Table 3 The relationship between KIT or PDGFRA mutation status and preceding TKIs.

From: Different efficacy of tyrosine kinase inhibitors by KIT and PGFRA mutations identified in circulating tumor DNA for the treatment of refractory gastrointestinal stromal tumors

Sample No.

Preceding TKIs

Mutational statusa

KIT

PDGFRA

Exon 9

Exon 10

Exon 11

Exon 13

Exon 17

Exon 18

Exon 20

Exon 18

1

IM

Resistant

A502_Y503dup

N822K

N822Y

2

SU

No-resistant

A502_Y503dup

3

SU

Resistant

D820Y

4

REG

Resistant

W557G

5

REG

Resistant

V654A

6

SU

No-resistant

V654A

7

SU

Resistant

V569_L576del

 

N822K

8

SU

Resistant

S628G

K642E

N822K

9

IM

Resistant

A829P

10

REG

Resistant

V654A

N822K

11

IM

No-resistant

W557_E561del

12

SU

Resistant

F529S

E554_K558del

V654A

13

IM

Resistant

A502_Y503dup

14

REG

Resistant

 

E925K

D842_S847 > EF

15

IM

Resistant

A502_Y503dup

 

D820E

16

IM

No-resistant

D579del

17-1

REG

Resistant

D842_S847 > EF

17-2

IM

Resistant

D901N

E925K

D842_S847 > EF

  1. TKIs tyrosine kinase inhibitors, IM imatinib, SU sunitinib, REG regorafenib, PD progression disease, dup duplication, del deletion, > deletion-insertion.
  2. aKIT and PDGFRA mutation status to the most prior tyrosine kinase inhibitor was judged according to the previous reports refs. [23, 24]