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. Author manuscript; available in PMC: 2021 Feb 16.
Published in final edited form as: Leukemia. 2021 Feb 12;35(9):2563–2569. doi: 10.1038/s41375-021-01165-w

Table 2. Demographics, clinical characteristics, and prognostic biomarkers in patients with versus without BRAF, FBXW7, NRAS, and/or XPO1 mutations (n=499 ‡).

Patient/disease characteristic BRAF, FBXW7, NRAS, and/or XPO1 mutation P
Yes % (n=73) No % (n=426)
Aged >70 years 34 30 0.5
Male 78 71 0.2
Binet stage C * 36 31 0.4
Randomised arm chlorambucil 52 47 0.5
Non-response to treatment 21 21 1.0
≥ 2 lines of treatment 73 66 0.3
Unmutated IGHV genes (>98% homology) ‡ 84 59 0.0002
β2 microglobulin ≥4 mg/L 55 47 0.3
CD38 positive (cut-off 7%) 78 61 0.02
Zap-70 positive (cut-off 10%) 65 47 0.02
Trisomy 12 29 14 0.003
11q deletion 24 20 0.5
Absence of 13q deletion 62 37 0.0001
17p deletion 8 5 0.5
ATM mutation 8 7 0.8
BIRC3 mutation 12 6 0.07
EGR2 mutation 1 3 0.5
KRAS mutation 15 4 0.0003
NOTCH1 mutation 21 11 0.02
SF3B1 mutation 15 26 0.05
TP53 mutation 15 9 0.09
*

Binet stage C disease was not significant because, while patients with these gene mutations were more likely than others to have anaemia (haemoglobin <100g/L; 33% vs. 18%; P=0.003), they were less likely to have thrombocytopenia (platelets <100x109/L; 10% v. 21%; P=0.02).

Eight variables had missing data, with the no. of cases ranging from 356 to 464.