Table 4.
Best response rates after CPX-351 induction
| CR/CRi, n (%) | P | |
|---|---|---|
| All patients treated | 61 (59) | |
| AML subtype | ||
| t-AML | 19 (70) | .01 |
| MRC-AML | 40 (55) | |
| With/without prior MDS | 15 (44)/46 (68) | .14 |
| With/without CMML | 2 (22)/59 (63) | .03 |
| Hyperleukocytosis | ||
| Presence/absence | 7 (13)/47 (87) | .21 |
| HMA experience | ||
| Prior HMA | 4 (22) | .001 |
| No prior HMA | 56 (69) | |
| Karyotype (presence/absence) | ||
| Complex karyotype | 17 (49)/44 (66) | .09 |
| Monosomal karyotype | 11 (39)/50 (68) | .009 |
| Chromosome 5 abnormalities | 13 (46)/48 (65) | .09 |
| Chromosome 7 abnormalities | 15 (47)/46 (66) | .07 |
| Chromosome 17 abnormalities | 6 (43)/55 (63) | .16 |
| 2017 ELN genetic risk stratification | ||
| Favorable | 2 (100) | .26 |
| Intermediate | 25 (66) | |
| Adverse | 33 (54) | |
| Lindsley’s classifier | ||
| De novo/pan-AML | 18 (86) | .009 |
| Secondary-type-mutation AML | 20 (56) | |
| TP53-mutated AML | 9 (41) | |
| Mutation status (mutated/nonmutated) | ||
| TP53 | 9 (41)/35 (66) | .04 |
| ASXL1 | 9 (53)/37 (67) | .28 |
| RUNX1 | 12 (57)/27 (66) | .50 |
| EVI1 | 1 (17)/50 (63) | .03 |
| FLT3-ITD | 6 (67)/53 (60) | .72 |
| FLT3-TKD | 3 (50)/56 (60) | .62 |
| NPM1 | 4 (57)/55 (59) | .92 |
| Functional group (presence/absence of mutation) | ||
| Epigenetic modifications | 24 (59)/22 (69) | .37 |
| Spliceosome complex | 14 (61)/32 (64) | .80 |
| Signaling and kinase pathway | 16 (55)/30 (68) | .26 |
| Cohesin complex | 6 (60)/40 (63) | .83 |
| Transcription factors | 17 (61)/29 (64) | .75 |