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Table 1 Clinical characteristic of 10 AML patients and their CI values

From: A loss-of-function genetic screening reveals synergistic targeting of AKT/mTOR and WTN/β-catenin pathways for treatment of AML with high PRL-3 phosphatase

Patient ID

Sex

Age (years)

FAB

Karyotype

FLT3

NPM1

PRL-3 status*

Average CI values

Pt#1

M

44

M5

47,XY,+8

FLT3-ITD

WT

35

0.29

Pt#2

M

70

M4

Normal

WT

N.A.

21

0.35

Pt#3

F

34

M4

Inv(16)(p13.1q22)

N.A.

N.A.

23

0.33

Pt#4

M

62

M3

add(14)(q24)

FLT3-ITD

Mutant

19

0.47

Pt#5

F

41

M2

Normal

FLT3-ITD

Mutant

15

0.68

Pt#6

F

37

M5

Normal

WT

N.A.

0.8

1.31

Pt#7

M

33

M4

t(3;7)(p25;q22)

N.A.

N.A.

1.9

0.96

Pt#8

F

75

M2

Normal

WT

N.A.

1.3

1.20

Pt#9

M

26

M0

Complex

WT

WT

0.7

1.45

Pt#10

F

68

M2

Normal

WT

Mutant

1.8

0.98

  1. Pt# indicates unique patient number
  2. FAB French-American-British, Normal normal karyotype, FLT3 FMS-like tyrosine kinase 3, ITD internal tandem duplication, NPM1 nucleophosmin 1, N.A. not available, WT wild type, CI combination index
  3. *qRT-PCR analysis was applied to determine the expression of PRL-3 gene in a serial of primary AML samples. The baseline expression of PRL-3 in OCI-AML2 was used to normalize the fold changes of PRL-3 gene in primary AML cells. Here, patients with PRL-3 expression more than 10fold higher than its expression in OCI-AML2 cells were defined as PRL-3 high, while for patients whose PRL-3 expression were less than twofold higher or lower than its expression in OCI-AML2 cells, they were classified as PRL-3 low