Pituitary neuroendocrine tumours (PitNETs): overview

Lesion

Most pituitary tumours are benign growths of one hormone-making cell line. They cause trouble by making too much hormone or by pressing on nearby nerves.

Updated Nov 12, 2026

What it is

Pituitary neuroendocrine tumours, the current name for pituitary adenomas, arise from the cells of the anterior lobe. They are now sorted by the transcription factor that marks their lineage (PIT1, TPIT or SF1) and by the hormones they contain, not by how the cytoplasm stains. A tumour can be functioning or silent, small or large, and its effects come from hormone excess, from compression of normal gland, optic chiasm and cavernous sinus, or from sudden haemorrhage.

Structure

Gross: soft, well-demarcated tan nodule; large tumours erode the sella, lift the diaphragma sellae and may invade the cavernous sinus.
H&E: sheets or cords of uniform, monotonous cells with a delicate capillary network; the mixed acinar pattern of normal gland is lost (reticulin breakdown).
Immunohistochemistry: hormones (GH, PRL, ACTH, TSH, FSH/LH) plus transcription factors (PIT1, TPIT, SF1); Ki-67 helps judge growth.
Corticotroph tumours: basophilic, PAS-positive cells; in Cushing disease the normal corticotrophs show Crooke hyaline change (keratin rings).
Invasion of bone or dura is common and does not by itself mean malignancy.

Step by step

A clone of anterior pituitary cells acquires a driver, often in a G-protein or signalling gene (GNAS in many somatotroph tumours, USP8 in corticotroph tumours).
The clone keeps its lineage factor and keeps making, to a variable degree, its normal hormone.
Excess hormone gives a syndrome: hyperprolactinaemia, acromegaly, Cushing disease or, rarely, central hyperthyroidism.
As it grows upward it presses on the chiasm; laterally it encases the cavernous sinus and cranial nerves III, IV and VI.
Compression of the remaining gland lowers other hormones; bleeding into the tumour causes apoplexy.

PitNET lineages and what each makes

Lineage (factor)	Tumour type	Hormone excess	Syndrome
PIT1	Lactotroph	Prolactin	Galactorrhoea, amenorrhoea, low libido
PIT1	Somatotroph (and mammosomatotroph)	Growth hormone (± prolactin)	Gigantism or acromegaly
PIT1	Thyrotroph	TSH	Central hyperthyroidism (rare)
TPIT	Corticotroph	ACTH	Cushing disease, or silent
SF1	Gonadotroph	FSH/LH, usually ineffective	Mostly silent; mass effects
None	Null-cell	None	Mass effects only

Markers

PIT1
TPIT
SF1
GH
PRL
ACTH
Ki-67
Synaptophysin

Clinical notes

Silent macroadenomas present late with headache, visual-field loss and hypopituitarism.
Corticotroph tumours are usually microadenomas; after bilateral adrenalectomy they can enlarge aggressively (Nelson syndrome) with hyperpigmentation.
PitNETs occur in MEN1 and MEN4, in Carney complex and in familial isolated pituitary adenoma (AIP).

Test yourself

Think of the answer, then tap the question to see it.

Which visual field defect does a pituitary macroadenoma typically cause, and why?

Bitemporal hemianopia, because it compresses the crossing nasal retinal fibres in the optic chiasm.

What defines a metastatic PitNET (formerly pituitary carcinoma)?

Spread outside the sella, to the craniospinal axis or distant sites; cytologic atypia or local invasion alone is not enough.

Which lineage factor marks corticotroph tumours?

TPIT (TBX19).

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Pituitary Adenoma (StatPearls (NCBI Bookshelf), 2025); Pituitary Tumors Treatment (PDQ®)–Health Professional Version (National Cancer Institute, 2025).

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Representative model, for educational purposes only.