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The five selected primary GISTs showed different primary mutations in KIT exon 11 and different emerging secondary KIT mutations in exon 13, 14 and 17.
This observation suggests that the development of a secondary KIT mutation is an important escape mechanism for tumour cells of which KIT-dependent proliferation is chronically inhibited by imatinib.
In gene mutation analysis, a secondary KIT gene mutation was detected in one case.
Moreover, gene mutation analysis revealed that lesions acquired resistance via secondary KIT mutations in addition to primary KIT mutations.
Moreover, with regard to nilotinib resistance, secondary KIT mutations might be involved, similarly to those involved in imatinib resistance.
In imatinib-resistant lesions, secondary KIT mutations were usually acquired in addition to primary KIT mutations [10 12].
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The bound primary antibody was detected using a ready-to-use secondary antibody kit (Histostain-Plus kit, Jingmei, Shenzhen, China) and the chromogenic substrate 3,3-diaminobenzidine tetrahydro-chloride.
In this setup, we can simulate faults in a transmission line in PSCAD; after that, the transient data for the fault is sent to a secondary test kit to generate three phase's fault voltage and current.
A universal peroxidase-conjugated secondary antibody kit (LSAB System, DakoCytomation, USA) was used for the detection system.
For immunohistochemistry, the anti-VHR antibody was revealed using an HRP secondary detection kit (Universal LSABTM 2 KIT/HRP, Rabbit/Mouse, DakoCytomation).
A universal peroxidase-conjugated secondary antibody kit (LSAB System, DakoCytomation, USA) was used for the detection system, and diaminobenzidine (DAB) was the applied chromogen.
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