REVIEW
Pathology of Pituitary Tumors Update: With World Health
Organization new Classification 2017
Robert Y. Osamura, MD
(AJSP: Reviews & Reports 2017;22: 189–195)
P ituitary adenomas constitute approximately 15% of all intra-
cranial neoplasms. The majority of pituitary tumors are adeno-
mas, which are benign and noninvasive (confined to the sella
turcica). Invasive adenomas are frequent. Pituitary carcinomas
are a rare condition, accounting for only 0.1% to 0.2% of all pitu-
itary endocrine tumors. The pituitary endocrine tumors are clini-
cally functioning with clinical hormonal symptoms, that include
acromegaly, Cushing disease, Graves disease; or nonfunctioning
without clinically apparent hormone production. Most of pituitary
adenomas are benign, and metastases (pituitary carcinoma) are
very rare. However, aggressive or invasive behavior is not uncom-
mon, and the tumor often (approximately 50%) extends beyond
the sellar region and reaches the sphenoid sinus and further to
the internal carotid artery. The pituitary adenomas are currently
classified according to the hormones they produce and to the basic
features of electron microscopy (EM). Recently, pituitary ade-
noma classification has changed regarding aggressive lesions.
The previous World Health Organization (WHO) classification
published in 2004 consisted of typical adenomas, atypical ade-
noma, and carcinoma. The atypical adenoma was defined as a
tumor with Ki67 index greater than 3% and strong p53 immu-
nostaining.1 The incidence of the atypical adenomas is rela-
tively low2,3 and not closely related to aggressive behavior,3
p53 mutation occurs predominantly in pituitary carcinoma, and
pituitary adenomas lack its mutation.4 The carcinomas can be di-
agnosed only when the tumor shows meningeal spread or metas-
tases, intracranial and extracranial.1 Now it has been clarified that
most of the “nonfunctioning” tumors are immunohistochemically
positive for hormones, that is, growth hormone (GH), prolactin
(PRL) and adrenocorticotropic hormone (ACTH),1 or gonadotroph
subunits or gonadotropin, that is, αSU, follicle stimulating hormone
βSU, and luteinizing hormone βSU.2 The former group1 has been
designated as “silent” adenoma,5,6 and the latter group2 has been
most frequently seen in the clinically nonfunctioning adenoma.
The pituitary carcinomas are rare, but they produce PRL or ACTH
when they produce hormones.
Since previous WHO classification was published in 2004,
new information has accumulated regarding pituitary adenomas
that has been integrated in the new WHO 2017 classification
(Table 1).7 Even though most terminology is based on the features
defined by EM, currently, immunohistochemistry is the method
for diagnosis in most cases. The classification of “typical or
atypical adenoma,” which was based on Ki67 and p53, is not
International University of Health and Welfare, Graduate School, Tokyo and
Department of Diagnostic Pathology, Nippon Koukan Hospital, Kawasaki,
Japan.
Reprints: Robert Y. Osamura, MD, Department of Diagnostic Pathology,
Nippon Kokan Hospital, 1-2-1 Koukandori, Kawasaki-ku, Kawasaki,
Kanagawa, Japan 210-0852. E‐mail: osamura@iuhw.ac.jp.
The author has no funding or conflicts to declare.
Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 2381-5949
DOI: 10.1097/PCR.0000000000000180
AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017
Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.
recommended in WHO 2017 classification. Instead, we encour-
age using the terminology of clinically aggressive adenoma.3
The basic concepts of the new WHO classification of pitui-
tary adenomas are summarized in the following list.
Basic concepts for WHO 2017 classification
1. Pituitary adenomas are derived from committed mature pitui-
tary cells: somatotroph adenoma, transcription factors.
2. Electron microscopy is not used as routine procedure. Immuno-
histochemistry is used for classification.
3. “Atypical adenoma” is not recommended. Ki67 index should
be analyzed. p53 is a good indicator of malignancy.
4. Morphologic subclassification for prognostication: sparsely
granulated somatotroph adenoma, Crooke cell (corticotroph)
adenoma and others
5. Multihormonal Pit-1–positive adenoma (previous silent sub-
type 3 adenoma)
6. Null cell adenomas—hormone negative and transcription
factor negative
7. Predictive biomarkers for therapy
8. Genetic predisposition
Key issues in the new WHO 2017 classification include
(1) transcription factors that promote differentiation of the pitui-
tary cells, (2) some morphologic features are associated with more
aggressive behavior, (3) various genetic background is associated
with pituitary adenomas, and (4) prognostic and predictive bio-
markers for pituitary adenomas.
Transcription Factors for Pituitary Hormone
Production: Prop-1, Pit-1, Sf-1, Gata-2,
Tpit, NeuroD1
Now it is well known that the differentiation of pituitary
hormone–producing cells is regulated by the transcription factors
with synergistic effects of cofactors. The differentiation toward
GH, PRL, and PRL depends on the transcription factor, Pit-1, to-
ward ACTH on Tpit, and toward FSH on SF-1, as indicated in the
diagrams (Figs. 1 and 2). By immunohistochemistry, these tran-
scription factors are detected in the nuclei.8
For new WHO classification, the diagnosis of plurihormonal
Pit-1–positive adenomas, designated as silent subtype 3 adeno-
mas, needs to demonstrate Pit-1 in the tumor cells,9 and the di-
agnosis of true null cell adenomas needs to be negative for
transcription factors in addition to negative pituitary hormones
or glycoprotein subunits.
Based on the transcription factors, it has been clarified that
the pituitary adenomas develop from the mature hormone-
producing cells, that is, somatotrophs (GH), lactotrophs (PRL),
thyrotrophs [thyroid stimulating hormone (TSH)], and gonadotrophs
(FSH, LH), and in the new WHO 2017 classification, we use termi-
nologies such as “somatotroph adenoma,” “lactotroph adenoma,”
“thyrotroph adenoma,” “corticotroph adenoma,” and “gonadotroph
adenoma” instead of previous “GH-, PRL-, TSH-, ACTH-, and FSH-
producing adenomas” (Table 2). Regarding the null cell adenomas,
Nishioka et al10 reported that 119 (95%) of hormone-negative adenomas
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Osamura AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017

TABLE 1. Morphofunctional Classification of Pituitary Adenomas (WHO 2017 Classification)

Transcription Factors
Adenoma Type Immunophenotype and Other Cofactors
Somatotroph adenoma Densely granulated GH ± PRL ± α subunit PIT1
somatotroph adenoma*
LMWCK: perinuclear or diffuse
Sparsely granulated somatotroph adenoma GH ± PRL PIT1
LMWCK: fibrous bodies
Mammosomatotroph adenoma GH + PRL (in same cell) ± α subunit PIT1, ER-α
Mixed somatotroph and GH + PRL (in different cells) ± α subunit PIT1, ER-α
lactotroph adenoma
Lactotroph adenoma Sparsely granulated lactotroph adenoma* PRL PIT1, ER-α
Densely granulated lactotroph adenoma PRL PIT1, ER-α
Acidophilic stem cell adenoma PRL, GH (focal and inconstant)LMWCK:
fibrous bodies (inconstant)
Thyrotroph adenoma TSH-β, α subunit PIT1, GATA2
Corticotroph adenoma Densely granulated corticotroph adenoma* ACTH, LMWCK: diffuse pattern TPIT
Sparsely granulated corticotroph adenoma ACTH, LMWCK: diffuse pattern TPIT
Crooke cell adenoma ACTH, LMWCK: ring-like pattern TPIT
Gonadotroph adenoma Sparsely granulated FSH-β, LH-β, α subunit SF-1, GATA2,
gonadotroph adenoma* (various combinations) ER-α (variable)
Null cell adenoma — No markers None
Plurihormonal adenomas Plurihormonal PIT1-positive adenoma† GH, PRL, TSH-β ± α subunit PIT1
Adenomas with unusual Various combinations Other transcription
immunohistochemical combinations factors (variable)
Double adenomas Distinct adenomas Usually PRL and ACTH, respectively PIT1 and TPIT,
respectively
*Most common subtype.
†Previously called silent subtype 3 adenoma.

showed mutually exclusive lineage-specific differentiation as Pathologic Predictors of Prognosis

gonadotrophs (SF-1 positive), corticotrophs (Tpit positive), or
somatotrophs/mammosomatotrophs/lactotrophs/thyrotrophs
(Pit-1 positive) in 79 cases (66.4%), 32 cases (26.9%), and 2
cases, respectively. Thus, the incidence of true null cell adenomas
should be very rare (Figs. 3 and 4).
In addition to proliferative activity associated with aggressive
behavior of the pituitary adenomas,11 some morphological charac-
teristics are associated with more aggressive behavior. These fea-
tures are sparsely granulated adenoma with fibrous bodies and

FIGURE 1. Differentiation of pituitary cells in rodents: transcription factors. Modified after Scully KM & Rosenfeld MG Science 2002.

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AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017
FIGURE 2. Differentiation of pituitary cells in human: transcription factors. Modified after Osamura RY et al. Pituitary 1999;1(3–4):269-271.
Crooke cell adenoma, null cell adenoma, and plurihormonal Pit-1–
positive adenoma (previous silent subtype 3 adenoma) (Fig. 5).12,13
(a) Sparsely granulated adenoma is the somatotroph adenoma
originally defined by EM as the tumor with fewer numbers of
secretory granules in contrast to densely granulated adenomas
with many dense secretory granules. The sparsely granulated
adenomas are also characterized by the presence of fibrous
bodies. The fibrous bodies are small globular inclusions of
keratin in the cytoplasm, demonstrated by immunohistochem-
istry. Thus, immunohistochemistry has substituted EM for
the diagnosis of this category. For diagnosis, we need
TABLE 2. Morphofunctional Classification of Pituitary Adenomas (WHO 2017 Classification)
Adenoma Type
Somatotroph adenoma
Lactotroph adenoma
Thyrotroph adenoma
Corticotroph adenoma
Gonadotroph adenoma
Null cell adenoma
Plurihormonal adenomas
Double adenomas
*Most common subtype.
†Previously called silent subtype 3 adenoma.
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Pathology of Endocrine Tumors Update
immunohistochemistry for GH and keratin (CAM5.2) to dem-
onstrate GH and fibrous bodies.
(b) Crooke adenomas are defined as one of the subtypes of
corticotroph adenomas, which are characterized by ring-like ac-
cumulation of keratin in the cytoplasm of ACTH-positive tumor
cells.14 For diagnosis, similarly, we need immunohistochemis-
try, ACTH, and CAM5.2.
(c) Plurihormonal Pit-1–positive adenoma (previous silent sub-
type 3 adenoma) is the tumor that is frequently nonfunction-
ing and is immunohistochemically positive for GH, PRL, and
sometimes TSH or ACTH. The tumor cells are positive for
Pit-1. Usually, the tumors are macroadenoma and invasive.13
Densely granulated somatotroph adenoma*
Sparsely granulated somatotroph adenoma
Mammosomatotroph adenoma
Mixed somatotroph and lactotroph adenoma
Sparsely granulated lactotroph adenoma*
Densely granulated lactotroph adenoma
Acidophilic stem cell adenoma
Densely granulated corticotroph adenoma*
Sparsely granulated corticotroph adenoma
Crooke cell adenoma
Sparsely granulated gonadotroph adenoma*
Plurihormonal PIT1-positive adenoma†
Adenomas with unusual immunohistochemical combinations
Distinct adenomas
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Osamura AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017

FIGURE 3. Densely granulated somatotroph adenoma. Acidophilic adenoma (left) and strong granular staining for GH in the cytoplasm of
the tumor cells (right).

Genetic Predisposition and Susceptibility
The majority of pituitary adenomas are sporadic. However, a
significant number of cases are related to germline genetic abnor-
malities, most commonly resulting in somatotroph and lactotroph
subtypes. Genetic background for the pituitary tumor development
includes multiple endocrine neoplasia type 1 (MEN1), MEN4, Car-
ney complex, SDHx-related familial syndrome, McCune-Albright
syndrome, and Dicer syndrome.
With this background (familial pituitary tumor syndrome),
the pituitary tumors are frequently associated with PRL or GH
production as follows.15 Clinical algorithm to approach this con-
dition has been proposed.15
MEN1: lactotroph adenomas (60%), somatotroph adenomas (10%);
Carney complex: somatotroph adenoma and/or lactotroph ade-
nomas or hyperplasia;
Familial isolated pituitary adenoma: lactotroph adenoma,
somatotroph adenoma, or mixed GH/PRL-secreting adenomas
(41%, 30%, and 7%, respectively).
and AIP, and it is known that the heterozygote knockout models
of these genes in rodents develop pituitary adenomas.
Predictive Biomarkers
The detection of certain molecules can be predictive for the
selection of molecular target therapies.
Somatostatin Receptor
It is well known that there are 5 subtypes, that is, SSTR1,
SSTR2, SSTR3, SSTR4, and SSTR5. The pituitary adenomas,
particularly somatotroph adenomas, are frequently positive for
SSTR2 and SSTR5. Recently, specific monoclonal antibodies
for immunohistochemistry are commercially available.17,18
It has been widely known that the detection of SSTR2 may
predict the effects of molecular target therapies, such as
octreotide (Fig. 6).

The unique situation in these syndromes is Dicer syndrome,
which includes pituitary blastoma,16 in addition to the other
various conditions.
The genetic background of these syndromes includes
germline mutations of MEN1, PRKAR1A, CDKN1A, SDHB,
MGMT and MSH6
Epigenetic silencing of the MGMT (O6-methylguanine–
DNA methyltransferase) DNA repair gene by promoter methylation
compromises DNA repair and has been associated with longer
survival in patients with glioblastoma who receive alkylating

FIGURE 4. Sparsely granulated somatotroph adenomas. Less acidophilic tumor cells (left), GH localized at the periphery of tumor
cells (middle), keratin-positive fibrous bodies are seen in the cytoplasm (right).

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AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017 Pathology of Endocrine Tumors Update

FIGURE 5. Crooke cell adenoma H&E staining (left), ACTH (middle) and Keratin (CAM5.2) (right) Ring-like pink cytoplasm (left), peripheral
staining for ACTH (middle) and ring-like keratin staining (right).

agents such as temozolomide (TMZ).19 In the pituitary adenomas
and carcinomas, decreased staining for MGMT by methylation is
associated with response to TMZ therapy.20,21 Hirohata et al22 re-
ported the association of MSH6 immunostaining with the effects
of TMZ therapy in pituitary adenomas and carcinoma (Fig. 7).
Pathology report on pituitary adenomas should include
the following:
Classification of adenoma (WHO 2017 classification);
Size of tumor: microadenoma, macroadenoma, giant adenoma
clinically functioning, clinically nonfunctioning, silent
invasive, noninvasive (Knosp grades 1–4);
Adenoma or carcinoma;
Immunohistochemistry for hormones and subunits-GH, PRL,
TSHβSU, ACTH, follicle stimulating hormone βSU, luteiniz-
ing hormone βSU, αSU;
Immunohistochemistry, in addition to hormones and subunits:
chromogranin A, keratin (low molecular weight: CK7/8
[CAM5.2], CK18);
Proliferative markers: Ki67, p53 (in some cases);
Transcription factors and cofactors: Pit-1, SF-1, ERa, Tpit,
GATA2, NeuroD1;
Predictive therapeutic factors: SSTR2, SSTR5, MGMT, MSH6.
SUMMARY
In this review, we discussed key issues in the new WHO
morphofunctional classification of pituitary tumors, mainly adeno-
mas (Tables 3 and 4). The new classification includes not only ad-
enoma types, but also immunophenotypes and transcription factors
with other cofactors. As atypical adenoma designation in 2004 is
rare and does not predict behavior, the new WHO classification
does not recommend using this terminology. In addition to pro-
liferative activity, other morphologic features suggest aggressive
behavior of pituitary adenomas, that is, sparsely granulated
somatotroph adenoma and Crooke cell adenoma. Some pituitary
adenomas, frequently along the Pit-1 lineage with GH and PRL
positivity, occur in MEN1, Carney complex, and others. Immuno-
histochemical detection of SSTR2, MGMT, and MSH6 is impor-
tant to predict the therapeutic response to octreotide and TMZ.

FIGURE 6. Immunohistochemical staining of SSTR2-positive rate of SSTR2 and SSTR5. Strong positive staining on the cell membrane of the
adenoma cells (right). Positive rate of the staining of SSTR2 and SSTR5 in pituitary adenomas. SSTR2 is frequently positive in somatotroph and
thyrotroph adenomas (left panel of the left), SSTR5 is frequently positive in corticotroph adenoma and somatotroph adenomas (right panel of
the left).

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Osamura AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017

FIGURE 7. Immunohistochemistry of MGMT and MSH6. Staining is negative when MGMT is methylated and lacks its function. The negative
MGMT staining is associated with response to TMZ. Nuclear staining for MSH6 is also associated with therapeutic response to TMZ in
pituitary adenomas and carcinomas.

TABLE 3. Additional Parameters That May Be Added to the Morphofunctional Types

Tumor size Microadenoma (<1 cm), macroadenoma (1–4 cm),

or giant adenoma (>4 cm)
Tumor’s clinical presentation Clinically functioning, clinically nonfunctioning, or silent
Invasiveness on magnetic resonance imaging (Knosp grade) Noninvasive (grade 1 or 2) or invasive (grade 3 or 4)
Metastasis or spinal spread Carcinoma
Additional immunohistochemistry • Chromogranin A
• Low-molecular-weight cytokeratin: CK7/8 (CAM5.2), CK18
• Proliferation markers: Ki67, p53 (in some cases)
• Transcription factors and cofactors: PIT1, SF-1, ER-α, TPIT,
GATA2, NeuroD1
• Predictive markers: SSTR2, SSTR5, MGMT, MSH6

TABLE 4. Genetic Predisposition to Pituitary Adenomas

Syndromic Diseases Isolated Pituitary Disease

MEN1 Familial isolated pituitary adenoma (somatotroph) (AIP)
Multiple endocrine neoplasia type 4 (CDKN1B) X-linked acrogigantism syndrome (GPR101)
SDH-related familial paraganglioma and pheochromocytoma syndromes Familial isolated pituitary adenoma (unknown)
(SDHA, SDHB, SDHC, SDHD, SDHAF2)
Carney complex (PRKAR1A, PRKACA)
McCune-Albright syndrome (mosaic GNAS)
Neurofibromatosis (very rare) (NF1)
Von Hippel-Lindau syndrome (VHL)
DICER1 syndrome (DICER1)

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AJSP: Reviews & Reports • Volume 22, Number 4, July/August 2017
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