Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

A
B
Fig. 2.61 A Adenocarcinoma in situ of urinary bladder. B Adenocarcinoma in situ. Note columnar epithelium with nuclear anaplasia involving mucosal surface.
cinoma {499}.
Cystitis glandularis is present in invasive
adenocarcinoma ranging from 14- 67%
of cases {24,2612}, but its role in the
pathogenesis of invasive adenocarcinoma
is not clear. However, in patients with
pelvic lipomatosis, which harbors cystitis
glandularis, adenocarcinoma may occur
{1088,2862}. Adenocarcinoma may also
arise in conjunction with villous adenomas,
S. haematobium infestation, and
endometriosis of the bladder {2885}.
Somatic genetics
To date, few studies have examined the
genetic alterations underlying adenocarcinoma
of the bladder. A partial allelotype
reported loss of chromosomal arm
9p (50%), 9q (17%), 17p (50%), 8p
(50%) and 11p (43%) in 8 schistosomiasis-associated
adenocarcinomas.
Chromosomal arms 3p, 4p and 4q, 14q
and 18q also showed LOH but no loss of
13q was seen {2380}. With the exceptions
of a lower frequency of loss of 9q
and 13q, this spectrum of chromosomal
loss is similar to urothelial and squamous
cell carcinoma of the bladder. LOH of 9p
likely targets the p16/p14 tumour suppressor
genes. The 17p LOH targets the
p53 gene as a separate study reported
4/13 adenocarcinomas to have p53 point
mutation {2784}. Further support for the
observation of 18q loss is provided by a
study that detected LOH of the D18S61
microsatellite marker in a patient’s adenocarcinoma
and urine DNA {628}.
Predictive factors
Clinical factors
Management of invasive adenocarcinoma
of the bladder includes partial or radical
cystectomy followed by consideration
of chemotherapy or radiotherapy according
to the extent of the lesion. Partial cystectomy
is usually associated with a relatively
high recurrence rate {2853}.
Poor prognosis of this variant is associated
with advanced stage at diagnosis.
These tumours typically arise in the bladder
base or dome, but can occur anywhere
in the bladder. Primary vesical
adenocarcinoma represents the most
common type of cancer in patients with
bladder extrophy. Signet-ring carcinoma
is a rare variant of mucus-producing
adenocarcinoma and will often produce
linitis plastica of the bladder {454}.
Morphologic factors
Stage is the most important prognostic
factors for this disease {953}. However,
the prognosis is poor since most adenocarcinomas
present at advanced stage
with muscle invasive disease and
beyond (T2/T3). Survival at 5 years is
31% {953} -35% {551}.
It is important to distinguish between
urachal and non-urachal adenocarcinomas
especially for treatment purposes.
Some studies have suggested that nonurachal
adenocarcinomas carry a worse
prognosis {95,953,2612}, but this was
not confirmed.
Among histologic types of adenocarcinoma,
pure signet ring cell carcinoma
carries the worst prognosis, otherwise
histologic type has no prognostic significance
{953}.
Immunohistochemical markers
Little is known about genetic factors
associated with prognosis of adenocarcinoma
of the bladder. Proliferation indices
of markers such as the nucleolar organizer
region (AgNOR), Ki-67, and proliferating
cell nuclear antigen (PCNA) are
associated with grade and stage of
nonurachal bladder adenocarcinomas
{1994}. There is an increased incidence
of local recurrence and distant metastasis
in patients with a high Ki-67, PCNA,
and AgNOR proliferation index.
Table 2.05
Variants of adenocarcinomas of the bladder.
Variant
Reference
Adenocarcinomas, NOS {953}
Enteric (colonictype) {953}
Signet ring cell {257,952}
Mucinous {953}
Clear cell {456,2901}
Hepatoid {344}
Mixed {953}
130 Tumours of the urinary system