Demographic and clinical characteristics of all patients (N = 31)
| Characteristic . | All (N = 31) . | FL (n = 14) . | R/R (n = 17) . |
|---|---|---|---|
| Median age (range), y | 69 (46-80) | 74 (46-80) | 66 (47-79) |
| Age ≥65 y, n (%)* | 21 (68) | 12 (86) | 9 (53) |
| Male sex, n (%) | 19 (61) | 9 (64) | 10 (59) |
| Primary MF, n (%) | 13 (42) | 7 (50) | 6 (35) |
| History of ET/PV, n† | 11/5 | 4/2 | 7/3 |
| Performance status ≥2, n (%) | 10 (32) | 5 (36) | 5 (29) |
| WBC, median (range), ×109/L* | 11.7 (0.1-76) | 13.2 (0.1-76) | 4.7 (0.5-47) |
| Platelets, median (range), × 109/L* | 71 (4-445) | 114 (5-445) | 35 (4-376) |
| Hemoglobin, median (range), g/dL | 8.4 (5-15) | 9.8 (7-15) | 8.5 (7.6-12) |
| Karyotype, n (%) | |||
| Diploid | 5 (16) | 3 (21) | 2 (12) |
| Abnormal | 12 (39) | 7 (50) | 5 (29) |
| Complex [3+ Abn]* | 14 (45) | 4 (28) | 10 (59) |
| Driver mutations, n (%) | |||
| JAK2 | 21 (68) | 9 (64) | 12 (71) |
| CALR/MPL‡ | 4 (13)/3 (10) | 1 (7)/2 (14) | 3 (17)/1 (1) |
| TN | 3 (10) | 2 (14) | 1 (1) |
| Additional mutation >10% patients, n (%) | |||
| ASXL1 | 10 (32) | 3 (21) | 7 (41) |
| NRAS/KRAS§ | 9 (29) | 3 (21) | 6 (35) |
| TET2 | 11 (32) | 5 (36) | 6 (35) |
| TP53§ | 8 (26) | 3 (21) | 5 (29) |
| IDH1/2§ | 8 (26) | 6 (43) | 2 (12) |
| RUNX1 | 7 (23) | 4 (28) | 3 (17) |
| U2AF1 | 5 (16) | 3 (21) | 2 (12) |
| SETBP1 | 4 (13) | 2 (14) | 2 (12) |
| Characteristic . | All (N = 31) . | FL (n = 14) . | R/R (n = 17) . |
|---|---|---|---|
| Median age (range), y | 69 (46-80) | 74 (46-80) | 66 (47-79) |
| Age ≥65 y, n (%)* | 21 (68) | 12 (86) | 9 (53) |
| Male sex, n (%) | 19 (61) | 9 (64) | 10 (59) |
| Primary MF, n (%) | 13 (42) | 7 (50) | 6 (35) |
| History of ET/PV, n† | 11/5 | 4/2 | 7/3 |
| Performance status ≥2, n (%) | 10 (32) | 5 (36) | 5 (29) |
| WBC, median (range), ×109/L* | 11.7 (0.1-76) | 13.2 (0.1-76) | 4.7 (0.5-47) |
| Platelets, median (range), × 109/L* | 71 (4-445) | 114 (5-445) | 35 (4-376) |
| Hemoglobin, median (range), g/dL | 8.4 (5-15) | 9.8 (7-15) | 8.5 (7.6-12) |
| Karyotype, n (%) | |||
| Diploid | 5 (16) | 3 (21) | 2 (12) |
| Abnormal | 12 (39) | 7 (50) | 5 (29) |
| Complex [3+ Abn]* | 14 (45) | 4 (28) | 10 (59) |
| Driver mutations, n (%) | |||
| JAK2 | 21 (68) | 9 (64) | 12 (71) |
| CALR/MPL‡ | 4 (13)/3 (10) | 1 (7)/2 (14) | 3 (17)/1 (1) |
| TN | 3 (10) | 2 (14) | 1 (1) |
| Additional mutation >10% patients, n (%) | |||
| ASXL1 | 10 (32) | 3 (21) | 7 (41) |
| NRAS/KRAS§ | 9 (29) | 3 (21) | 6 (35) |
| TET2 | 11 (32) | 5 (36) | 6 (35) |
| TP53§ | 8 (26) | 3 (21) | 5 (29) |
| IDH1/2§ | 8 (26) | 6 (43) | 2 (12) |
| RUNX1 | 7 (23) | 4 (28) | 3 (17) |
| U2AF1 | 5 (16) | 3 (21) | 2 (12) |
| SETBP1 | 4 (13) | 2 (14) | 2 (12) |
Abn, abnormality; MF, myelofibrosis; TN, triple negative; WBC, white blood cell count.
*Statistically significant.
†Five of these 16 patients (3 ET) had no obvious MF phase before transformation to AML.
‡One patient had 2 functional driver mutations, CALR L367fs and MPL R592Q.
§More than 1 mutation of these genes was identified in individual patients (eg, 1 patient with 2 TP53 mutations, 1 patient with both KRAS and NRAS mutation).