Results from a systematic review and meta-analysis published in Critical Reviews in Oncology/Hematology indicated there was no association between mutations in SF3B1 and overall survival (OS) in patients with myelodysplastic syndrome (MDS).

Mutations in the SF3B1 gene are the most common mutations in MDS, though the prognostic implications of these mutations are unclear.

In this study, researchers searched PubMed, Embase, and the Cochrane Library for meeting abstracts and primary studies in humans that evaluated the association between mutations in SF3B1 and prognosis in MDS, provided survival information with hazard ratios (HRs) and 95% CIs, and were published before or during October 2017. The researchers excluded review articles, reanalyses, editorials, case reports, or commentaries.

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Across the 15 included studies, the overall HR for OS was 0.90 in patients with MDS who had SF3B1 mutations compared with patients without mutations; this was not statistically significant (95% CI, 0.60-1.35; P =.61).

Decreased leukemia-free survival was associated with SF3B1 mutations. Both Asian ethnicity and Illumina HiSeq 2000 sequencing methods were significantly correlated with OS, though SF3B1 mutations were not. However, presence of SF3B1 mutations was significantly associated with decreased levels of blast cells and increased platelet counts and bone marrow ring sideroblast levels.

These results describe a potentially complex role of SF3B1 mutations in the prognosis and clinical outcomes of patients with MDS, though these mutations appear to have no significant influence on the OS of patients with MDS. “A potential explanation for this discrepancy is that the SF3B1 mutation coexisted with other genetic alterations related to unfavorable outcomes, thereby mitigating the positive effect on survival,” the authors concluded.

Reference

  1. Tang Y, Miao M, Han S, et al. Prognostic value and clinical feature of SF3B1 mutations in myelodysplastic syndromes: A meta-analysis [published online August 3, 2018]. Crit Rev Oncol Hematol. doi:10.1016/j.critrevonc.2018.07.013

This article originally appeared on Hematology Advisor