Tumors of Testis

2022

Dr.Nidal Al-Jebrini
Dr.Hisham ALAamleh
Outlines: -
❑ Overview.
❑ Types
❑ Presentation
❑ Diagnosis
❑ treatment
Overview: -
• Primary testicular tumors are the most common solid
malignant tumor in men 20 to 35 years of age in the
United States. For unknown reasons, the incidence of this
cancer—principally, testicular seminomas—increased
during the last century. Over the past decade, the
incidence of testicular cancer has risen approximately
1.2% per year, although the rate of increase has been
slowing. Germ cell cancers account for more than 90% of
all testicular cancers. Approximately 9,000 new cases have
been diagnosed in United States every year, although only
about 400 deaths have occurred annually.
Cont.
• In patients with localized disease, painless swelling or a
nodule in one testicle is the most common presenting sign. A
dull ache or heavy sensation in the lower abdomen could be
the presenting symptom. Patients with disseminated disease
can present with manifestations of lymphatic or
hematogenous spread.
• Ultrasound can distinguish intrinsic from extrinsic testicular
lesions and can identify masses within testes. Once the
diagnosis of testicular cancer is suspected, a high-resolution
CT scan of the abdomen and pelvis and a chest x-ray are
ordered as part of the initial staging workup. Radical inguinal
orchiectomy is the definitive procedure to permit histologic
evaluation of the primary tumor and to provide local tumor
control.
Cont.
• Initial therapy is selected according to the following features of the
cancer:
I. Stage group
II. Risk stratification (good, intermediate, or poor risk)
III. Histology (seminoma versus nonseminoma)
• With stage I seminoma, cure can sometimes be achieved by radical
inguinal orchiectomy alone. Patients with more advanced disease
require adjuvant chemotherapy or radiation therapy.
Cont.
• Testicular cancers are very sensitive to chemotherapy and are curable
even when metastatic. Cure rates for good-risk disease are 90%-95%.
However, patients cured of testicular cancer have approximately a 2%
cumulative risk of developing a cancer in the opposite testicle during
the 15 years after initial diagnosis. The risk of subsequent
contralateral testis tumors appears to be higher in men whose
primary tumor was a seminoma than in those with nonseminomatous
primary tumors.
Types: -
• Tumors of Non- germinal (germ) cells (3%)
• Lymphoma (7%)
• Germ cell tumors (90%)
(1) Tumors of Non- germinal cells
• These are benign tumors
• They may secrete steroids and cause endocrinopathies
• (1) Leydig (interstitial) cell adenoma
It produces androgens
1- Before puberty it leads to sexual precocity.
2- After puberty, no body change are detected.
• (2) Sertoli cell adenoma
It produces estrogen leading to feminizing characters
(2) Lymphoma

• It represents 7% of testicular tumors and usually occurs

above 65 years of age.
(3) Germ cell tumors
• Most of these tumors are malignant and the peak incidence is from
19 to 35 years old.
• Predisposing factors:
1- Genetic factors
2- Undescended testis
3- Atrophic testis
4- Venereal diseases
Cont.
• Types:
1- Seminoma (commonest malignant tumor of testis).
2- Teratoma.
3- Combined seminoma and teratoma.
4- Yolk sac tumor (spaces lined by malignant epithelium). also called
endodermal sinus tumor, are the most common testicular tumor in
infants and young children. The tumor secretes  - feto protein.
Cont.
• Seminoma :
• 40-50 years of age. Unknown before puberty
• Germ cells with gonadal differentiation.
• N/E
Shape: Well defined rounded mass
Consistency: Fleshy
C/S: homogenous, grayish white and opaque (potato like)
Cont.
• M/E
-sheets and cords of spermatogenic cells. -fibrous
stroma with lymphocytic infiltration.
-The cells are uniform, large.
Cont.
• Spread
• 1- local:-
• tunica vaginalis, epididymis, Invade testicular tissue to reach
spermatic cord and scrotal skin
• 2- lymphatic:
• Common iliac, pancreatic L.N.
later mediastinal and supraclavicular L.N
• 3- blood:
Lung, then brain and bones.
 Cont.

• Teratoma :
• Germ cell with embryonic differentiation.
• N/E
o Irregular rounded or oval mass
•C/S
oNot uniform, it is solid, Show variable sized cystic cavities
with areas of hemorrhage and necrosis
Cont.
• M/E:
oTumor tissue which is:
- Foreign to the locality
- Formed of mixture of tissues derived from 3 germ layers.
• It may be:
❑Differentiated (mature) teratoma.
❑Intermediate (immature) teratoma.
❑Undifferentiated teratoma
• Spread :
o Same as seminoma
 Presentation:
• Any solid, firm mass within the testis should be considered testicular
cancer until proven otherwise. Prompt diagnosis and early treatment are
required for cure.
• Testicular cancer may be painless, in which case the patient may be
unaware of its presence. In patients with scrotal pain, testicular cancer
must be differentiated from epididymitis. The clinician should consider
the full differential diagnosis of a testicular mass, which includes not only
epididymitis but the following:
I. Epididymo-orchitis
II. Testicular torsion
III. Hydrocele
IV. Hernia
V. Hematoma
VI. Spermatocele
VII.Varicocele
Risk factors:
• Cryptorchidism: -In patients with cryptorchidism, the risk of
developing germ cell tumor is increased fourfold to eightfold.
• Prior Testicular Cancer: -a previous history of testicular cancer
is the strongest risk factor for germ cell tumor. Approximately
1-2% of testicular cancer patients will develop a second
primary testicular cancer contralaterally—a 500-fold higher
rate than in the general population.
• Genetics: -Patients with Klinefelter syndrome (47XXY) have
higher incidence of germ cell tumor, particularly primary
mediastinal germ cell tumor. Family members of Klinefelter
syndrome patients has a six fold to 10-fold increased risk of
germ cell tumor. Patients with Down syndrome also are at
increased risk for germ cell tumors.
Cont.
• Family history: -First-degree relatives have a higher risk of developing
testicular cancer than the general population, although the incidence
is low. About 2% of testicular cancer patients report having an
affected relative.
 Diagnosis:
• The workup of patients with suspected testicular cancer starts with a
complete history and physical examination. Lab tests and imaging
studies include the following :
1.Serum alpha-fetoprotein
2.Serum beta subunit of human chorionic gonadotropin (beta- hCG)
3.Lactate dehydrogenase (LDH)
4.Chemistry profile
5.Testicular ultrasound
6.High-resolution computed tomography (CT) scan of the abdomen
and pelvis
7.Chest x-ray
8.Magnetic resonance imaging (MRI) of the brain should be performed
if brain metastasis is suspected after clinical examination
Treatment:
• Testicular cancers are curable even in the presence of metastatic
disease. If the cancer progresses or recurs despite initial
chemotherapy, these patients are candidates for salvage therapy.
• Nonseminoma is more aggressive than seminoma. When the
elements of both seminoma and nonseminoma are present or the
alpha-fetoprotein (AFP) concentration is elevated, the tumor should
be treated as a nonseminoma.
• Radical inguinal orchiectomy is considered the primary treatment for
most patients who present with a suspicious testicular mass;
 Recurrent disease and salvage treatment:

Patients who do not have a complete response to first-line therapy,

or whose disease recurs after complete response, are categorized
into favorable and unfavorable prognostic groups.
• Salvage treatment for patients with a favorable prognosis:
❖This group includes patients with low tumor marker levels, low-
volume disease, complete response to first-line chemotherapy, and
testis primary. These patients are treated with chemotherapy—
VeIP or TIP. If they have an incomplete response or relapse, they
should be considered for high-dose chemotherapy with autologous
stem cell transplantation or enrollment in a clinical trial. In patients
with a solitary metastatic site, salvage surgery should be
considered. Patients who have a complete response should be
followed closely and if they experience relapse, should be
considered for clinical trials or high-dose chemotherapy.
• Salvage treatment for patients with an unfavorable prognosis:
❖This group includes patients with an incomplete response to first-line
chemotherapy, high tumor marker levels, high-volume disease,
extratesticular primary, and late relapse. In these patients, enrollment
in a clinical trial is preferred. Other options include high-dose
chemotherapy plus autologous stem cell support, conventional
chemotherapy with either VeIP or TIP, or best supportive care. Third-
line chemotherapy with or without cyclophosphamide/ifosfamide can
produce a durable complete response in 15%-20% of patients and
should be considered for patients with good performance scores.
• High-dose chemotherapy and stem cell rescue:
❖High-dose chemotherapy with tandem courses of carboplatin and
etoposide followed by hematopoietic stem cell rescue can produce
complete remission in 5%-10% of cisplatin-refractory testicular
cancers. Non–cisplatin-refractory testicular cancers have much better
responses; more than 60% of these patients can be cured with high-
dose chemotherapy.