Table 4.

Prognostic significance of mutations in theKITgene in CBF AML patients.

Chromosome AberrationAge, Range (Median) YearsNo. PatientsTotalExon 8Exon 17OtherPrognostic SignificanceRef.
Abbreviations: KIT, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog; pts, patients; OS, overall survival; RI, relapse incidence; EFS, event-free survival; RFS, relapse-free survival; CIR, cumulative incidence of relapse; RR, relapse rate; NA, not analyzed; NR, not reported. 
* Numbers of patients for whom clinical data were available. 
† Median age and range of all 1940 patients analyzed for KIT mutations. 
‡ Age range and median provided for all patients with CBF AML, including 56 with t(8;21) and 47 with inv(16)/t(16;16). 
§ Mean age. 
|| One patient with inv(16) whose clinical outcome was analyzed had a non-exon 17 mutation, but it is unclear if this was an exon 8 or other KIT mutation. 
t(8;21) 16–76 (40.5) 36 17 (47%) 5 (14%) 12 (33%) 2 (6%) OS: Significantly shorter for pts with any KIT mutation (24 mo OS rates: 42% vs 77%, P = 0.017) and for pts with exon 17 mutation (24 mo OS rates: 25% vs 77%, P = 0.006) compared with pts without KIT mutations. 42  
  34 15 (44%) 5 (15%) 10 (29%) 2 (6%) RI: Significantly higher for pts with any KIT mutation (24 mo RI rates: 77% vs 35%, P = 0.005) and for pts with exon 17 mutation (24 mo OS rates: 90% vs 35%, P = 0.002) compared with pts without KIT mutations.  
t(8;21) 15–90 64 8 (13%) NA 8 (13%) NA OS: Significantly shorter for pts with exon 17 KIT mutation (median: 304 d vs 1836 d, P < 0.001).
 EFS: Significantly shorter for pts with exon 17 KIT mutation (median: 244 d vs 744 d, P = 0.003). 43  
t(8;21) 1–75 (33)‡ 50 6 (12%) 3 (6%) 3 (6%) NA OS: Significantly shorter for pts with any KIT mutation ( P = 0.03).
 EFS: Significantly shorter for pts with any KIT mutation ( P = 0.006).
 RFS: Significantly shorter for pts with any KIT mutation ( P = 0.005). 44  
t(8;21) 18–71 (37) 49 11 (22%) 2 (4%) 9 (18%) NA OS: No significant difference between pts with or without KIT mutations.
 CIR: Significantly higher for patients with any KIT mutation (5-year CIR 70% vs 36%, P = 0.017) compared with those without KIT mutations. 45  
inv(16) 15–74 (44)§ 63 20 (32%) 15 (24%) 5 (8%) NA OS: No significant difference between pts with and without exon 8 mutations. Mutations in exon 17 not analyzed.
 RR: Significantly higher for pts with exon 8 mutations compared with pts without exon 8 mutations. Mutations in exon 17 not analyzed. 46  
inv(16)/ t(16;16) 17–88 (51) 17 8 (47%) NR|| 7 (41%) NR|| OS: No significant differences between pts with any KIT mutation or with exon 17 mutation and those without KIT mutations.
 RI: No significant difference between pts with any KIT mutation or with exon 17 mutation and those without KIT mutations. 42  
inv(16)/ (16;16) 1–75 (33)‡ 46 10 (22%) 9 (20%) 1 (2%) NA OS: No significant difference between pts with any KIT mutation and those without KIT mutations. 44  
inv(16)/ t(16;16) 19–57 (40) 61 18 (30%) 8 (13%) 10 (16%) NA OS: No significant differences between pts without KIT mutations and those with any KIT mutation, with exon 17 mutation and exon 8 sole mutation. In multivariable analyses, any KIT mutation predicted worse overall survival (OS) after adjusting for sex.
 CIR: Significantly higher for patients with any KIT mutation (5-year CIR 56% vs 29%, P = 0.05) and pts with exon 17 mutation (5-year CIR 80% vs 29%, P = 0.002) compared with those without KIT mutations. No significant difference between pts with exon 8 sole mutation and those without KIT mutations. 45  
Chromosome AberrationAge, Range (Median) YearsNo. PatientsTotalExon 8Exon 17OtherPrognostic SignificanceRef.
Abbreviations: KIT, v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog; pts, patients; OS, overall survival; RI, relapse incidence; EFS, event-free survival; RFS, relapse-free survival; CIR, cumulative incidence of relapse; RR, relapse rate; NA, not analyzed; NR, not reported. 
* Numbers of patients for whom clinical data were available. 
† Median age and range of all 1940 patients analyzed for KIT mutations. 
‡ Age range and median provided for all patients with CBF AML, including 56 with t(8;21) and 47 with inv(16)/t(16;16). 
§ Mean age. 
|| One patient with inv(16) whose clinical outcome was analyzed had a non-exon 17 mutation, but it is unclear if this was an exon 8 or other KIT mutation. 
t(8;21) 16–76 (40.5) 36 17 (47%) 5 (14%) 12 (33%) 2 (6%) OS: Significantly shorter for pts with any KIT mutation (24 mo OS rates: 42% vs 77%, P = 0.017) and for pts with exon 17 mutation (24 mo OS rates: 25% vs 77%, P = 0.006) compared with pts without KIT mutations. 42  
  34 15 (44%) 5 (15%) 10 (29%) 2 (6%) RI: Significantly higher for pts with any KIT mutation (24 mo RI rates: 77% vs 35%, P = 0.005) and for pts with exon 17 mutation (24 mo OS rates: 90% vs 35%, P = 0.002) compared with pts without KIT mutations.  
t(8;21) 15–90 64 8 (13%) NA 8 (13%) NA OS: Significantly shorter for pts with exon 17 KIT mutation (median: 304 d vs 1836 d, P < 0.001).
 EFS: Significantly shorter for pts with exon 17 KIT mutation (median: 244 d vs 744 d, P = 0.003). 43  
t(8;21) 1–75 (33)‡ 50 6 (12%) 3 (6%) 3 (6%) NA OS: Significantly shorter for pts with any KIT mutation ( P = 0.03).
 EFS: Significantly shorter for pts with any KIT mutation ( P = 0.006).
 RFS: Significantly shorter for pts with any KIT mutation ( P = 0.005). 44  
t(8;21) 18–71 (37) 49 11 (22%) 2 (4%) 9 (18%) NA OS: No significant difference between pts with or without KIT mutations.
 CIR: Significantly higher for patients with any KIT mutation (5-year CIR 70% vs 36%, P = 0.017) compared with those without KIT mutations. 45  
inv(16) 15–74 (44)§ 63 20 (32%) 15 (24%) 5 (8%) NA OS: No significant difference between pts with and without exon 8 mutations. Mutations in exon 17 not analyzed.
 RR: Significantly higher for pts with exon 8 mutations compared with pts without exon 8 mutations. Mutations in exon 17 not analyzed. 46  
inv(16)/ t(16;16) 17–88 (51) 17 8 (47%) NR|| 7 (41%) NR|| OS: No significant differences between pts with any KIT mutation or with exon 17 mutation and those without KIT mutations.
 RI: No significant difference between pts with any KIT mutation or with exon 17 mutation and those without KIT mutations. 42  
inv(16)/ (16;16) 1–75 (33)‡ 46 10 (22%) 9 (20%) 1 (2%) NA OS: No significant difference between pts with any KIT mutation and those without KIT mutations. 44  
inv(16)/ t(16;16) 19–57 (40) 61 18 (30%) 8 (13%) 10 (16%) NA OS: No significant differences between pts without KIT mutations and those with any KIT mutation, with exon 17 mutation and exon 8 sole mutation. In multivariable analyses, any KIT mutation predicted worse overall survival (OS) after adjusting for sex.
 CIR: Significantly higher for patients with any KIT mutation (5-year CIR 56% vs 29%, P = 0.05) and pts with exon 17 mutation (5-year CIR 80% vs 29%, P = 0.002) compared with those without KIT mutations. No significant difference between pts with exon 8 sole mutation and those without KIT mutations. 45  

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