Patient characteristics at baseline according to random assignment for induction with or without lenalidomide
. | No. of patients evaluated . | Control induction treatment . | Lenalidomide induction treatment . |
---|---|---|---|
Total | 392 (100) | 388 (100) | |
Male sex | 210 (54) | 233 (60) | |
Age, y | |||
Median (range) | 53 (18-65) | 54 (18-65) | |
≤45 | 110 (28) | 99 (26) | |
46-60 | 194 (49) | 195 (50) | |
>60 | 88 (22) | 94 (24) | |
WHO/ECOG performance status | |||
0 | 239 (61) | 264 (66) | |
1 | 138 (35) | 113 (29) | |
2 | 15 (4) | 11 (3) | |
Diagnostic subgroup | |||
AML | 356 (91) | 351 (90) | |
High-risk RAEB | 33 (8) | 35 (9) | |
Leukemia with ambiguous lineage | 3 (1) | 2 (1) | |
AML type | |||
De novo | 358 (91) | 351 (90) | |
sAML | 19 (5) | 24 (6) | |
tAML | 15 (4) | 13 (3) | |
WBC, × 109/L | |||
Median (range) | 8.0 (0-265) | 6.7 (0.4-297) | |
≤20 | 259 (66) | 257 (66) | |
20-100 | 109 (28) | 103 (27) | |
>100 | 23 (6) | 27 (7) | |
Unknown | 1 (0) | 1 (0) | |
Median blasts in bone marrow, % | 52 | 52 | |
Cytogenetics* | |||
t(8;21) | 11 (3) | 22 (6) | |
inv(16) or t(16;16) | 23 (6) | 26 (7) | |
CN-X-Y | 211 (54) | 199 (51) | |
CA rest | 97 (25) | 95 (24) | |
Monosomal karyotype | 39 (10) | 34 (9) | |
Unknown | 11 (3) | 12 (3) | |
Gene mutations† | |||
NPM1-mut | 744 | 129 (33) | 115 (30) |
FLT3-ITD-mut | 742 | 85 (22) | 69 (18) |
FLT3-TKD835-mut | 742 | 34 (9) | 33 (9) |
NPM1-mut FLT3-ITD-negative | 741 | 69 (18) | 77 (20) |
NPM1-mut FLT3-ITD-mut | 59 (15) | 38 (10) | |
NPM1-wt FLT3-ITD-negative | 217 (55) | 224 (58) | |
NPM1-wt FLT3-ITD-mut | 26 (7) | 31 (8) | |
DNMT3A-mut | 739 | 108 (28) | 105 (27) |
IDH1-mut | 739 | 35 (9) | 34 (9) |
IDH2-mut | 739 | 45 (11) | 45 (12) |
TET2-mut | 739 | 54 (14) | 41 (11) |
Biallelic CEBPA-mut | 739 | 16 (4) | 12 (3) |
RUNX1-mut | 742 | 41 (10) | 49 (13) |
ASXL1-mut | 742 | 39 (10) | 31 (8) |
TP53-mut | 742 | 28 (7) | 29 (7) |
SF3B1-mut or SRSF2-mut‡ | 739 | 46 (12) | 43 (11) |
SRSF2-mut‡ | 739 | 30 (8) | 28 (7) |
PTPN11-mut | 739 | 44 (11) | 33 (9) |
KRAS-mut | 739 | 23 (6) | 18 (5) |
NRAS-mut | 739 | 60 (15) | 69 (18) |
JAK2-mut | 739 | 3 (1) | 4 (1) |
BCOR-mut or BCOR1-mut | 739 | 29 (7) | 25 (6) |
EVI1 overexpression | 594 | 21 (5) | 28 (7) |
Prognostic risk according to 2017 ELN criteria§ | |||
Favorable | 134 (34) | 150 (39) | |
Intermediate | 127 (32) | 94 (24) | |
Adverse | 119 (30) | 139 (36) | |
Unknown | 12 (3) | 5 (1) |
. | No. of patients evaluated . | Control induction treatment . | Lenalidomide induction treatment . |
---|---|---|---|
Total | 392 (100) | 388 (100) | |
Male sex | 210 (54) | 233 (60) | |
Age, y | |||
Median (range) | 53 (18-65) | 54 (18-65) | |
≤45 | 110 (28) | 99 (26) | |
46-60 | 194 (49) | 195 (50) | |
>60 | 88 (22) | 94 (24) | |
WHO/ECOG performance status | |||
0 | 239 (61) | 264 (66) | |
1 | 138 (35) | 113 (29) | |
2 | 15 (4) | 11 (3) | |
Diagnostic subgroup | |||
AML | 356 (91) | 351 (90) | |
High-risk RAEB | 33 (8) | 35 (9) | |
Leukemia with ambiguous lineage | 3 (1) | 2 (1) | |
AML type | |||
De novo | 358 (91) | 351 (90) | |
sAML | 19 (5) | 24 (6) | |
tAML | 15 (4) | 13 (3) | |
WBC, × 109/L | |||
Median (range) | 8.0 (0-265) | 6.7 (0.4-297) | |
≤20 | 259 (66) | 257 (66) | |
20-100 | 109 (28) | 103 (27) | |
>100 | 23 (6) | 27 (7) | |
Unknown | 1 (0) | 1 (0) | |
Median blasts in bone marrow, % | 52 | 52 | |
Cytogenetics* | |||
t(8;21) | 11 (3) | 22 (6) | |
inv(16) or t(16;16) | 23 (6) | 26 (7) | |
CN-X-Y | 211 (54) | 199 (51) | |
CA rest | 97 (25) | 95 (24) | |
Monosomal karyotype | 39 (10) | 34 (9) | |
Unknown | 11 (3) | 12 (3) | |
Gene mutations† | |||
NPM1-mut | 744 | 129 (33) | 115 (30) |
FLT3-ITD-mut | 742 | 85 (22) | 69 (18) |
FLT3-TKD835-mut | 742 | 34 (9) | 33 (9) |
NPM1-mut FLT3-ITD-negative | 741 | 69 (18) | 77 (20) |
NPM1-mut FLT3-ITD-mut | 59 (15) | 38 (10) | |
NPM1-wt FLT3-ITD-negative | 217 (55) | 224 (58) | |
NPM1-wt FLT3-ITD-mut | 26 (7) | 31 (8) | |
DNMT3A-mut | 739 | 108 (28) | 105 (27) |
IDH1-mut | 739 | 35 (9) | 34 (9) |
IDH2-mut | 739 | 45 (11) | 45 (12) |
TET2-mut | 739 | 54 (14) | 41 (11) |
Biallelic CEBPA-mut | 739 | 16 (4) | 12 (3) |
RUNX1-mut | 742 | 41 (10) | 49 (13) |
ASXL1-mut | 742 | 39 (10) | 31 (8) |
TP53-mut | 742 | 28 (7) | 29 (7) |
SF3B1-mut or SRSF2-mut‡ | 739 | 46 (12) | 43 (11) |
SRSF2-mut‡ | 739 | 30 (8) | 28 (7) |
PTPN11-mut | 739 | 44 (11) | 33 (9) |
KRAS-mut | 739 | 23 (6) | 18 (5) |
NRAS-mut | 739 | 60 (15) | 69 (18) |
JAK2-mut | 739 | 3 (1) | 4 (1) |
BCOR-mut or BCOR1-mut | 739 | 29 (7) | 25 (6) |
EVI1 overexpression | 594 | 21 (5) | 28 (7) |
Prognostic risk according to 2017 ELN criteria§ | |||
Favorable | 134 (34) | 150 (39) | |
Intermediate | 127 (32) | 94 (24) | |
Adverse | 119 (30) | 139 (36) | |
Unknown | 12 (3) | 5 (1) |
All data are n (%) unless otherwise indicated. RAEB is defined as having a Revised International Prognostic Scoring System score >4.5.16
CA, abnormal cytogenetics; CN, normal cytogenetics; ECOG, Eastern Cooperative Oncology Group; mut, mutation; sAML, secondary AML (after myelodysplastic syndrome and antecedent hematologic disease); tAML, therapy-related AML (in case of previous chemotherapy or radiotherapy) (for details see “Patients and methods”); WHO, World Health Organization; wt, wild-type.
AML with core binding factor abnormalities: t(8;21)(q22;q22), inv(16)(p13.1;q22), or t(16;16)(p13.1;q22); monosomal karyotype defined as described in Breems et al.20
Gene mutations include ASXL1, additional sex combs–like 1; CEPBA, CCAAT/enhancer-binding protein α; DNMT3A, DNA methyltransferase 3 α; EVI1, ecotropic virus integration 1; FLT3, fms-like tyrosine kinase-3; FLT3-ITD-negative, FLT3 without internal tandem duplications (ITDs); FLT3-TKD835, FLT3-tyrosine kinase domain 835, FLT3 gene with point mutation at position D835; IDH1/IDH2, isocitrate dehydrogenase 1 and 2; NPM1, nuclephosmin-1; PTPN11, protein tyrosine phosphatase nonreceptor type 11; RUNX1, runt-related transcription factor 1; SF3B1, splicing factor 3B subunit; SRSF2, serine/arginine-rich splicing factor 2; TET2, Tet methylcytosine dioxygenase 2.
We considered the frequencies of SRSF2 alone and SRSF2 and SF3B1 in combination.
The ELN prognostic risk categories as described in Döhner et al.1