Biomedical Engineering Reference
In-Depth Information
During the early stages of imatinib therapy, decrease in tumor
size may not follow changes in tumor density but patients may
experience clinical benefit with improvement of symptoms even
in the absence of tumor shrinkage. Tumor size may even increase
in size in case of intratumoral bleeding or myxoid degeneration.
Peritoneal tumor implants may resolve rapidly whereas tumors in
the liver may take longer time to regress. Maximum response may
be seen until 6 to 12 months or longer with imatinib. Stable disease
in CT has been demonstrated to predict time to treatment failure.
The results of a pilot study on the predictive power of change in
CT bidimensional measurements,
change in PET SUV
, and PET
max
SUV
of treatment was reported by
Holdsworth and colleagues [126]. They found that no reduction in
the CT bidimensional tumor measurements at 1 month is an effective
indicator of prolonged clinical benefit in patients with advanced
GIST. PET seems to detect earlier and greater number of responses
than CT. Responses can be observed within 24 hours of initiating
imatinib.
at 1 month after initiation
max
9.4.3.2
Adjuvant therapy
The primary therapy for localized GIST is surgery with complete
resection and negative margins. Although the majority of patients
with localized GIST are able to undergo complete surgical resection,
only about one-half are free of recurrence at 5 years or longer. In a
single institution report of 200 patients with GIST, patient, tumor,
and treatment variables were analyzed to identify patterns of tumor
recurrence and factors that predict survival. Tumor size was found
to be predictive of disease-specific survival in patients with primary
disease who undergo complete gross resection [127, 128].
9.4.4
Biomarkers That Predict Benefit, Response, and
Resistance to Therapy
9.4.4.1
Response predictors in GIST
As discussed in Section 9.2, the majority of GISTs harbor activating
mutations of
. A number of randomized
clinical trials have demonstrated that the mutational status of these
oncoproteins, especially
KIT
,
PDGFRA or BRAF
KIT
, is predictive of clinical response to
