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PIT1
master switch shared by the cells that make prolactin, GH, and TSH
(high levels of prolactin suppress GnRh in the hypothalamus)
TPIT
corticotroph cell type —> ACTH excess causing Cushing disease
SF1
develops gonadotrophs (LH and FSH)
most common silent PitNET
Thyroid cancers
papillary/follicular —> oncoytic —> poorly differentiated —> anaplastic
moving along this spectrum, tumors lose thyroid-specific features
also become more aggressive and accumulate more mutations
Papillary carcinoma
BRAF V600E is the classic mutation
spread through lymphatics (commonly goes to cervical lymph node)
most common type of thyroid cancer
generally excellent prognosis
Follicular carcinoma
driver: RAS mutations (feed into growth-signaling pathways)
spread: invade blood vessels, spread hematogenously to bone and lung
rarely goes to lymph nodes
oncocytic carcinoma
follicular-derived tumor
cells are packed with abnormal mitochondria
mitochondria DNA mutations and widespread chromosomal loses
low RAI avidity, RAI therapy is less effective
poorly differentiated carcinoma
high-grade follicular cell cancer (btwn differentiated and anaplastic)
starts with RAS or BRAF mutation
acquires additional hits, especially TERT and p53 mutations
aggressive
reduced iodine avidity
anaplastic carcinoma
follicular cells that are undifferentiated
genetics: BRAF, RAS, p53, TERT
rapid, locally invasive growth
most lethal human cancers
fast-growing neck mass
near-complete loss of follicular cell identity
does not take up iodine
medullary carcinoma
parafollicular C cells (neuroendocrine cells)
RET mutations (germline in MEN2 or somatic)
biomarkers: calcitonin and CEA
doesn’t come from follicular cells —> doesn’t take up iodine, RAI is not useful
MEN1
menin
Parathyroid
Pituitary
Pancreatic
neuroendocrine tumors
MEN2A
RET
medullary thyroid carcinoma
pheochromocytoma
parathyroid disease hyperplasia
MEN2B
medullary thyroid carcinoma
pheochromocytoma
marfanoid habitus
MEN4
rare MEN 1 -like tumor predisposition syndrome