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Prostate Cancer BJUI Mini Reviews - Rare and Unusual Histological Variants of Prostatic Carcinoma: Clinical Significance
Prostate Cancer BJUI Mini Reviews - Rare and Unusual Histological Variants of Prostatic Carcinoma: Clinical Significance
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| BJUI Mini Reviews - Rare and Unusual Histological Variants of Prostatic Carcinoma: Clinical Significance |
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| Sunday, 04 November 2007 | ||
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This review examines the clinicopathological features
of several unusual histological
variants of prostatic carcinoma including small cell
carcinoma, ductal adenocarcinoma,
sarcomatoid (carcinosarcoma), basal cell,
squamous cell and adenosquamous, and
urothelial carcinoma.
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![©
2008 THE AUTHORS
JOURNAL COMPILATION
©
2008 BJU INTERNATIONAL | 102, 1369–1374 | doi:10.1111/j.1464-410X.2008.08074.x
1369
Roberta Mazzucchelli, Antonio Lopez-Beltran*, Liang Cheng
†
,
Marina Scarpelli, Ziya Kirkali
‡
and Rodolfo Montironi
Section of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals,
Ancona, ItalySection of Pathological Anatomy, Polytechnic University of the Marche Region, School of Medicine, United Hospitals,
Ancona, Italy, *Department of Pathology, Reina Sofia University Hospital and Faculty of Medicine, Cordoba, Spain,
†
Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN, USA,
and
‡
Department of Urology, School of Medicine, Dokuz Eylül University, Izmir, Turkey
Accepted for publication 14 May 2008
that originate in the prostate. Some
develop from acinar adenocarcinoma after
hormonal or radiation therapy. They are
usually aggressive tumours that often
present with secondary deposits. The
outcome is generally poor. Only basal cell
carcinoma is seen as a low-grade
carcinoma.
KEYWORDS
small cell carcinoma, ductal
adenocarcinoma, carcinosarcoma, unusual
carcinomas
We review the clinicopathological features
of the following unusual histological
variants of prostatic carcinoma: small cell
carcinoma, ductal adenocarcinoma,
sarcomatoid (carcinosarcoma), basal cell,
squamous cell and adenosquamous, and
urothelial carcinoma. These variants are
rare and account for 5–10% of carcinomas
INTRODUCTION
Prostate cancer is the most common cancer in
men, often discovered after serum PSA testing
[1]. Morphologically, most of the cancers
are referred to as acinar, microacinar, or
conventional adenocarcinomas. Carcinomas
with architectural or cytological variations,
e.g. atrophic, pseudohyperplastic, foamy
gland, colloid and signet-ring, oncocytic and
lymphoepithelioma-like, are descriptive terms
used to help pathologists to recognize the
diagnostic pitfalls. They have no known
prognostic significance other than that of
acinar adenocarcinoma, of which they are
considered to be variants [2].
Unusual histological prostatic carcinomas,
that account for 5–10% of the carcinomas
that originate in the prostate, have been
described, i.e. small cell (SCC), ductal
adenocarcinoma (DA), sarcomatoid (SC,
carcinosarcoma), basal cell (BCC), squamous
cell (SqCC) and adenosquamous (ASC), and
urothelial carcinoma (UC) [2]. Most of these
variants are aggressive and with a poor
prognosis. It is important for the urologist to
be acquainted with their morphological
features and their clinical significance, to
manage patients appropriately. The aim of
this review was to discuss the morphological
features and the clinical significance of
unusual histological variants of prostatic
carcinoma.
SCC
SCC as a primary in the prostate [3–18] is a
rare, extremely aggressive tumour that often
presents with secondary deposits. Estimates
of the incidence range from 0.3% [11] to 1%
[16] of all prostatic carcinomas. In about half
of cases it is pure SCC, while in the other half
there is a mixture with prostatic acinar
adenocarcinoma. In a third of patients there
is an initial diagnosis of adenocarcinoma,
followed by therapy, usually hormonal, in turn
followed by a subsequent diagnosis of SCC
[4,9,16].
CLINICAL FEATURES
Most patients are aged 65–72 years (range
24–89). The most frequent presenting
symptoms are related to BOO and
disseminated disease [3]. In a few cases
paraneoplastic syndromes have been
reported. These include Cushing’s syndrome
due to tumoral adrenocorticotropic
hormone production, hypercalcaemia,
hyperparathyroidism, thyrotoxicosis, and
hyperglucagonaemia [3]. The presence of
a paraneoplastic syndrome in a patient
with prostatic carcinoma should prompt
a histological search for a small-cell
component. Between a third and two-thirds
of patients with SCC present with an elevated
serum PSA level. The DRE is often suspicious
for malignancy, with an enlarged, irregular
and stony-hard prostate.
MORPHOLOGY
Macroscopically, there is usually extensive
involvement of the gland. The cut surface is
grey-whitish and nodular. Extraprostatic
extension into the seminal vesicles,
periprostatic soft tissue and bladder can be
easily visualized.
Microscopically, SCC is identical to its more
common counterpart in the lung. The tumour
grows as sheets, with ribbons, nesting and
pallisading along fibrous bands (Fig. 1A). An
‘Indian file’ pattern and rosette-like structures
are occasionally noted. The polygonal, round
or spindled tumour cells have scanty
cytoplasm, with hyperchromatic nuclei,
‘salt and pepper’ stippled chromatin and
inconspicuous nucleoli. Nuclear moulding can
be evident. Both individual cell necrosis,
manifested by karryorhectic debris, and large
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areas of geographical necrosis can be seen.
Crush artefact is present in most cases.
The acinar adenocarcinoma component in
mixed small-cell adenocarcinoma varies
from focal to 70% [16] of the tumour. In
most cases, particularly those where
adenocarcinoma precedes a diagnosis of SCC
[9], the adenocarcinoma portion is of low
grade. However, high-grade Gleason pattern
4 is reported in about a third of cases. In
two-thirds of cases the two components
merge directly into each other, while in a
third the separation between them is sharp.
In metastatic deposits derived from primary
mixed SCC-adenocarcinoma, the SCC
element is often found, although both
components can be seen. Rare examples of
admixture of SCC with malignant cells other
than adenocarcinoma include coexistence
with Paneth cell-like change, squamous
cells, and a spindle-cell sarcomatoid
component.
IMMUNOPHENOTYPIC PROFILE
In most cases, the cells are positive for at least
one of the neuroendocrine markers (Fig. 1A,
insert), i.e. chromogranin A, synaptophysin,
neurone-specific enolase and CD56 [3,17].
Prostatic SCC expresses thyroid transcription
factor-1, such that this marker is not useful in
distinguishing prostatic and lung SCC. The
prostatic markers PSA and prostate-specific
acid phosphatase (PSAP) are identified only
in a small percentage of prostatic SCCs. The
adenocarcinomatous component of mixed
SCC-adenocarcinoma is positive for PSA and
PSAP in almost all cases.
PROSTATIC SCC VS PROSTATIC
ACINAR ADENOCARCINOMA
There are significant clinical differences
between SCC and prostatic acinar
adenocarcinoma; 92% of patients with SCC
have advanced disease at presentation, and
three-quarters of them have metastatic
disease [3]. The sites of the metastases are
also different, with spread to viscera,
including liver and lung, being common
in SCC. Widespread dissemination and
metastatic deposits in unusual locations, e.g.
axillary lymph node, omentum, pericardium
and soft tissue, are more often seen with
prostatic SCC than acinar adenocarcinoma
[4,13–16].
PROGNOSIS
The outcome for patients with SCC is dismal,
with a median survival of 9–17 months [12].
There is no difference in prognosis between
patients with pure SCC and those with mixed
glandular and SCC. It is not responsive to
hormonal therapy; there might be an initial
response to chemotherapy.
DA
The incidence of pure DA, also termed
endometrioid, endometrial, papillary, or
papillary DA, is 1.3%, while the incidence of
mixed DA-acinar adenocarcinoma is 4.8%
[2,19–28].
CLINICAL FEATURES
Men with prostatic DA are typically aged
63–72 years (range 41–89); obstruction and
haematuria are common manifestations.
Most patients have a serum PSA level of
>
4 ng/mL. A substantial minority can present
with ‘metastatic’ levels of serum PSA in the
hundreds to thousands of ng/mL, bone pain
and skeletal metastases. the DRE is usually
abnormal and often suspicious for
malignancy. The clinical stage is more
often advanced than standard acinar
adenocarcinomas [26,28,29]. By urethroscopy,
DA appears, in many cases, as an exophytic,
villous/polypoid growth, with white fronds of
‘worm-like’ tumour protruding into the
urethra at or near the verumontanum.
MORPHOLOGY
Centrally occurring tumours appear as
exophytic polypoid or papillary masses
protruding into the urethra around the
verumontanum (Fig. 1B). Peripherally
occurring tumours typically show a white-
grey firm appearance similar to acinar
adenocarcinoma [23,28].
Microscopically, DA is characterized by tall
columnar cells with abundant cytoplasm,
which form a single or pseudostratified layer
reminiscent of endometrial carcinoma. The
cytoplasm of DA is often amphophilic and
might occasionally appear clear. In some
cases, there are numerous mitoses and
marked cytological atypia. In other cases, the
FIG. 1.
A
, Prostatic SCC (insert: immunohistochemical expression of neurone-specific enolase).
B
, Whole-
mount section of the prostate with DA showing an endourethral exophytic component (arrow) and involving
the entire prostate gland.
C
, DA with a papillary pattern.
D
, SC (carcinosarcoma); the carcinomatous and
sarcomatous components are admixed, with blending of the two (insert: osteosarcomatous component).
E
,
BCC (insert: perineural invasion).
F
, Prostate biopsy with adenocarcinoma (arrow) and SqCC , both intraductal
and invasive (insert).
G
, ASC; the glandular and squamous components show a direct transition.
H
, Whole-
mount section of the prostate with UC involving the periurethral region.
I
, Invasive urothelial carcinoma
(same case of Fig. 1H).
UNUSUAL CARCINOMAS OF THE PROSTATE
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cytological atypia is minimal, which makes a
diagnosis difficult particularly on needle
biopsy. It usually spreads along the urethra or
into the prostatic ducts with or without
stromal invasion. DA has a variety of
architectural patterns which are often
intermingled, i.e. cribriform, papillary (Fig. 1C),
individual glands and solid. Some patterns
might represent ductal carcinoma
in situ.
In a
half of the cases, there is a coexisting acinar
component, which is most often of a Gleason
score of 6 or 7 [21].
The histological grade of DA is usually high
Gleason pattern 4 [30], but pattern 3 and
pattern 5 can be seen. For mixed DA-acinar
adenocarcinomas, separate grades should not
be given, but rather a combined score, just as
for pure acinar adenocarcinomas. The ductal
component is usually of higher grade than the
acinar proliferation.
IMMUNOPHENOTYPIC PROFILE
The immunophenotype of prostatic DA is
similar to that of acinar adenocarcinoma.
Immunostains for PSA and PSAP are almost
always positive, in both primary and
metastatic sites.
α
-methylacyl CoA racemase
can be detected in DA [25,31], but at a
reduced level [25]. Tumour cells are typically
negative for basal cell-specific high-
molecular weight cytokeratins (detected by
34
β
E12) [32] and p63 [33].
PROGNOSIS
Most studies show that DA is aggressive;
25–40% of patients have metastases at the
time of diagnosis, with a poor 5-year survival
rate, of 15–43%. Even limited DA on biopsy
warrants definitive therapy. Androgen-
deprivation therapy might provide palliative
relief, even though this cancer is less
hormonally responsive than acinar
adenocarcinoma [21].
SC (CARCINOSARCOMA)
SC, also termed metaplastic carcinoma,
spindle-cell carcinoma, and malignant mixed
mesodermal tumour, is a rare biphasic
malignancy in the prostate [34,35]. The two
elements of SC are a malignant epithelial
(carcinomatous) component and a malignant
mesenchymal-like or mesenchymal
(sarcomatous) component. SC can be either
homologous, where the mesenchymal-
like areas have the appearance of an
undifferentiated sarcoma, or heterologous,
where the sarcoma has differentiation along
the lines of specific mesenchymal cells, such
as bone and cartilage. Carcinosarcoma is
synonymous with heterologous SC. Fewer
than 60 cases have been reported [2].
CLINICAL FEATURES
Most patients are
≈
70 years old (range 50–89)
and present with urinary tract obstruction
and symptoms of frequency, urgency and
nocturia. On DRE, the prostate is enlarged,
nodular and hard. An equal number of men
have normal and elevated serum PSA levels. In
about half of the cases the initial diagnosis
is acinar adenocarcinoma, followed by
hormonal and/or radiation therapy, with a
subsequent diagnosis of SC. The mean time
for the development of SC after acinar
adenocarcinoma is
≈
3 years [36,37].
Treatment is not the sole trigger, as SCs can
occur de novo.
MORPHOLOGY
Macroscopically, prostatic SCs are large
(5.5–18 cm), grey-white to pink masses with
haemorrhage, necrosis and local extension
into surrounding structures such as seminal
vesicles and rectal wall. Microscopically, the
carcinomatous and sarcomatous components
are admixed, with blending of the two in some
areas (Fig. 1D). The carcinomatous element is
almost always of acinar type. Two cases were
ductal adenocarcinoma [38], three had
squamous differentiation or adenosquamous
carcinoma [39], and one had urothelial
and squamous components [40]. The
adenocarcinoma is typically of high grade,
with a mean Gleason score of 9, and range of
7–10. A Gleason score can be assigned only to
the glandular component of SC.
The sarcomatoid component often has large
areas of undifferentiated spindled and
pleomorphic cells arranged in sheets or
fascicles. Cellularity is variable, from higher
degrees to lower degrees in more hyalinized
areas. Osteosarcoma (Fig. 1D, insert) and
chondrosarcoma are frequently identified.
Areas of fibrosarcoma, leiomyosarcoma,
angiosarcoma, and rhabdomyosarcoma are
rare. Different types of sarcoma can be found
together in the same case. Cytologically,
nuclear pleomorphism is moderate to marked,
with numerous mitotic figures, including
atypical ones, readily identified.
IMMUNOPHENOTYPIC PROFILE
Immunohistochemical stains show
mesenchymal or epithelial differentiation
in the sarcomatoid component. Epithelial
markers (cytokeratins, PSA, PSAP) and
muscle markers can be detected by
immunohistochemistry in the malignant
spindle cells. Vimentin immunostains are
uniformly positive, and S-100 protein is
consistently found in chondrosarcomatous
regions. Skeletal muscle and vascular
differentiation is substantiated by positivity
for myoglobin and CD31 or CD34, respectively
[41].
PROGNOSIS
The outcome of patients with prostatic SC is
poor, with a median survival of 3 years and
7-year survival rate of 14%. The disease can
be locally aggressive, with local recurrences
and formation of large pelvic masses. Sites of
metastasis include, in order of frequency,
lung, bone, lymph nodes, and brain, with rare
cases of metastatic spread to skin, liver,
peritoneum, adrenal, pleura, and kidney. Both
epithelial and/or mesenchymal components
can be seen in metastatic deposits. The
histological pattern does not predict
progression and survival [2]. Treatment has
varied; nonsurgical therapy is ineffective.
BCC
BCC of the prostate includes malignant
basaloid proliferations (basaloid carcinomas)
and neoplasms that resemble, to some degree,
adenoid cystic carcinomas of the salivary
glands [42–44]. Many terms have been used
for these neoplasms and related growths such
as adenoid basal cell tumour, adenoid cystic
tumour, adenoid cystic-like tumour, BCC, and
adenoid basal proliferation of uncertain
significance. Some of these cases probably
represent adenoid cystic-like hyperplasia.
The difficulty in classification of these
proliferations resides in the fact that they are
rare, there is no agreement on histological
criteria, and follow-up is available for only a
few cases. BCCs are quite rare, with only
≈
50
reported cases [44].
CLINICAL FEATURES
There are only a few reports in English on this
entity [44]. Patients are generally elderly,
presenting with urinary obstruction, with
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TURP being the most common tissue source
of diagnosis.
MORPHOLOGY
The macroscopic features have been reported
for fewer than 10 cases [42]. The tumours are
white and solid, sometimes with microcysts.
Microscopically, two morphological variants
of BCCs can be recognized in the prostate.
Islands and cords of epithelial cells with
peripheral pallisading characterize the first
type, morphologically similar to BCC of the
skin (Fig. 1E). The second type, also called
adenoid cystic carcinoma, is composed of
nests of infiltrating tumour cells with an
adenoid cystic pattern, morphologically
similar to the adenoid cystic carcinoma
of the salivary glands. Focal squamous
differentiation and clear cell appearance can
be seen.
The diagnostic criteria for malignancy in BCC
include: (i) extensive infiltration between
normal prostate glands; (ii) extension out of
the prostate; (iii) perineural invasion (Fig. 1E,
insert); or (iv) necrosis [44]. Histological
grading of BCC is generally not done.
IMMUNOPHENOTYPIC PROFILE
The cells are strongly stained with 34
β
E12
and p63, and negative for PSA, PSAP and
α
-methylacyl CoA racemase [45]. Cells can
be stained with antibodies to
α
-smooth
muscle actin, S-100 protein and c-erbB-2
oncoprotein [44].
PROGNOSIS
BCC is generally considered a low-grade
carcinoma.
SqCC AND ASC
The incidence of SqCC of the prostate is
<
0.6% of all prostate cancers [46–49]. Even
more rare is ASC of the prostate [50]. SqCC
can originate either in the periurethral glands
or in the prostatic acini, probably from the
lining basal cells which show a divergent
differentiation pathway. About half of ASC
can arise in patients with prostate cancer
after endocrine therapy or radiotherapy. The
time course for the appearance of squamous
differentiation in the carcinoma varies from
3 months to many (up to 9) years after
therapy. In addition to admixture with
adenocarcinoma, a few patients have had
prostatic SqCC mixed with UC and
adenocarcinoma [50] and UC [49].
The mechanism underlying the development
of SqCC or ASC after radiation or androgen-
deprivation therapy is not known. It is not
possible to completely exclude a second
squamous malignancy in these cases,
although a more plausible explanation would
be clonal evolution/divergence of persistent
carcinoma, secondary to the selective
pressure of therapy. Other pathways for
squamous prostatic carcinogenesis must
exist, as in some cases no therapy is
administered before the diagnosis of SqCC.
Prostatic SqCC has been shown to occur in
association with prostatic schistosomiasis.
CLINICAL FEATURES
The largest series is of 33 cases [48], in which
men with a mean age of 68 years presented
with BOO and dysuria. The vast majority of
patients with prostatic SqCC have normal
serum PSA and PSAP levels.
MORPHOLOGY
Macroscopically, the tumours are usually
large, up to 6.5 mm in greatest dimension,
and often replacing a substantial portion of
the prostate. Cut surfaces reveal a solid, firm,
whitish-yellow, white-grey, to grey-tan mass.
Central extension, with compression of
prostatic urethra, and local invasion into the
bladder, rectum and seminal vesicles, is
macroscopically apparent in several cases.
Microscopically, pure SqCC is typified by
infiltrating nests, strands, and sheets of
polygonal cells with nuclear atypia, with
squamous differentiation manifested as
individual cell keratinization, intercellular
bridges, and/or keratin pearl formation. ASC is
defined by the presence of both glandular
(acinar) and SqCC components. Glandular and
squamous components could be distinct
(Fig. 1F, including insert) or could show direct
transition (Fig. 1G).
The application of a three-tiered grading
scheme, with well, moderately or poorly
differentiated categories, to SqCC of the
prostate seems reasonable. The Gleason
grading scheme can be used for the glandular
component, but not for the squamous
component, of ASC. The adenocarcinoma
element is often high-grade, while the grade
of the squamous portion is variable.
IMMUNOPHENOTYPIC PROFILE
It is identical to that of SqCC originating in
other organs and sites such as bladder; it is
negative for PSA and PSAP immunostains.
PROGNOSIS
Prostatic SqCC and ASC, like glandular
adenocarcinomas, can spread along nerves,
extend locally into periprostatic soft tissue,
bladder and seminal vesicles, and metastasize
to lymph nodes and bone. However, in bone
the metastases are routinely osteolytic rather
than osteoblastic [46]. In widely disseminated
disease, metastatic deposits have been
detected in peritoneum, diaphragm, liver and
lung. The mean survival for prostatic SqCC is
not long, at 6–24 months.
UC
The frequency of primary UC, also known as
TCC is 0.7–2.8% of prostatic tumours in adults
[2,51–54]. In patients with invasive bladder
carcinoma, there is involvement of the
prostate gland in up to 45% of cases [55].
CLINICAL FEATURES
Patients have similar age distribution to UC of
the bladder (range 45–90 years). Primary UC
presents in a similar fashion to other prostatic
masses including urinary obstruction and
haematuria. The DRE is abnormal in most
patients but is infrequently the presenting
sign. There are limited data on PSA levels. In
some cases patients present with signs and
symptoms related to metastases.
MORPHOLOGY
No reliable macroscopic features of prostatic
TCC have been reported. The full range of
histological types and grades of urothelial
neoplasms can be seen in the prostate.
Papillary urothelial neoplasms arising from
the prostatic urethra and/or within prostatic
ducts have been described. However, the vast
majority are high-grade and are associated
with carcinoma
in situ
(CIS) in prostatic
urethra and/or within prostatic ducts
(Fig. 1H).
Prostatic UC has a striking propensity for
growth within prostatic ducts and acini.
Rounded or elongated cylinders and plugs of
solid tumour within ducts are characteristic
UNUSUAL CARCINOMAS OF THE PROSTATE
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profiles. Comedo necrosis can also commonly
be found, and might undergo dystrophic
calcification. Partial involvement of benign
prostatic glands is typical. Pagetoid spread
can also be seen.
Prostatic stromal invasion by UC is typified by
irregular solid nests (Fig. 1I) and cords that
extend beyond the rounded, smooth outer
profile of the UC
in situ
. It is associated
with lymphovascular space invasion in a
substantial percentage (44%) of cases [53].
Cytologically, UC in the prostate has a high
nuclear grade with nucleomegaly, and with
nuclear pleomorphism and hyperchromasia.
The cytoplasm often has an eosinophilic
‘squamoid’ appearance. Stromal sclerosis and
inflammation can be pronounced.
IMMUNOPHENOTYPIC PROFILE
The immunophenotypic profile of prostatic
UC is the same as for UCs elsewhere, and
is useful in the differential diagnostic
distinction from poorly differentiated
prostatic adenocarcinoma. They are PSA- and
PSAP-negative, and are frequently positive for
the cytokeratins CK20, CK7, 34
β
E12, p63,
thrombomodulin and uroplakins.
PROGNOSIS
The distinction between prostatic urothelial
CIS and stromal invasion, with or without an
associated bladder carcinoma, is critical for
prognosis [52,56]. The outcome for patients
diagnosed with primary invasive UC of the
prostate has been dismal, with an average
survival of 17–29 months [2]. By contrast, the
prognosis for men with pure urothelial CIS
and noninvasive papillary neoplasms in the
prostate is excellent [51,52].
CONCLUSIONS
Patients with unusual prostate cancers can
have different clinical presentations and the
histopathological diagnosis can sometimes be
challenging. As in the case with SCC of the
prostate, they do not respond to hormonal
therapy, and require chemotherapy. Most of
these tumours behave quite aggressively and
the prognosis can be poor. Only BCC is seen as
a low-grade carcinoma. Both the urologist
and the pathologist should be aware of these
unusual types of prostate cancer.
CONFLICT OF INTEREST
None declared.
REFERENCES
1
Stamey TA, Yang N, Hay AR, McNeal JE,
Freiha FS, Redwine E.
Prostate-specific
antigen as a serum marker for
adenocarcinoma of the prostate.
N Engl J
Med
1987;
317
: 909–16
2
Epstein JI, Algaba F, Yang XJ
et al.
Tumours of the prostate. In Eble JN,
Sauter G, Epstein JI, Sesterhenn IA eds,
Tumours of the Urinary System and Male
Genital Organs
, Chapter 3. Lyon: IARC
Press, 2004: 160–208
3
Abbas F, Civantos F, Benedetto P,
Soloway MS.
Small cell carcinoma of the
bladder and prostate.
Urology
1995;
46
:
617–30
4
Amato RJ, Logothetis CJ, Hallinan R, Ro
JY, Sella A, Dexeus FH.
Chemotherapy
for small cell carcinoma of prostate origin.
J Urol
1992;
147
: 935–7
5
Christopher ME, Seftel AD, Sorenson K,
Resnick MI.
Small cell carcinoma
of the genitourinary tract: an
immunohistochemical, electron
microscopic and clinicopathological
study.
J Urol
1991;
146
: 382–8
6
Di Sant’Agnese PA.
Divergent
neuroendocrine differentiation in
prostatic carcinoma.
Semin Diagn Pathol
2000;
17
: 149–61
7
Evans AJ, Humphrey PA, Belani J,
van der Kwast TH, Srigley JR.
Large
cell neuroendocrine carcinoma of the
prostate. A clinicopathologic summary of
7 cases of a rare manifestation of advance
prostate cancer.
Am J Surg Pathol
2006;
30
: 684–93
8
Helpap B, Kollermann J.
Undifferentiated carcinoma of the
prostate with small cell features:
immunohistochemical subtyping and
reflections on histogenesis.
Virchows Arch
1999;
434
: 385–91
9
Hindson DA, Knight LL, Ocker JM.
Small-cell carcinoma of prostate.
Transient complete remission with
chemotherapy.
Urology
1985;
26
: 182–
4
10
Huang J, Wu C, di Sant’Agnese PA,
Yao JL, Cheng L, Na Y.
Function and
molecular mechanisms of neuroendocrine
cells in prostate cancer.
Anal Quant Cytol
Histol
2007;
29
: 128–38
11
Losi L, Di Gregori C, Brausi M, Fante R,
Hurlimann J.
Expression of p53 protein in
prostate cancers of different histologic
types.
Pathol Res Pract
1994;
190
: 384–8
12
Mackey JR, Au H-J, Hugh J, Venner P.
Genitourinary small cell carcinoma.
Determination of clinical and therapeutic
factors associated with survival.
J Urol
1998;
159
: 1624–9
13
Oesterling JE, Hanzeur CG, Farrow GM.
Small cell anaplastic carcinoma in clinical,
pathological, and immunological study of
27 patients.
J Urol
1992;
147
: 804–7
14
Papandreou CN, Daliani DD, Thall PF
et al.
Results of a phase II study with
doxorubicin, etoposide, and cisplatin in
patients with fully characterized small cell
carcinoma of the prostate.
Am J Surg
Pathol
2002;
20
: 3072–80
15
Schwartz LH, Latrenta LR, Bonaccio E,
Kelly WK, Scher HI, Panicek DM.
Small
cell and anaplastic prostate cancer-
correlation between CT findings and
prostate-specific antigen level.
Radiology
1998;
208
: 735–8
16
Têtu B, Ro JY, Ayala AB, Johnson DE,
Logothetis CJ, Ordonez NG.
Small cell
carcinoma of the prostate. Part 1. A
clinicopathologic study of 20 cases.
Cancer
1987;
59
: 1803–9
17
Wang W, Epstein JI.
Small cell
carcinoma of the prostate. A morphologic
and immunohistochemical study of 95
cases.
Am J Surg Pathol
2008;
32
: 65–71
18
Yao JL, Huang J, di Sant’Agnese PA.
Small cell carcinoma of the prostate.
Diagn Histopathol
2008;
14
: 117–21
19
Bock BJ, Bostwick DG.
Does prostatic
ductal adenocarcinoma exist?
Am J Surg
Pathol
1999;
23
: 781–5
20
Bostwick DG, Kindrachuk RW,
Rouse RV.
Prostatic adenocarcinoma
with endometrioid features. Clinical,
pathologic, and ultrastructural findings.
Am J Surg Pathol
1985;
9
: 595–609
21
Brinker DA, Potter SR, Epstein JI.
Ductal adenocarcinoma of the prostate
diagnosed on needle biopsy. Correlation
with clinical and radical prostatectomy
findings and progression.
Am J Surg
Pathol
1999;
23
: 1471–9
22
Christensen WN, Steinberg G,
Walsh PC, Epstein JI.
Prostatic duct
adenocarcinoma. Findings at radical
prostatectomy.
Cancer
1991;
67
: 2118–
24
23
Dube VE, Farrow GM, Greene LF.
Prostatic adenocarcinoma of ductal
origin.
Cancer
1973;
32
: 402–9
MAZZUCCHELLI
ET AL.
24 Epstein JI, Woodruff JM.
Adenocarcinoma of the prostate
with endometrioid features. A light
microscopic and immunnohistochemical
study of ten cases. Cancer 1986; 57: 111–
9
25 Kelemen K, Adley B, Yang XJ, Wang HL,
Humphrey PA. Ductal adenocarcinoma
of the prostate. A clinicopathologic study
of 50 cases. Lab Invest 2006; 86: 144A
26 Lemberger RJ, Bishop MC, Bates CP,
Blundell W, Ansell ID. Carcinoma of the
prostate of ductal origin. Br J Urol 1984;
56: 706–9
27 Millar EKA, Sharma NK, Lessels AM.
Ductal (endometrioid) adenocarcinoma of
the prostate: a clinicopathological study
of 16 cases. Histopathology 1996; 29: 11–
9
28 Ro JY, Ayala AG, Wishnow KI, Ordoñez
NG. Prostatic duct adenocarcinoma
with endometrioid features.
Immunohistochemical and electron
microscopic study. Semin Diagn Pathol
1988; 5: 301–11
29 Tannenbaum M. Histopathology of the
prostate gland. In Tannenbaum M ed.,
Urologic Pathology: The Prostate.
Philadelphia: Lea & Febiger, 1977: 312–5
30 Epstein JI, Allsbrook WC Jr, Amin MB
et al. The 2005 International Society of
Urological Pathology (ISUP) Consensus
Conference on Gleason grading of
prostatic carcinoma. Am J Surg Pathol
2005; 29: 1228–42
31 Adley BP, Yang XJ. Application of alpha-
methylacyl coenzyme A racemase
immunohistochemistry in the diagnosis
of prostate cancer: a review. Anal Quant
Cytol Histol 2006; 28: 1–13
32 Samaratunga H, Singh M. Distribution
pattern of basal cells detected by
cytokeratin 34 Beta E12 in primary
prostatic duct adenocarcinoma. Am J Surg
Pathol 1997; 21: 435–40
33 Beach R, Gown AM, De Peralta-
Venturina MN et al. P504S
immunohistochemical detection in 405
prostatic specimens including 376 18-
gauge needle biopsies. Am J Surg Pathol
2002; 26: 1588–96
34 Dundore PA, Cheville CJ, Nascimento
AG, Farrow GM, Bostwick DG.
Carcinosarcoma of the prostate. Report of
21 cases. Cancer 1995; 76: 1035–42
35 Shannon RL, Ro JY, Grignon DJ et al.
Sarcomatoid carcinoma of the prostate. A
clinicopathologic study of 12 patients.
Cancer 1992; 69: 2676–82
36 Ray ME, Wojno KJ, Goldstein KJ, Olson
KB, Shah RB, Cooney KA. Clonality
of sarcomatous and carcinomatous
elements in sarcomatoid carcinoma of the
prostate. Urology 2006; 67: 423e5–423e8
37 Delahunt B, Eble JN, Nacey JN,
Grebe SK. Sarcomatoid carcinoma of
the prostate: progression from
adenocarcinoma associated with p53
over-expression. Anticancer Res 1999;
19: 4279–83
38 Poblet E, Gomez-Tierno A, Alfaro L.
Prostatic carcinosarcoma: a case
originating in a previous ductal
adenocarcinoma of the prostate. Pathol
Res Pract 2000; 196: 569–72
39 Berney DM, Ravi R, Baithun SI. Prostatic
carcinosarcoma with squamous cell
differentiation: a consequence of
hormonal therapy. Report of two cases
and review of the literature. J Urol Pathol
1979; 11: 123–32
40 Rogers CG, Parwani A, Tekes A,
Schoenberg MP, Epstein JI.
Carcinosarcoma of the prostate with
urothelial and squamous components.
J Urol 2005; 173: 439–40
41 Wick MR, Young RH, Malvesta R, Beebe
DS, Hansen JJ, Dehner LP. Prostatic
carcinosarcomas. Clinical, histologic, and
immunohistochemical data on two cases,
with a review of the literature. Am J Clin
Pathol 1989; 92: 131–9
42 Iczkowski KA, Ferguson KL, Grier DD
et al. Adenoid cystic/basal cell carcinoma
of the prostate. Am J Surg Pathol 2003;
27: 1523–9
43 Mastropasqua MG, Pruneri G, Renne G,
De Cobelli O, Viale G. Basaloid cell
carcinoma of the prostate. Virchows Arch
2003; 443: 787–91
44 Montironi R, Mazzucchelli R,
Stramazzotti D, Scarpelli M, Lopez-
Beltran A, Bostwick DG. Basal cell
hyperplasia and basal cell carcinoma of
the prostate: a comprehensive review and
discussion of a case with c-erbB2
expression. J Clin Pathol 2005; 58: 290–6
45 Zhou M, Magi-Galluzzi C, Epstein JI.
Prostate basal cell lesions can be negative
for basal cell keratins: a diagnostic pitfall.
Anal Quant Cytol Histol 2006; 28: 125–
9
46 Little NA, Wiener JS, Walther PJ,
Paulson DF, Anderson EE. Squamous cell
carcinoma of the prostate: 2 cases of a
rare malignancy and review of the
literature. J Urol 1993; 149: 137–9
47 Mohan H, Bal A, Punia RPS, Bawa AS.
Squamous cell carcinoma of the prostate.
Int J Urol 2003; 10: 114–6
48 Parwani AV, Kronz JD, Genega EM,
Gaudin P, Chang S, Epstein JI.
Prostate carcinoma with squamous
differentiation: an analysis of 33 cases.
Am J Surg Pathol 2004; 28: 651–7
49 Wernert N, Goebbels R, Bonkhoff H,
Dhom G. Squamous cell carcinoma of the
prostate. Histopathology 1990; 17: 339–
44
50 Bennett RS, Edgerton EO. Mixed
prostatic carcinoma. J Urol 1973; 110:
561–3
51 Cheville JC. Urothelial carcinoma of the
prostate. An immunohistochemical
comparison with high grade prostatic
adenocarcinoma and review of the
literature. J Urol Pathol 1998; 9: 141–54
52 Cheville JC, Dundore PA, Bostwick DG
et al. Transitional cell carcinoma of the
prostate. Clinicopathologic study of 50
cases. Cancer 1998; 82: 703–7
53 Goebbels R, Amberger L, Wernert N,
Dhom G. Urothelial carcinoma of the
prostate. Appl Pathol 1985; 3: 242–54
54 Oliai BR, Kahane H, Epstein JI. A
clinicopathologic analysis of urothelial
carcinomas diagnosed in prostate needle
biopsy. Am J Surg Pathol 2001; 25: 794–
801
55 Nixon RG, Chang SS, Lafleur BJ, Smith
JA, Cookson MS. Carcinoma in situ and
tumor multifocality predict the risk of
prostatic urethral involvement at radical
cystectomy in men with transitional cell
carcinoma of the bladder. J Urol 2002;
167: 502–5
56 Greene FL, Page DL, Fleming ID et al.
Urethra. In Greene FL, Page DL, Fleming ID
et al. eds, AJCC Cancer Staging Manual,
6th edn. New York: Springer Verlag, 2002:
341–3
Correspondence: Rodolfo Montironi,
Pathological Anatomy, Polytechnic University
of the Marche Region, School of Medicine,
United Hospitals, Via Conca 71, I-60126
Torrette, Ancona, Italy.
e-mail:
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Abbreviations: SCC, small cell carcinoma;
DA, ductal adenocarcinoma; SC, sarcomatoid
carcinoma; BCC, basal cell carcinoma;
SqCC, squamous cell carcinoma; ASC,
adenosquamous carcinoma; PSAP, prostate-
specific acid phosphatase; CIS, carcinoma
in situ; BOO, bladder outlet obstruction; UC,
urothelial carcinoma.](http://www.urotoday.com/images/stories/bju_2008_11_cover.gif)
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