Table 1.
Characteristics | 2014-2019 cohort |
|
---|---|---|
N | (%) | |
Total number of patients | 110 | (100) |
Demographics | ||
Sex | ||
Male | 78 | (71) |
Female | 32 | (29) |
Age, y | ||
Median (IQR) | 73 (67-78) | |
≤65 | 22 | (20) |
>65 | 88 | (80) |
Blood counts, median (IQR) | ||
Hb, g/dL∗ | 11.0 (9.0-12.4) | |
Platelets, ×109/L∗ | 150 (95-273) | |
Neutrophils, ×109/L† | 31.8 (18.6-60) | |
Monocytosis (>1 × 109/L)∗ | 59 | (54) |
Blasts, %‡ | 1 (1-4) | |
Bone marrow features | ||
Blast data available, n/N (%) | 93/110 (85%) | |
Median (IQR), % | 2 (1-4) | |
<5% | 72 | (77) |
≥5% | 21 | (23) |
Fibrosis data available, n/N (%) | 87/110 (79%) | |
Fibrosis present§ | 66 | (76) |
Cytogenetics | ||
Available | 98 | (89) |
Normal karyotype | 83 | (85) |
Abnormal karyotype‖ | 15 | (15) |
Trisomy‖ | 10 | (10) |
Molecular genetics | ||
Available | 101 | (92) |
ASXL1 mutation | 22 | (22) |
SETBP1 mutation | 18 | (18) |
SRSF2 mutation | 12 | (12) |
CSFR3 mutation | 12 | (12) |
JAK2 mutation | 9 | (9) |
TET2 mutation | 8 | (8) |
RUNX1 mutation | 6 | (6) |
EZH2 mutation | 3 | (3) |
Other mutations¶ | 8 | (8) |
Number of mutations | ||
No mutations | 52 | (51) |
One mutation | 22 | (22) |
Two mutations | 11 | (11) |
Three or more mutations | 16 | (16) |
First-line treatment | ||
BSC only | 33 | (30) |
Antineoplastic therapy without alloSCT | 62 | (56) |
Antineoplastic therapy with alloSCT | 15 | (14) |
Death during follow-up | 92 | (84) |
Median follow-up, mo (IQR) | 16.8 (9.4-33.1) |
alloSCT, allogeneic stem cell transplantation.
Missing in 1 patient.
Missing in 13 patients.
Missing in 18 patients.
Fibrosis data: 21 (19%) patients had no bone marrow fibrosis. 47 had grade 1 (42%), 18 had grade 2 (16%), 1 had grade 3 (1%), and 23 had an unknown grade (21%).
Abnormal karyotype includes 10 trisomies (ie, +8 [n = 6], +13 [n = 2], +21 [n = 1], and add(10p) [n = 1]). There remaining 5 patients had either a −20, -Y, del(13p), der(5p), or t(16;17). One patient had 2 abnormalities: add (10p) and i(17q). Notably, none of the patients had a complex karyotype.
Includes patients with the following mutations: CALR (n = 1), DNMT3A (n = 1), KIT (n = 2), CEPBA (n = 1), NPM1 (n = 1), IDH2 (n = 1), ETNK1 (n = 1), and KRAS/NRAS mutation (n = 2). Notably, a patient can harbor several mutations.