Studies evaluating the impact of donor KIR haplotype or activating KIRs in related or unrelated donor HSCT
| Study . | Kröger 200673 . | Cooley 200983 . | Cooley 201085 . | Stringaris 201087 . | Cooley 201486 . | Oevermann 201484 . |
|---|---|---|---|---|---|---|
| No. of patients | 142 | 448 | 1409 | 246 | 1532 | 85 |
| Disease | AML, ALL, CML, MDS | AML | AML, ALL | AML, ALL, CML, CLL, MDS, NHL | AML | Childhood ALL |
| Donor | URD | URD | URD | HLA-identical sibling | URD | Haploidentical |
| TCD (%) | In vivo 100 (ATG) | 0 | 0 | 100 | 0 | 100 |
| Study group | Donor activating KIRs | Donor genotype B/x | Centromeric B/B donors vs others | Donor KIR B haplotype genes (2DS1, 3DS1, and 2DL5A) | C1/x patient receiving an HSCT from a donor with ≥2 KIR B genes vs other donor | Donor genotype B/x |
| Proportion of patients with aGVHD (grade 2-4) | NS | NS | NS | — | NS | — |
| Relapse | Higher with increasing number of donor activating KIRs | NS | Lower with centromeric B/B donors AML only) | Lower in study group (AML only) | Lower in study group | Lower with genotype B/x donor |
| Risk | HR, 1.37 | RR, 0.34 | HR, 0.24 | RR, 0.70 | RR, 2.82 | |
| 95% CI | 1.1-1.7 | 0.20-0.57 | 0.56-0.87 | 1.37-5.77 | ||
| P | .005 | .001 | .02 | .0018 | .005 | |
| DFS | Lower with increasing number of donor activating KIRs | Higher with genotype B/x donor | Higher with centromeric B/B donors (AML only) | — | Higher in study group | Higher with genotype B/x donor |
| Risk | HR, 1.16 | RR, 0.70 | RR, 0.72 | RR, 0.78 | 50.6% vs 29.5% at 5 years | |
| 95% CI | 0.55-0.88 | 0.55-0.93 | 0.67-0.91 | |||
| P | .04 | .002 | .01 | .0015 | .033 | |
| OS | NS | Higher with genotype B/x donor | Higher with centromeric B/B donors AML only) | NS; (AML only); higher in study group (all patients) | — | — |
| Risk | 31% vs 20% | NR | HR, 0.64 | |||
| 95% CI | 26%-36% vs 13%-27% | 0.43-0.94 | ||||
| P | .007 | .024 |
| Study . | Kröger 200673 . | Cooley 200983 . | Cooley 201085 . | Stringaris 201087 . | Cooley 201486 . | Oevermann 201484 . |
|---|---|---|---|---|---|---|
| No. of patients | 142 | 448 | 1409 | 246 | 1532 | 85 |
| Disease | AML, ALL, CML, MDS | AML | AML, ALL | AML, ALL, CML, CLL, MDS, NHL | AML | Childhood ALL |
| Donor | URD | URD | URD | HLA-identical sibling | URD | Haploidentical |
| TCD (%) | In vivo 100 (ATG) | 0 | 0 | 100 | 0 | 100 |
| Study group | Donor activating KIRs | Donor genotype B/x | Centromeric B/B donors vs others | Donor KIR B haplotype genes (2DS1, 3DS1, and 2DL5A) | C1/x patient receiving an HSCT from a donor with ≥2 KIR B genes vs other donor | Donor genotype B/x |
| Proportion of patients with aGVHD (grade 2-4) | NS | NS | NS | — | NS | — |
| Relapse | Higher with increasing number of donor activating KIRs | NS | Lower with centromeric B/B donors AML only) | Lower in study group (AML only) | Lower in study group | Lower with genotype B/x donor |
| Risk | HR, 1.37 | RR, 0.34 | HR, 0.24 | RR, 0.70 | RR, 2.82 | |
| 95% CI | 1.1-1.7 | 0.20-0.57 | 0.56-0.87 | 1.37-5.77 | ||
| P | .005 | .001 | .02 | .0018 | .005 | |
| DFS | Lower with increasing number of donor activating KIRs | Higher with genotype B/x donor | Higher with centromeric B/B donors (AML only) | — | Higher in study group | Higher with genotype B/x donor |
| Risk | HR, 1.16 | RR, 0.70 | RR, 0.72 | RR, 0.78 | 50.6% vs 29.5% at 5 years | |
| 95% CI | 0.55-0.88 | 0.55-0.93 | 0.67-0.91 | |||
| P | .04 | .002 | .01 | .0015 | .033 | |
| OS | NS | Higher with genotype B/x donor | Higher with centromeric B/B donors AML only) | NS; (AML only); higher in study group (all patients) | — | — |
| Risk | 31% vs 20% | NR | HR, 0.64 | |||
| 95% CI | 26%-36% vs 13%-27% | 0.43-0.94 | ||||
| P | .007 | .024 |
CLL, chronic lymphoid leukemia; NR, not reported.