CDC25c expression in patients with myelofibrosis is associated with stronger myeloproliferation and shorter overall survival (CROSBI ID 307311)
Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija
Podaci o odgovornosti
Galusic, Davor ; Lucijanic, Marko ; Livun, Ana ; Radman, Maja ; Lucijanic, Jelena ; Drmic Hofman, Irena ; Kusec, Rajko
engleski
CDC25c expression in patients with myelofibrosis is associated with stronger myeloproliferation and shorter overall survival
Background: Cell-division-cycle-25c (CDC25c) is a gene coding a phosphatase controlling entry into mitosis upon activation through Polo-like-kinase-1 (PLK1) and serves as a key regulator of cell division. CDC25c was reported to be dysregulated in some malignant diseases, but its role in myelofibrosis has not yet been elucidated. Methods: We have retrospectively investigated CDC25c mRNA expression in bone marrow aspirates of 43 patients with myelofibrosis (28 primary/PMF, 15 secondary myelofibrosis/SMF) and 12 controls. Results: CDC25c mRNA expression did not significantly differ between PMF, SMF and controls (median ΔCT 3.08 vs 2.86 vs 2.29 for PMF, SMF and controls, respectively ; P=0.162). Patients presenting with higher CDC25c mRNA expression were of older age (P=0.037), had statistically significantly higher white-blood-cells (P=0.017), larger liver size (P=0.022), higher absolute neutrophil (P=0.010), monocyte (P=0.050), basophil (P=0.012), and eosinophil counts (P=0.013). Patients presenting with high CDC25c mRNA expression had statistically significantly inferior overall survival compared to low CDC25c expression group (HR=2.99 ; P=0.049). Median overall survival was not reached in patients with low and was 44 months in patients with high CDC25c expression. Conclusion: Our data suggest that CDC25c might be implicated in disease pathogenesis and could represent interesting novel therapeutic target in myelofibrosis. Future studies investigating these interesting associations are warranted.
myelofibrosis ; myeloproliferative neoplasm ; survival ; cell cycle control
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Podaci o izdanju
134 (1-2)
2020.
83-85
objavljeno
0043-5325
1613-7671
10.1007/s00508-020-01738-2
Povezanost rada
Kliničke medicinske znanosti