Step 1: Identify what RET codes for - a transmembrane receptor tyrosine kinase. Like other such receptors, when a gain-of-function mutation locks it in the active state it triggers uncontrolled proliferation of whichever cells normally express it.
Step 2: Map RET to its tissues. RET is switched on in the thyroid C cells, adrenal medulla and parathyroid precursors. The thyroid C cell tumour that springs from constitutive RET activation is the medullary carcinoma, which secretes calcitonin and clusters in the MEN 2 syndromes. So the correct association is medullary carcinoma of the thyroid.
Step 3: Eliminate the distractors. Astrocytoma is a glial CNS tumour without a RET link. Paraganglioma is the hallmark of succinate dehydrogenase (SDH) mutations. Hurthle cell tumour is a follicular-cell oncocytic neoplasm, distinct from the C-cell origin of RET-driven cancer.
\[\boxed{\text{Medullary carcinoma of the thyroid}}\]