Table 1 AML patients’ main characteristics

From: MEK inhibition enhances the response to tyrosine kinase inhibitors in acute myeloid leukemia

Demographic data

Clinical features

Performed analysis

P (#)

Sex (M/F)

Age (y)

AML subtype (FAB)

Moment

Sample type

Blasts (%)

Cytogenetics (FISH)

FLT3 status

Other mutations

TKI treatment

Methods

1

M

71

M1

Diagnosis

BM

80

46, XY

L576P

No

Sorafenib

A

d + 5

PBMC

67 (PB)

B

d + 15

PBMC

40 (PB)

C

d + 188

PBMC

81 (PB)

C

d + 191

PBMC

81 (PB)

B

d + 195

PBMC

81 (PB)

B

2

M

63

M1

Diagnosis

BM clot

93

47, XY; der (2;8), +5, −7, +8

L576Q

No

Sorafenib

D

Relapse

BM clot

35

D

3

F

36

M2

Diagnosis

BM clot

77

46, XX

ITD

NPM1, DNMT3A, CBL

Midostaurin

D

Relapse

BM clot

39

D

4

M

66

M1

Relapse

BMMC

94

46, XY; +13,−21

WT

biCEBPA

No

E

5

F

59

M5

Diagnosis

BMMC

71

46, XX; del (8p)

WT

NPM1

No

E

6

M

76

M1

Relapse

BMMC

40

46, XY; −21

WT

No

No

E

7

M

75

M1

Diagnosis

BMMC

90

46, XY; del (8p)

WT

CEBPA

No

E

8

F

57

M5

Diagnosis

BMMC

78

47,XX; + 8, inv (16) (p13q22)

WT

CBFB/ MYH11

No

E

  1. P (#), patient number; M, male; F, female; y, years; d + , day; PBMC, peripheral blood mononuclear cells; BM, bone marrow; BMMC, bone marrow mononuclear cells; PB, peripheral blood; ITD, internal tandem duplication; WT, wildtype; biCEBPA, biallelic CEBPA mutations; TKI, tyrosine kinase inhibitor; A, whole exome sequencing; B, western blot; C, liquid chromatography tandem-mass spectrometry analysis; D, immunohistochemistry analysis; E, drug sensitivity assay.