Biomedical Engineering Reference
In-Depth Information
imatinib. The type of mutation in
also correlate
with clinical outcome to imatinib. In the B2222 phase II trial,
activating mutations in
KIT
and
PDGFRA
were observed in 88 and
4.7 percent, respectively. All KIT mutant isoforms were associated
with positive response to imatinib. However, only a subset of patients
with
KIT
and
PDGFRA
PDGFRA
mutation responded to imatinib. The patients with
exon 11
mutations experienced partial response rate of 86%,
whereas patients with tumors containing exon 9
KIT
KIT
mutations or
no detectable mutation of
KIT
or
PDGFRA
had partial response rates
of 48% (
< .0001), respectively [28]. Patients
whose tumors demonstrated exon 11
p
= .0006) and 0.0% (
p
mutations had a longer
event-free and overall survival than those whose tumors expressed
either exon 9
KIT
KIT
mutations or had no detectable kinase mutation
(Fig. 9.5).
Figure 9.5
Tumor genotype is of major prognostic significance for overall
survival in patients treated with imatinib for advanced GISTs.
Overall survival according to
mutational status.
LL, lower limit; UL, upper limit; N/A, not available. Adapted
with permission from Blanke [28].
KIT
and
PDGFR
