Table 1 Patient characteristics by treatment.

From: Molecular ontogeny underlies the benefit of adding venetoclax to hypomethylating agents in newly diagnosed AML patients

 

Overall (N = 314)

Treatment group, N (%)

p-value

HMAa (N = 148)

HMA + VEN (N = 166)

Sex (male)

186 (59)

91 (61)

95 (57)

0.5

Age (years, median, range)

73.7 (25.2, 89.6)

74.0 (42.4, 88.5)

73.7 (25.2, 89.6)

0.4

Age categories (% within age group)

– <60 years

32 (10)

11 (7)

21 (13)

0.4

– 60 to <75 years

152 (48)

72 (49)

80 (48)

>0.9

– ≥75 years

130 (41)

65 (44)

65 (39)

0.8

Prior MDS, MPN or MDS/MPN overlap

111 (35)

48 (32)

63 (38)

0.3

Prior myeloid disease directed therapy

– HMA

35 (11)

17 (11)

18 (11)

0.9

– Prior alloHCT

29 (9)

12 (8)

17 (10)

0.6

– t-AML

87 (28)

39 (26)

48 (29)

0.7

Cytogeneticsb

– Normal

80 (29)

38 (29)

42 (29)

0.9

– 5/7/17 abnormalities

94 (34)

47 (36)

47 (32)

0.4

– Complex karyotype

116 (42)

55 (43)

61 (41)

>0.9

ELN 2022 risk stratification

– Favorable

39 (12)

15 (10)

24 (14)

>0.9

– Intermediate

40 (13)

21 (14)

19 (11)

>0.9

– Adverse

235 (75)

112 (76)

123 (74)

0.8

Ontogeny group

– De-novo

88 (28)

50 (34)

38 (23)

0.1

– Secondary

115 (37)

47 (32)

68 (41)

0.2

– TP53

111 (35)

51 (34)

60 (36)

0.8

  1. HMA hypomethylating agents, VEN venetoclax, MDS myelodysplastic syndrome, MPN myeloproliferative syndrome, alloHCT allogeneic hematopoietic stem cell transplantation, t-AML - therapy related AML, CBF core binding factor, ELN European leukemia network, AML acute myeloid leukemia, Ven venetoclax.
  2. a21/148 (14%) in the HMA group received additional non-venetoclax drug: FLT3 inhibitors (n = 5), CD33 antibody (n = 5),APR246 (n = 3), Syk inhibitor (n = 2), ipilimumab (n = 2) and one of each of the following – CD123 antibody, CD47 antibody, IDH1 inhibitor, MUC1 inhibitor.
  3. bCytogenetics known for 77 De-novo patients, 102 Secondary patients and 103 TP53 patients.