DISEASE

Seminom
a

ETIOLOGY

The etiology of
tumors of the
testis is not
known, but risk
factors include:
Cryptorchidism
is the most
important; it is
associated with
10% of cases.
Testicular
dysgenesis
syndrome (TDS)
includes
cryptorchidism,
hypospadias,
and poor sperm
quality; TDS has
been related to
pesticide and
non-steroidal
estrogen
exposures in
utero.
Genetic factors
are reflected by
familial
clustering and an
increased
incidence of
testicular
carcinoma
among brothers
and sons of
affected
individuals.

PATHOLOGY

Most testicular
germ cell tumors
originate
from a precursor
lesion called
intratubular germ
cell neoplasia
(ITGCN). ITGCN is
believed to arise in
utero and stay
dormant until
puberty, after
which it may
progress to
seminoma or
nonseminomatous
tumors.
Seminomas
contain
isochromosome
12p and express
transcription
factors OCT3/4 and
NANOG, which are
important in
maintenance of
pluripotent stem
cells.
Approximately 25%
of these tumors
have KIT activating
mutations. KIT
amplification and
KIT overexpression
through other
unknown
mechanisms have
also been reported.

HISTOLOGIC
FEATURE/MORPHOL
OGY
GROSS
APPEARANCE
Grossly: Seminomas
are homogeneous,
lobulated, gray-white
masses, generally
devoid of hemorrhage
or necrosis; the
tunica albuginea
usually remains
intact.
Microscopically: This
germ cell neoplasm is
the one most likely to
exhibit a single
histologic pattern.
The mass is
composed of large
polyhedral seminoma
cells containing
abundant pale and
eosinophilic or clear
cytoplasm (since it
has considerable
glycogen and some
lipid), large nuclei,
and prominent
nucleoli. A fibrous
stroma of variable
density divides the
neoplastic cells into
irregular lobules, and
there is a lymphocytic
(and occasionally
granulomatous)
infiltrate.
Seminomas resemble
ovarian
dysgerminoma
microscopically. Cells
grow in nests or

INCIDENCE

CLINICAL
PRESENTATION

In the 15- to
34-year age
group,
testicular
germ cell
tumors
constitute the
most common
tumor of men
and cause
approximately
10% of all
cancer deaths.
Of all testicular
germ cell
tumors,
seminoma
accounts for
50%; it has a
peak incidence
between ages
30 and 40 years
and they almost
never occur in
infants.

Seminomas are
usually
progressively
growing scrotal
masses that are
often diagnosed
while still
curable by
orchiectomy,
with or without
abdominal lymph
node dissection;
usually presents
as unilateral
painless
enlargement of
the testis.
Tumor cells are
diffusely positive
for c-KIT, OCT4,
and placental
alkaline
phosphatase
(PLAP).
Roughly 15%
contain
syncytiotrophobl
asts; human
chorionic
gonadotropin
(hCG) is present
in such cells.

TREATMENT

Diagnosis
a. Ultrasound
b. CT scan or
MRI of pelvis
and abdomen
** Testicular
cancer most
often involves
para-aortic
lymph nodes
Treatment
a. Inguinal
orchiectomy
b. Adjuvant
chemotherapy

PROGNOSIS

Seminomas
metastasize
late, are highly
radiosensitive,
and
radiotherapy is
important in
treating tumors
that are cured
by surgery
alone. Even in
advanced stages
of
dissemination,
chemotherapy
can be curative.
The cure rate
for all
histologic
subtypes of
seminoma is
now over 90%.
Excellent
prognosis.

sheets separated by
fibrous septa
infiltrated with
lymphocytes, plasma
cells and
macrophages.
Septa may contain
granulomas with
giant cells. Seminoma
cells resemble
immature
spermatogonia.
.