Resident Short Reviews
Adenocarcinoma of the Urinary Bladder
Somak Roy, MD; Anil V. Parwani, MD, PhD
Nmon
Primary adenocarcinoma of urinary bladder is an uncom-
neoplasm and is a source of diagnostic confusion with
adenocarcinomas arising in adjacent organs, especially
colon. These tumors show varied histologic picture and
degree of differentiation. Clinical association with bladder
exstrophy and schistosomiasis has been well documented.
Primary bladder adenocarcinomas have overlapping histo-
logic and immunohistochemical features with adenocarci-
nomas arising from other primary sites and the suggested
immunohistochemical panel includes cytokeratins 7
and 20, 34bE12, thrombomodulin, CDX2, and b-catenin.
Clinical, imaging, histologic, and immunohistochemical
correlation should be done while rendering this diagnosis,
as prognosis and therapeutic options for primary versus
metastatic adenocarcinoma vary widely.
(Arch Pathol Lab Med. 2011;135:1601–1605; doi:
10.5858/arpa.2009-0713-RS)
A denocarcinoma of the urinary bladder arising from the
urothelial lining is an uncommon malignant neo-
plasm, accounting for 0.5% to 2.0% of all malignant vesical
tumors.1 The histologic variants show a predominant
colonic (enteric) type glandular morphology with varied
histologic patterns. Based on the morphology they are
classified as follows: colonic (enteric) type, adenocarcino-
ma not otherwise specified, mucinous, signet ring cell
(SRC), clear cell type, hepatoid, and mixed forms.2,3 These
tumors are also grouped as urachal and nonurachal type,
the latter being the focus of this review.
Irrespective of the various histologic patterns, there is
usually evidence of cystitis cystica et glandularis or
surface glandular metaplasia in the adjacent benign
urothelium.2 Recent molecular studies using quantitative
fluorescence in situ hybridization hypothesize that intes-
tinal metaplasia in the bladder could be a precursor lesion
for vesical adenocarcinoma.4,5
CLINICAL FEATURES
Patients are usually in their sixth decade of life with a
male predilection. The most common clinical presentation
is hematuria.6 Bladder irritation symptoms are also
frequently reported.1 About 90% of the tumors arising in
Accepted for publication December 27, 2010.
From the Department of Pathology, University of Pittsburgh Medical
Center, Pittsburgh, Pennsylvania.
The authors have no relevant financial interest in the products or
companies described in this article.
Reprints: Somak Roy, MD, Department of Pathology, University of
Pittsburgh Medical Center, A615, Scaife Hall, 3550 Terrace St,
Pittsburgh, PA 15261 (e-mail: roys911@gmail.com).
Arch Pathol Lab Med—Vol 135, December 2011
exstrophied bladder are adenocarcinomas.2 They are also
more prevalent in settings of vesical schistostomiasis.7,8
Adenocarcinomas can arise anywhere in the urinary
bladder. However, they involve the trigone and posterior
bladder wall in most cases.2 About two-thirds of the
adenocarcinomas present as solitary, discrete lesions,
unlike the ‘‘usual’’ urothelial carcinomas, which tend to
be multifocal.2,9
GROSS AND MICROSCOPIC PATHOLOGY
Adenocarcinomas can have a papillary, nodular, flat, or
ulcerated architecture. Some of the adenocarcinoma
variants (SRC) tend to present with prominent bladder
wall thickening (‘‘linitis plastica’’ like) without apparent
growth due to diffuse infiltration of the bladder wall by
tumor cells.2,10
Microscopically, these tumors show pure glandular
morphology. Usually they show well to moderately
differentiated colonic-type infiltrating glands with or
without abundant extracellular mucin (Figure 1). How-
ever, in some cases, highly cellular and poorly differen-
tiated morphology may be seen in the absence of the more
common colonic glandular histology.2 The not otherwise
specified type shows nonspecific glandular growth
pattern. Foci of cystitis cystica may also be seen in some
of these tumors (Figure 2).
The SRC variant of bladder adenocarcinoma is an
aggressive, poorly differentiated rare subtype. This entity
is defined as a tumor composed entirely of SRCs or as a
poorly differentiated round cell tumor with intracytoplas-
mic mucin without extracellular mucin.2,10–12 This variant
resembles mammary lobular carcinoma with the excep-
tion of large cell size. A dense layer of cells in the lamina
propria with diffuse infiltration into the muscularis is
commonly seen. The tumors tend to be aggressive with
propensity for extravesical soft tissue extension at the time
of presentation (higher stage).2,10–12 This variant can bear
morphologic resemblance to plasmacytoid urothelial
carcinoma, an unusual bladder tumor13,14 that is charac-
terized by large cells with abundant eosinophilic cyto-
plasm and eccentrically placed vesicular nucleus with
prominent nucleolus, closely resembling a plasma cell.13,14
Signet ring cell variant, in contrast, has cells with a clear
cytoplasmic vacuole and an indented eccentrically placed
nucleus. The plasmacytoid urothelial carcinomas are
poorly differentiated high-grade tumors and often have
a coexisting high-grade conventional urothelial carcinoma
or a sarcomatoid carcinoma component.14 This is, howev-
er, an uncommon finding in SRC variant.
The mucinous (colloid) variant displays abundant pools
of extracellular mucin with groups of tumor cells floating
Vesical Adenocarcinoma—Roy & Parwani 1601
Figure 1. Adenocarcinoma of bladder, enteric type. Invasive small- to medium-sized well-formed glands with luminal dirty necrosis and focal
cribriform pattern. Stroma is desmoplastic and edematous. Histologic features are indistinguishable from colonic adenocarcinoma (hematoxylin-
eosin, original magnification 3100).
Figure 2. Adenocarcinoma of bladder, enteric type (transurethral resection specimen) showing fragment of urothelium-lined tissue with cystitis
cystica (hematoxylin-eosin, original magnification 3200).
Figure 3. Invasive adenocarcinoma of bladder, mucinous type. Extensive extracellular pools of mucin with malignant glands and cells floating on
it. Right lower field shows benign reactive urothelium (hematoxylin-eosin, original magnification 340).
Figure 4. Invasive adenocarcinoma of bladder, mucinous type. Occasional signet ring cells in pool of mucin. This, however, does not qualify for
diagnosis of signet ring cell adenocarcinoma (hematoxylin-eosin, original magnification 3100).

on it.2,3,15 This variant is usually well differentiated and
mimics many extravesical mucinous tumors histologically
(Figure 3). They may show SRCs with intracellular mucin
(Figure 4); however, they do not qualify to be classified as
SRC variant by the definition stated previously.
The grading system of bladder adenocarcinomas is
based on the degree of glandular differentiation and
nuclear pleomorphism (well, moderate, and poorly
differentiated).3
DIFFERENTIAL DIAGNOSIS
AND IMMUNOHISTOCHEMISTRY
Bladder adenocarcinoma needs to be distinguished
from the more common metastatic adenocarcinoma
(direct spread, lymphatic, and hematogenous). The
principal primary organs to be considered include
prostate, colon, female genital tract, appendix, stomach,
and breast.2,15,16
1602 Arch Pathol Lab Med—Vol 135, December 2011
The evidence supporting the fact that the entity
represents a primary vesical adenocarcinoma is the
presence of flat carcinoma in situ. The latter is difficult
to document, particularly in transurethral resection
specimens due to extensive thermal artefact, incomplete
sampling, and presence of mucosal ulcerations.2 Also,
secondary adenocarcinomas tend to colonize the native
epithelium mimicking a carcinoma in situ component. The
most frequent and challenging differential diagnosis
remains metastatic or directly spreading colonic adeno-
carcinoma. The latter is virtually indistinguishable on
histomorphology as well as on immunohistochemis-
try.2,3,15,17,18 Differential diagnosis is even more difficult
on small biopsies with poorly differentiated tumors.
The extreme similarity of vesical and colonic adenocar-
cinomas has raised the interesting, though controversial,
proposition of the pathogenic relationship of these
tumors. It is hypothesized that due to the common
Vesical Adenocarcinoma—Roy & Parwani
Figure 5. A, Adenocarcinoma of bladder. Tumor cells show focal strong positivity for cytokeratin 20. B, Adenocarcinoma of bladder. Tumor cells
demonstrating weak immunoexpression of thrombomodulin. C, Adenocarcinoma of bladder; strong diffuse nuclear expression of CDX2. D,
Adenocarcinoma of bladder; membranous staining pattern of b-catenin (original magnification 3200 [A]; original magnification 3400 [B]; original
magnification 3100 [C]; original magnification 3400 [D]).

embryologic origin of the bladder and the rectum from the
cloaca, vesical adenocarcinomas may arise from pluripo-
tent cloacal cells that undergo similar genetic changes as
seen in colonic adenocarcinomas.15
The immunohistochemical panel used to distinguish
primary vesical adenocarcinoma from metastatic colonic
adenocarcinoma includes cytokeratin (CK) 7, CK20,
34bE12, thrombomodulin, villin, CDX-2, and b-cate-
nin.3,15–21 CK7 and CK20 are reported to be positive in
more than half of primary bladder adenocarcinomas
(Figure 5, A).15,16,21 The typical colonic adenocarcinoma
staining profile, CK7 negative and CK20 positive, has been
reported in 29% of primary vesical adenocarcinomas.15
A combination of CK7 and CK20 by itself does not
appear to differentiate primary bladder from colonic
adenocarcinomas.
Thrombomodulin, an endothelial thrombin receptor, is
a sensitive urothelial marker. Wang et al15 reported 90%
expression of thrombomodulin in urothelial carcinoma.
However, only 59% of the bladder adenocarcinomas and
none of the colonic adenocarcinomas were positive for this
marker (Figure 5, B).
Arch Pathol Lab Med—Vol 135, December 2011
CDX-2 is a homeobox gene implicated in regulation of
growth and differentiation of intestinal epithelial cells. It
acts as a nuclear transcription factor and therefore
demonstrates nuclear staining in normal colonic epithelial
cells and colonic adenocarcinoma.15,19 Its expression was
initially thought to be restricted to colonic adenocarcino-
mas. However, recent studies have shown the immunoex-
pression of CDX-2 in vesical adenocarcinomas as well
(Figure 5, C).19 This overlapping immunophenotype di-
minishes the utility of CDX-2 in the differential diagnosis
between the 2 entities.
b-catenin is a key component of the cadherin-mediated
cell-cell adhesion system and is abnormally accumulated
in the nucleus of tumor cells (colorectal adenocarcinomas)
due to impaired adenomatous polyposis coli–b-catenin
interaction. Wang et al15 found consistent nuclear expres-
sion of b-catenin in 81% of colonic adenocarcinomas
metastatic to the bladder. Nuclear pattern of staining was
restricted to this group of tumors. Membranous staining
pattern was observed in 88% of primary vesical adeno-
carcinomas and in all cases of colorectal adenocarcinomas
(Figure 5, D). It was concluded that the b-catenin
Vesical Adenocarcinoma—Roy & Parwani 1603
dysregulation mechanism is not functional in bladder
adenocarcinomas and also that nuclear versus membra-
nous staining pattern is a good marker for distinction
between these 2 tumor entities. Thomas et al22 studied b-
catenin expression in conjunction with E-cadherin expres-
sion in SRC primary bladder adenocarcinoma. They
demonstrated membranous staining of b-catenin in all
foci of colonic-type adenocarcinoma and 78% of the SRC
foci. The study concluded that the decreased expression of
both markers in SRC foci might be attributed to alteration
in the signaling pathway. Sordo et al11 demonstrated only
membranous expression in all cases of SRC adenocarci-
noma. No nuclear staining was observed. Gopalan et al21
in their study of urachal adenocarcinomas demonstrated
93% of cases with membranous expression of b-catenin
with focal nuclear staining in 1 of the cases. They
concluded that the presence of predominant nuclear
expression of b-catenin would not be compatible with
primary urachal adenocarcinoma.
34bE12, a high-molecular-weight cytokeratin, is a sensi-
tive and relatively specific marker for basal cells of prostatic
acini. It demonstrates strong cytoplasmic staining in these
cells. Gopalan et al21 reported 66% and 11% positivity of
34bE12 in urachal and colonic adenocarcinomas, respec-
tively. They concluded that a strong diffuse positivity
would favor urachal over colonic adenocarcinoma.
Urachal carcinoma is a less common tumor that can
present as a bladder mass and should be considered in the
list of differential diagnoses.3,21 This tumor tends to occur
in the dome and anterior bladder wall and usually has a
male predominance.21 Adenocarcinoma with enteric fea-
tures is the most common histologic subtype and can also
show mucinous and SRC variants.3,21 Diagnostic criteria
for urachal carcinoma include (1) tumor in the dome; (2)
absence of cystitis cystica and cystitis glandularis; (3)
predominant invasion of the muscularis or deeper tissues
with a sharp demarcation between the tumor and surface
bladder urothelium that is free of glandular or polypoid
proliferation; (4) urachal remnants within the tumor; (5)
extension into the bladder wall with involvement of the
space of Retzius, anterior abdominal wall, or umbilicus;
and (6) no evidence of a primary neoplasm elsewhere.23
The previous criteria help in differentiating it from
primary vesical adenocarcinomas. Immunohistochemical
profile is similar to primary vesical adenocarcinoma and
hence is of no practical utility.21 The management of
urachal carcinoma is typically a partial cystectomy as
opposed to a radical cystectomy for primary bladder
adenocarcinomas.
Prostatic adenocarcinomas often directly extend into the
bladder and may coexist with a bladder adenocarcinoma.
The most reliable immunohistochemical marker is pros-
tate-specific antigen, which stains approximately 90% of
poorly differentiated prostatic adenocarcinomas and is
negative in bladder adenocarcinomas.3,16
CA 125, which stains the tumor cells of endometrial and
ovarian malignancies, has been reported to be of use to
differentiate endometrial and ovarian carcinoma from
primary bladder adenocarcinomas.16 Vimentin highlights
endometrial carcinoma cells as opposed to bladder
adenocarcinoma cells.3
Metastatic breast carcinoma may be differentiated from
SRC vesical carcinoma using estrogen receptor and gross
cystic disease fluid protein 15, which stain breast
carcinoma cells.11
1604 Arch Pathol Lab Med—Vol 135, December 2011
OTHER VARIANTS OF VESICAL ADENOCARCINOMA
Clear Cell Adenocarcinoma
Clear cell adenocarcinoma is an unusual and rare
variant of bladder adenocarcinoma with a particularly
strong predilection for females, with a reported mean age
of 57 years.24,25 Gross hematuria, dysuria, suprapubic pain,
and discharge are the usual presenting symptoms. Clear
cell adenocarcinoma is histologically and ultrastructurally
similar to clear cell tumors of the female genital tract of
possible müllerian origin.2,3,25,26 The tumor has an exo-
phytic, polypoidal, or papillary appearance and usually
involves the posterior and lateral walls or the trigone.3,24
Histology is characterized by varied architectural patterns
of tubulocystic to papillary or diffuse sheets of cells. The
tumor cells range from flat, cuboidal to columnar cells
with eosinophilic to clear cytoplasm, often containing
glycogen. They occasionally demonstrate prominent
hobnailing. There is moderate to severe nuclear atypia
with frequent mitosis. Associated histologic features
include concurrent presence of urothelial carcinoma,
adenocarcinoma not otherwise specified type, cystitis
cystica glandularis, and prominent inflammatory infil-
trate.3,24,25
Immunohistochemically, the tumor cells are positive for
CA 125.3,25,27 The tumor cells also express pancytokeratin,
CK7, and CK20 (variable).23,25,27 The tumor cells variably
express S100 protein, carcinoembryonic antigen, Leu-M1,
and CA 19.9 and are consistently negative for prostate-
specific antigen and prostatic acid phosphatase.25,27 Neph-
rogenic adenoma is the most important differential
diagnosis. Both entities have overlapping morphologic
and immunohistochemical profiles. However, clear cell
adenocarcinomas demonstrate pronounced nuclear atypia
and numerous mitoses. A higher MIB-1 index and a
stronger p53 staining have been reported in clear cell
adenocarcinomas unlike in nephrogenic adenomas.27
Urothelial carcinomas can occasionally display abundant
glycogen-rich clear cells and lack the other histologic
features of clear cell adenocarcinoma.25 Other lesions that
need to be distinguished from clear cell adenocarcinoma
include vaginal or cervical clear cell carcinomas, clear cell
prostatic adenocarcinoma, and metastatic clear cell renal
cell carcinoma. Overall, these entities are rare and
clinicoradiologic correlations with immunohistochemistry
are helpful in arriving at the correct diagnosis.3,25
Hepatoid Adenocarcinoma
Hepatoid adenocarcinoma is an extremely rare tumor of
the bladder, described in very few case reports.28
Clinically, this is an aggressive tumor primarily affecting
elderly men. Diagnosis is based on morphologic resem-
blance to hepatocellular carcinoma and positive immuno-
staining for a-fetoprotein. The tumor cells are large and
polygonal with abundant granular eosinophilic cytoplasm
and vesicular nuclei with prominent nucleoli. The cells are
arranged in a trabecular pattern. Hyaline globules and bile
production can also be seen. Hepatocellular differentia-
tion can be documented by expression of a-fetoprotein,
a1-antitrypsin, albumin, HepPar-1, epithelial membrane
antigen, and carcinoembryonic antigen.28
THERAPY AND PROGNOSIS
The main stay of treatment is surgery with or without
adjuvant radiation or chemotherapy. Radical or partial
Vesical Adenocarcinoma—Roy & Parwani
cystectomy with or without node dissection is the common-
ly used surgical procedure.1 The most important prognostic
factor is tumor stage.1 Histologic subtypes especially SRC
and clear cell variants behave more aggressively.
CONCLUSION
Primary adenocarcinoma of the bladder is an uncom-
mon neoplasm with a spectrum of histomorphologic
appearances. The more common metastatic adenocarci-
nomas, especially colonic, need to be ruled out before
making a diagnosis of primary vesical adenocarcinoma.
Because histologically and immunohistochemically there
is considerable overlap between colonic and vesical
adenocarcinoma, extensive clinical and radiologic workup
is required for diagnostic accuracy. The panel of markers
required for primary versus secondary adenocarcinomas
should be carefully selected based on the morphology of
the tumor and its related entities in the differential
diagnosis. Although the immunomarkers discussed pre-
viously do not individually prove to be diagnostically
significant, a panel of stains is helpful such as a
combination of CK7, CK20, thrombomodulin, b-catenin,
34bE12, and prostate-specific antigen.
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