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. Author manuscript; available in PMC: 2016 Sep 7.
Published in final edited form as: Clin Cancer Res. 2015 Feb 18;21(10):2289–2296. doi: 10.1158/1078-0432.CCR-14-1630

Table 3.

Clinical melanoma subtype, associated KIT alterations, clinical response to prior therapy with a KIT inhibitor and clinical response to nilotinib in those with CNS involvement.

Study
Subject #
Melano
ma
Subtype
KIT
Mutatio
n
KIT
Amplificati
on
Prior
KIT
Inhibito
r+
RECIS
T
Respons
e to
Prior
KIT
Inhibito
r
PFS to
Prior
KIT
Inhibito
r
(Month
s)
RECIST
Respons
e to
Nilotinib
in non-
CNS
Lesions
(Best
Percent
Respons
e)
RECIST
Respons
e to
Nilotinib
in CNS
Lesions
(Best
Percent
Respons
e)
PFS to
Nilotini
b
(Month
s)
4 Mucosal Exon 11
V560D
Not Present
(FISH)
None n/a n/a SD
(−20%)
PR
(−36%)*
3.9
6 Acral Exon 11
W577R
Not Present
(FISH)
Imatinib Unk Unk SD
(−23%)
SDa
(11%)
6.6
7 Acral None Present
(qPCR)
Imatinib PD 1.7 SD
(3%)
PD
(37.5%)
2.1
10 Cutaneo
us
Exon 11
V560D
Not tested Imatinib PR 4.6 PD
(44%)
PD
(40%)
2.4
15 Mucosal Exon 11
L576P
Not tested None n/a n/a n/ab SD
(−25%)
2.9
16 Mucosal Exon 13
Y646D
Not tested Imatinib SD ~ 4 Uneval Uneval 0.2
17 Mucosal Exon 18
L831P
Not Present
(FISH)
Imatinib SD ~ 7 n/ab SD
(9%)
1.6
18 Mucosal Exon 11
L576P
Not tested Imatinib SD 2.8 SD
(14%)
PD
(0%)*
1.8

Abbreviations: Unk – Unknown

+

- All patients previously treated with a KIT inhibitor experienced progression on those agents and were not enrolled onto this study due to intolerance of prior therapy

*

- Signifies the development of progression in non-target lesions or the development of new lesions

a

– Patient 6 underwent resection of one symptomatic brain target lesion 1.6 months after initiation of therapy; a second CNS target lesion remained stable for 6.6 months after initiation of therapy; however, new CNS lesions were noted at that time and the patient was taken off for POD

b

- No non-CNS lesions present.