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Figure 1.
Overview of the KIT gene and protein. (A) Schematic
representation of KIT showing location of functional domains,
primary (1°) and secondary (2°) mutations (mut.).
Frequencies of primary KIT genotypes, specific secondary KIT
mutations, and resistance (R) or sensitivity (S) to imatinib
(IM) or sunitinib (SU) were those reported in a phase I/II trial
of sunitinib in advanced GIST after imatinib failure (6). V560D,
substitution of Asp for Val at residue 560. (B) The unactivated,
autoinhibited and activated forms of WT KIT (7, 8). The JM
domain (red), A-loop (green), and C α-helix (cyan) are oriented
differently in the autoinhibited and activated states. *V560D
generally occurs as a primary mutation.
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