In some instances, splicing factor (SF) mutations have provided diagnostic utility and information on clinical outcomes as exemplified by <i>SF3B1</i> mutations associated with increased ring sideroblasts (RS) in MDS-RS or MDS/MPN-RS with thrombocytosis.
In vitro and in vivo experiments revealed that tumor-derived G-CSF and G-CSF-mediated IL-6 production from the tumor microenvironment are involved in the development of leukocytosis and thrombocytosis in patients with endometrial cancer.
In vitro and in vivo experiments revealed that tumor-derived G-CSF and G-CSF-mediated IL-6 production from the tumor microenvironment are involved in the development of leukocytosis and thrombocytosis in patients with endometrial cancer.
Sequential mutational evaluation of CALR -mutated myeloproliferative neoplasms with thrombocytosis reveals an association between CALR allele burden evolution and disease progression.
The PLT-CA125 scores (0, 1, and 2) were defined basing on the presence of thrombocytosis (PLT count > 400,000/μL), an elevated CA125 level (CA125 > 1200 U/mL), or both.
Three patients with TRNT1 mutations exhibited severe early onset microcytic anaemia associated with thrombocytosis, and two exhibited B-cell immunodeficiency, inflammatory syndrome and psychomotor delay.
Thrombopoietin overproduction by BRAFV600E-mutated hepatocytes may contribute to hepatocyte proliferation via thrombocytosis, platelet activation, and the interaction of platelets with hepatic sinusoidal cells, while hematologic, renal, and pulmonary disorders due to aberrant platelet activation may lead to spontaneous death in the transgenic mice.
Additionally, although elevated plasma C-reactive protein (CRP) levels and thrombocytosis are strongly correlated and both indicate a poor prognosis for RCC patients, the bridge connecting inflammation and coagulation remains poorly understood.
The excellent response to treatment with the IL-1β receptor antagonist, suggests a key pathogenic role of IL-1β in thrombocytosis as well as in the associated systemic symptoms of inflammation.
Elevated Ca-125 and thrombocytosis were associated with a <i>moderate</i> increase in risk of LNM; lymphadenopathy on imaging with a <i>large</i> increase.
Thrombocytosis during acute exacerbation of COPD (AECOPD) has been associated with mortality; however, the relationship between platelet count and mortality in stable COPD is unknown.
Lethally irradiated mice that were engrafted with bone marrow transduced with the different CALR mutations developed thrombocytosis, but to a much lesser extent with ins5 and the type 2-like CALR mutation.
Diagnostic criteria include the following: persistent thrombocytosis (>450 × 10<sup>9</sup> /L) with clustering of atypical megakaryocytes, refractory anemia, dyserythropoiesis with ring sideroblasts, and the presence of the spliceosome factor 3b subunit (SF3B1) mutation.
The ESR (median 70 vs. 40 mm/h, P = 0.000) and CRP (median 214 vs. 114 mg/dL, P < 0.0001) were found to be increased in ID-associated thrombocytosis patients, similarly for each ID.
We detected SF3B1 mutations in 15 cases (10%) and set to investigate the clinical, morphologic, and molecular features of SF3B1 mutated (SF3B1+) MPNs in comparison to SF3B1 wild-type (SF3B1-) cases and to identify distinctive features with myelodysplastic/myeloproliferative neoplasms with ring sideroblasts (RS) and thrombocytosis, which can show partial clinical and morphological overlap with MPNs.
Identification of commonly deleted genes such as RPS14, miRNA-145, HSPA9, CD78, and CSNK1a1 have elucidated the precise biological changes responsible for the anemia, leukopenia, and thrombocytosis that characterizes del(5q) MDS and highlighted the importance of allelic haploinsufficiency in the hematological phenotype.
Some mice transplanted with RUNX1-EVI1-expressing bone marrow cells developed acute megakaryoblastic leukemia within eight months, and the other non-leukemic mice showed thrombocytosis at around a year.
Some mice transplanted with RUNX1-EVI1-expressing bone marrow cells developed acute megakaryoblastic leukemia within eight months, and the other non-leukemic mice showed thrombocytosis at around a year.