AI Article Synopsis

  • * In a study of 68 patients with myeloproliferative neoplasms, DTA mutations were linked to an increased risk of thrombotic events, especially in those with PV, where having one or more DTA mutations raised the risk significantly.
  • * The findings indicate that pathogenic DTA mutations, particularly those within the specified genes, may serve as independent risk factors for thrombosis in PV patients, though the effects of these

Article Abstract

The development of thrombotic events is common among patients with polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). We studied the influence of pathogenic mutations frequently associated with myeloid malignancies on thrombotic events using next-generation sequencing (NGS) in an initial cohort of 68 patients with myeloproliferative neoplasms (MPN). As expected, the presence of mutations in and (DTA genes) was positively associated with age for the whole cohort ( = 0.025, OR: 1.047, 95% CI: 1.006-1.090). Also, while not related with events in the whole cohort, DTA mutations were strongly associated with the development of vascular events in PV patients ( = 0.028). To confirm the possible association between the presence of DTA mutation and thrombotic events, we performed a case-control study on 55 age-matched patients with PV (including 12 PV patients from the initial cohort, 25 with event vs. 30 no event). In the age-matched case-control PV cohort, the presence of ≥1 DTA mutation significantly increased the risk of a thrombotic event (OR: 6.333, = 0.0024). Specifically, mutations in were associated with thrombotic events in the PV case-control cohort (OR: 3.56, 95% CI: 1.15-11.83, = 0.031). Our results suggest that pathogenic DTA mutations, and particularly mutations, may be an independent risk factor for thrombosis in patients with PV. However, the predictive value of and DTA mutations in ET and PMF was inconclusive and should be determined in a larger cohort.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226609PMC
http://dx.doi.org/10.3390/cancers12040934DOI Listing

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