Table 1 Clinicopathologic characteristics of seven patients with FLT3-ITD+ AML treated on sorafenib monotherapy trial.

G, gender; A, age (in years); FAB, French-American-British classification; WCC, white cell count (109/liter); Blast, percentage of bone marrow blast cells; NPM1, nucleophosmin 1 mutation status; Karyo., karyotype; FLT3-TKD, FLT3 tyrosine kinase domain mutation status; Naïve, pre-sorafenib sample; Res., sample collected after disease evolution upon sorafenib treatment; NS, not specified; NA, not available; WT, wild type; Mut, mutated; 7 + 3, daunorubicin and cytarabine; HDAC, high-dose cytarabine; MTZ/VP16/AC, mitoxantrone, etoposide, and cytarabine; MACE-DEX, mitoxantrone, cytarabine, etoposide, and dexamethasone; ICE, idarubicin, cytarabine, etoposide; CLARA, clofarabine, cytarabine; MTZ/MDAC, mitoxantrone, medium-dose cytarabine; 5AZA, 5-azacytidine; Y and N, presence or absence of TKD mutations in sorafenib-naïve and sorafenib-resistant samples.

PatientG/AFABWCCBlastNPM1Karyo.Previous treatmentsFLT3-TKD*
NaïveRes.
AML#1M/54NS16781NAComplex7 + 3, HDAC×2, MACE-DEXNN
AML#2M/34M626 (75)WT46, XY7 + 3, ICE, CLARA, MTZ/MDAC, 5AZANY
AML#3F/57M11954WT46, XX7 + 3, MTZ/MDAC×3NN
AML#4§F/47NS2578Mut.46, XX7 + 3, ICE×2NY
AML#5F/87M126094NA46, XXNot eligibleNY
AML#6F/43NS1855WTComplex7 + 3, HDAC×2, MTZ/VP16/ACNN
AML#7F/67M110295NA46, XX7 + 3, HDAC×2, 5AZANY

*D835 mutation of FLT3-TKD was examined as described (18) on peripheral blood cells. †42~48,XY,del(5)(p13),+del(6)(q16),del(12)(p11.2),-14,-15,-17,t(17;19)(q21;p13),-20,+1~6mar[cp8]/46,XY[7]. ‡The percentage of blast cells of bone marrow was 75% among the nucleated cells. §The clinical information and the FLT3-TKD status of patient AML#7 have been reported (18). ¶46,XX,i(17)(q10)[6]/46,XX,del(5)(q34)[3]/46,XX,add(11)(p11.2)[2]/46,XX,del(11)(15.2)[2]/46,XX[20].