Do both mutated and wild-type c-KIT MCTs respond to RTK inhibitors?

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Study for the ACVIM Small Animal Internal Medicine Exam to enhance your veterinary knowledge. Prepare with flashcards and multiple-choice questions, featuring hints and explanations. Ensure success in your exam journey!

Multiple Choice

Do both mutated and wild-type c-KIT MCTs respond to RTK inhibitors?

Explanation:
RTK inhibitors work by blocking KIT signaling, which is essential for mast cell tumor cell survival and proliferation. When KIT is mutated, it’s constitutively active, making the tumor highly dependent on KIT signaling and often highly responsive to inhibition. Wild-type KIT tumors can also respond if they rely on KIT signaling—through ligand-driven activation (SCF), overexpression, or other mechanisms—so blocking KIT can slow growth or cause tumor regression. In practice, both mutated and wild-type KIT mast cell tumors can show a response to RTK inhibitors, though the response is typically stronger and more predictable with KIT mutations.

RTK inhibitors work by blocking KIT signaling, which is essential for mast cell tumor cell survival and proliferation. When KIT is mutated, it’s constitutively active, making the tumor highly dependent on KIT signaling and often highly responsive to inhibition. Wild-type KIT tumors can also respond if they rely on KIT signaling—through ligand-driven activation (SCF), overexpression, or other mechanisms—so blocking KIT can slow growth or cause tumor regression. In practice, both mutated and wild-type KIT mast cell tumors can show a response to RTK inhibitors, though the response is typically stronger and more predictable with KIT mutations.

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