Table. 1 Demographic data of AML patients with their cytogenetic abnormalities and genetic lesions classified by functions.

From: Interrogation of novel CDK2/9 inhibitor fadraciclib (CYC065) as a potential therapeutic approach for AML

Sample

Sex

Age (years)

Karyotype

Genetic lesions

Signaling genes

DNA methylation-related genes

Chromatin-modifying genes

Nucleophosmin gene

Cohesin complex genes

Spliceosome complex genes

Transcription factor fusions

An investigation of the effect of fadraciclib on primary AML cells harboring KMT2A-PTD or KMT2A WT

AML 22

M

68

Normal

FLT3-ITD

DNMT3A, TET2

KMT2A-PTD

  

SRSF2

RUNX1

AML 20B

M

80

NA

  

KMT2A-PTD

   

U2AF1

 AML H002

NA

NA

Normal

 

IDH2

KMT2A-PTD, ASXL1

    

 AML 12

F

65

Normal

 

DNMT3A

KMT2A-PTD

    

 AML 17

M

72

Trisomy 21

NRAS

 

KMT2A-PTD, ASXL1

NPM1

  

U2F1

 AML 18

M

68

Normal

NRAS

TET2

ASXL1, EZH2

    

 AML 13

F

43

Normal

FLT3-ITD

  

NPM1

   

 AML 44

M

79

Monosomy 7

FLT3-ITD

DNMT3A, IDH2

     

 AML 5

M

46

Trisomy 8 t(15;17)

 

TET2

ASXL1

  

SRSF2

 

 AML 36

M

78

Trisomy 11

 

DNMT3A, IDH1

  

STAG2

SRSF2

 

Drug combination studies

 AML H002

NA

NA

Normal

 

IDH2

KMT2A-PTD, ASXL1

    

 AML 44

M

79

Monosomy 7

FLT3-ITD

DNMT3A, IDH2

     

 AML 52

M

73

Normal

FLT3-ITD

DNMT3

 

NPM1

RAD21

  

 AML 31

F

56

Complex

KIT

  

NPM1

   

 AML 36

M

78

Trisomy 11

 

DNMT3A, IDH1

  

STAG2

SRSF2

 

 AML 22

M

68

Normal

FLT3-ITD

DNMT3A TET2

KMT2A-PTD

  

SRSF2

RUNX1