferative neoplasms on the basis of causal biologic mechanisms. Mutations in JAK2, CALR, or MPL being the sole abnormality in 45% of the patients.
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MPL and CALR genotypes show a similar clinical picture at essential thrombocythaemia diagnosis. Bone marrow histology in MPL-mutated ET is characterized by prominent megakaryocytic proliferation.
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These results indicate that lusutrombopag acts on human TPOR to upregulate differentiation and proliferation of megakaryocytic cells, leading to platelet production.
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The expression of TPO and c-Mpl was significantly decreased in the cITP group compared to the nITP group, suggesting that TPO and its receptor may play important roles in childhood cITP pathogenesis.
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In 94.9% of PV, 85.5% ET and 85.2% PMF, authors found mutations in JAK2, MPL or CALR. 74.9% carried JAK2V617F, 12.3% CALR mutations, 2.1% MPL mutations and 10.7% were triple negative.
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A novel germ-line mutation of c-mpl gene in a sporadic case of essential thrombocythemia.
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In 136 patients with myelofibrosis and a median age of 58 years who underwent allogeneic stem cell transplantation (AHSCT) for molecular residual disease, the percentage of molecular clearance on day 100 was higher in CALR-mutated patients (92%) in comparison with MPL- (75%) and JAKV617F-mutated patients (67%).
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This study demonstrated that absence of MPL mutation in stroke.
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MPL mutations and splenomegaly are risk factors for essential thrombocythemia progression into primary nyelofibrosis.
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goals were: (i) to identify other MPL mutations that should be tested in MPN patients by mutation-specific PCR; and (ii) to determine the amino acid requirements at position 515 to prevent TpoR self-activation
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Concurrent MPL W515L and Y591D mutations in a patient with myelofibrosis.
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MPL is up regulated in JAK2(V617F) ECs and contributes to the maintenance/expansion of the JAK2(V617F) clone over JAK2(WT) clone in vitro