Testicular Tumours

Presented by : Emmanuel Kamalondo

Choongo Simawawa
 Introduction
 Testicular tumors are rare.

 1 – 2 % of all malignant tumors.

 Most common malignancy in men in the 15 to 35 year

age group.

 Benign lesions represent a greater percentage of cases

in children than in adults.

 Most curable solid neoplasm

• Age - 3 peaks
2 – 4 yrs
20 – 40 yrs
above 60 yrs

• Testicular cancer is one of the few neoplasms

associated with accurate serum markers.

• Most curable solid neoplasms and serves as a

paradigm for the multimodal treatment of
malignancies.
 Improvement in Survival
 Effective diagnostic techniques

 Improved tumor markers

 Multi-model treatment
 Surgical

 Radiotherapy

 Multi-drug chemotherapy regimens

 Mortality
 before 1970 – 50 %

 1997 – 5 %
 AETIOLOGY OF TESTICULAR TUMOUR
• Cryptorchidism
• Intersex disorder – Klinefelter’s syndrome
• Testicular atrophy
• Trauma- prompts medical evaluation
• Chromosomal abnormalities - loss of chromosome 11, 13, 18,
abnormal chromosome 12p.
• Sex hormone fluctuations, estrogen administration
during pregnancy
• Race
• Carcinoma in situ
• Previous testicular cancer
 Germ cell tumors
1. Seminomas - 40%
(a) Classic Typical Seminoma
(b) Anaplastic Seminoma
(c) Spermatocytic Seminoma
2. Embryonal Carcinoma - 20 - 25%
3. Teratoma - 25 - 35%
(a) Mature
(b) Immature
4. Choriocarcinoma - 1%
5. Yolk Sac Tumour
 Non Germ Cell Tumors
1. Specialized gonadal stromal tumor
(a) Leydig cell tumor
(b) sertoli cell tumor

2. Gonadoblastoma

3. Miscellaneous Neoplasms
(a) Carcinoid tumor
(b) Tumors of ovarian epithelial sub
types
 Age wise incidence of
testicular tumour
Tumour Type Age group (years)
1. Seminoma 35-40
2. Pure Teratoma Pediatric age group
3. Embryonal CA 25-30
4. Chorio CA 25-35
5. Yolk sac Tumour infancy & child hood
6. Mixed terato CA 25-30
7. Lymphoma > 50
 Germ cell tumors
 Favourable outcome - GCT
 Sensitive to both
 Radiotherapy
 Chemotherapy

 Differentiation
 Rapid rate of growth
 Young – no co-morbid

 Extra Gonadal Germ Cell Tumors (EGCT)

 Prognosis is ½ GCT
 Seminoma
 The commonest variety of testicular tumour
 Adults are the usual target (4th and 5th decade);
never seen in infancy
 Right > Left Testis
 Starts in the mediastinum: compresses the
surrounding structure.
 Patients present with painless testicular mass
 30 % have metastases at presentation, but only
3% have symptoms related to metastases
• Serum alpha fetoprotein is normal
• Beta HCG is elevated in 30% of patients with
Seminoma
• Classification
a) Typical
b) Anaplastic
c) Spermatocytic
  Anaplastic
Spermatocytic

2% - 12% of seminomas  5% - 10

Old age > 50 yr  Middle age

Extremely low metastatic potential  Aggressive - lethal

Good prognosis  Greater mitotic activity

 Typical/ Classical  Higher local invasion

 82% - 85%  Higher metastatic potential

 Middle age  Higher rate of β

 PLAP – 90%  -HCG production

 Syncytiotrophoblsts – ↑Beta HCG (10%)  Inguinal orchidectomy +

 Very slow growth Radiation

 Inguinal orchidectomy + Radiation

 Macroscopically:
Characterized by a
circumscribed lobular
gray white fleshy
tumor that have areas
of necrosis &
hemorrhage
Cut surface in
homogenous and
greyish white or
pinkish in colour
• Microscopically:
 Typical seminoma Cells have
round to oval nuclei with
one to several nucleoli &
clear to eosinophillic
cytoplasm.
 Cell borders are well defined
arranged in solid nests
separated by fibrous septa.
 Active lymphocytic
infiltration in 80% cases.
 Strongly positive for
placental Alkaline
phosphatase (PLAP)
 Embryonal Carcinoma
 2nd most common germ cell tumor
 Present in majority of mixed germ cell tumors
 Most men present in their 20s to 30s with a
testicular mass
 Highly malignant tumours; may invade the cord
stuctures
 High degree of metastasis
 Serum AFP is normal , & beta HCG is elevated in
60 % of cases
 Macroscopically:
Tan to yellow neoplasms
(fleshy tumor) that
exhibit large areas of
hemorrhage and
necrosis.

• Most undifferentiated;
capacity to differentiate
to other NSGCT within
primary or mets
 Microscopically:
 Undifferentiated malignant cells
with crowded pleomorphic
nuclei
 Solid sheets,
 Papillary
 Glandular
 Tubular arrangement of cells
 Choriocarcinoma
 A rare and aggressive tumour (5yrs survival is 5%)
 Typically elevated hCG
 Presents with disseminated disease
 Metastasis to lungs and brain
 Primary is very small and often exhibit NO TESTICULAR
ENLARGEMENT
 Small palpable nodule may be present.
 Prone to hemorrhage, sometimes spontaneous (lungs
and brain)
 Catastrophic hemorrhage immediately after
chemotherapy;
 Macroscopically:
Primary lesion may be a
hemorrhagic or a clotted
mass in which bits of grey
tumor can be seen
Presents as nodules
• Microscopically:
Consists of both
syncitiotrophoblast and
cytotrophoblast
Prominent areas of
hemorrhage and necrosis.
 Yolk Sac Tumour
 Most common germ cell tumor ( & most
common testicular tumor ) in children, where
it occurs in its pure form.
 In adults, it is unusual in pure form, but is
found approx. 50 % of mixed germ cell
tumors.
 Testicular mass the most usual presentation.
 Always produce AFP, never hCG
 Easily detectable, lower relapse
 Macroscopically:
White to tan masses, with myxoid & cystic
changes
• Microscopically:
Reticular network of medium sized cuboidal
cellswith cytoplasmic and extracytoplasmic
eosinophil, hyaline like goblets (84%)
Glandular, papillary or microcystic pattern
Schiller-Duval bodies are characteristic
 TERATOMA
 Teratoma in greek means “monster tumor”
 Occurs in its pure form with a mean age of
diagnosis at 20 months
 In adults, occur as a component of mixed
germ cell tumor & is identified in > 47 % of
mixed tumors.
 Pure teratomas are uncommon.
 Normal serum markers.
◦ Mildly elevated AFP levels
 Macroscopically:
Largely depends on elements within it with solid & cystic areas
 Microscopically:
Contain more than one germ cell layers(ectoderm, endodermand
mesoderm).
Range from “mature” with well differentiated tissue to
“immature” with undifferentiated primitive tisuue.
Composed of somatic type of tissues that include enteric type
glands, respiratory epithelium, cartilage, muscles, hair etc.
Immature Teratomas contain immature neuroepithelium,
blastema or cellular stroma.
Can give rise to carcinoma, such as adenocarcinoma , or
sarcoma, such as rhabdomyosarcoma.
• Growing Teratoma Syndrome:
May grow uncontrollably, invade the surrunding
tissueand become unresectable
• Teratoma with malignant transformation
Rarely teratoma may transform into a somatic
malignancy such as rhabdomyosarcoma,
adenocarnoma or primitive neuroectodermal
tumour
Cut surface
Variably sized cysts
Gelatinous, mucinous,
hyalinized material
Intersposed solid islands –
cartilage/ bone/pancreatic/
liver/ intesttinal/ muscle/
neural/ connective tissue
 Secondary Tumors of Testis
• Lymphoma – most common secondary tumor
- most common testicular tumor in patients
above 50 years
- most common variety is histiocytic
• Leukamic Infilteration of testis
-primary site of relapse after ALL remission
-occurs mainly in the interstitial space
-biopsy for diagnosis
- no orchidectomy
- testicular irradiation for treatment
• Metastases to testis
- rare cases reported
 Tumors of adnexa / Paratesticular
tissue
• Adenomatoid tumor
-most common paratesticular tumor
-benign in nature
• Mesothelioma
-metastatic in 15% cases to inguinal lymph nodes
• Cystadenoma
- bilateral cases are associated with Von Hippel Lindau
syndrome
• Rhabdomyosarcoma
- most commonly seen in second decade of life
 Intratubular Germ Cell Neoplasia
(ITGCN)

Adjacent to germ cell tumor: 98%

•Cryptorchidism: 2-8%
•Prior germ cell tumor (contralateral testis): 5%
•50% risk of developing GCT in 5y
•Treat with observation, XRT (20 Gy) or orchiectomy
•Chemo reduces risk but still 25% - 45% risk of GCT at 10y
(Christensen et al. Ann. Oncol. 1998)
•Can be precursor to all types of GCT except
spermatocytic seminoma
 Metastasis
1. Direct Spread:
 This spread occurs by invasion.
 Whole of testis in involved and restricted
 Tunica albuginea is rarely penetrated
 May be crossed by “blunder biopsy”
 Scrotal skin involvement
 Fungation on the anterior aspect
 Spread to spermatic cord and epidedymis may
occur : points towards bad prognosis
2. Lymphatic spread:
Seminoma metastasize exclusively
through lymphatics
They drain primarily to para-aortic
lymph nodes in the region of origin
of tetsticular arteries
Left supraclavicular fossa through
the thoracic duct
Lymph from medial side of testes
run along the artery to the vas to
drain to nodes at the bifurcation of
common iliac
No inguinal nodes until scrotal skin
involvement
3. Blood Spread
 NSGCT spread through blood route
 Lungs, liver, bones and brain are the usual sites
usually involved
 GCT – Unique Features
Chemo and radiation sensitive
Capacity to differentiate
Consistent pattern of metastasis
Ability to produce marker substances (AFP/HCG)
NSGCT: unique potential for teratomatous differentiation
High growth rates 10-30 days

Retroperitoneum is usually the first and only site of metastatic

disease
Landing zones for right-sided tumors: Interaortocaval, precaval
lymph nodes

Landing zones for left-sided tumors: Para-aortic, left hilar

lymph nodes

Right to Left Crossover extremely common

 Clinical Features / Presentaion
1. Due to primary tumor
a) Painless testicular lump
b) Sensation of heaviness if size > than 2-3 times
c) Rarely dragging pain is complained of (1/3rd
cases)
d) May mimic epidedymo-orchitis
e) Sudden pain and enlargement due to
hemorrhage mimicking torsion
f) History of trauma (co-incidental
2. Due to metastasis
 Abdominal or lumbar pain (lymphatic spread)
 Mass in epigastrium
 Dyspnoea, hemoptysis and chest pain with lung mets
 Jaundice with liver mets
 Hydronephrosis by para-aortic lymph nodes
enlargement
 Pedal oedema by IVC obstruction
 Troiser’s sign
 Differential Diagnosis
• Testicular torsion

• Epididymitis, or epididymo-orchitis

• Hydrocele,

• Hernia,

• Hematoma,

• Spermatocele,

• Syphilitic gumma .
 Investigations
1. USG testes: gold standard
2. Tumor markers/ hormones
a) AFP
b) Beta hCG
3. Chest radiography
4. USG abdomen
5. CT abdomen
6. MRI: intra-abdominal and intra-thoracic
secondaries
7. IVP and RFT : obstruction on ureters
 Radiological work up

Plain X-Ray
chest:
Metastasis
USG :
Hypoechoic
relative to the
surrounding
parenchyma
 Seminoma
• Seminomas are well defined within the tunica
albuginea and homogeneously hypoechoic
 Embryonal cell cancers

• Embryonal cell cancers are

heterogeneous.

• The borders of the tumor are

less distinct.

• More aggressive in behavior.

• The tunica albuginea may be

invaded
 Yolk Sac Tumor

• Imaging findings are

nonspecific,especially in
children, in whom the only
finding may be testicular
enlargement without a defined
mass.
 Teratoma

• Well-circumscribed complex
masses. a common feature
and may be a

• Cysts are anechoic or complex,

depending on the cyst
contents (ie, serous, mucoid,
or keratinous fluid)
• Choriocarcinomas are often
heterogeneous with multiple
internal calcifications present.
• Leydig and Sertoli
cell, are generally
well defined and
hypoechoic.

• Calcifications are
frequently
described.
Testicular lymphoma
generally appears as
discrete hypoechoic
lesions, which may
completely infiltrate
the testicle &
epididymis
 “Burned-out" Germ Cell Tumor
• The patient may present with
widespread metastases even though the
primary tumor has involuted.

• These tumors are clinically occult, with

the testis being normal to small upon
palpation.

• These primary tumors have a variable

appearance. They are generally small
and can be hypoechoic, hyperechoic, or
merely an area of focal calcification.
 Clinical Staging TNMS

• Findings at Inguinal Orchiectomy Histology, size,

extent of invasion, LVI

• •Imaging Chest and Retroperitoneum

• CT scan with IV contrast
• PET CT more accurate for seminoma rather than
NSCGT

• •Serum Tumor Markers AFP, bHCG , LDH

 Serum Markers
TWO MAIN CLASSES
• Onco-fetal Substances : AFP & HCG
• Cellular Enzymes : LDH & PLAP
AFP - Trophoblastic Cells
HCG - Syncytiotrophoblastic Cells
( PLAP- placental alkaline phosphatase, & LDH lactic
acid dehydrogenase)
 AFP –( Alfafetoprotein)
NORMAL VALUE: Below 16 ngm / ml
HALF LIFE OF AFP – 5 and 7 days

Raised AFP :
• Pure embryonal carcinoma
• Teratocarcinoma
• Yolk sac Tumor
• Combined tumors,
• AFP not raised in pure choriocarcinoma , & in
pure seminoma
 HCG – ( Human Chorionic
Gonadotropin)
Has  and  polypeptide chain

NORMAL VALUE: < 1 ng / ml

HALF LIFE of HCG: 24 to 36 hours

RAISED  HCG -
100 % - Choriocarcinoma
60% - Embryonal carcinoma
55% - Teratocarcinoma
25% - Yolk Cell Tumour
7% - Seminomas
 ROLE OF TUMOUR MARKERS
• Helps in Diagnosis - 80 to 85% of Testicular Tumours have Positive
Markers

• Most of Non-Seminomas have raised markers

• Only 10 to 15% Non-Seminomas have normal marker level

• After Orchidectomy if Markers Elevated means Residual Disease or

Stage II or III Disease

• Elevation of Markers after Lymphadenectomy means a STAGE III

Disease
• Degree of Marker Elevation Appears to be Directly
Proportional to Tumour Burden

• Markers indicate Histology of Tumour:

If AFP elevated in Seminoma - Means Tumour has Non-
Seminomatous elements

• Negative Tumour Markers becoming positive on follow up

usually indicates -
Recurrence of Tumour

• Markers become Positive earlier than X-Ray studies

 LDH HCG AFP
Miu/ml Ng/ml
S0 _< N <N <N

S1 <1.5 x N < 5000 < 1000

S2 1.5-10x N 5000 to 1000 to

50000 10000
S3 >10x N > 50000 >10000
 PRINCIPLES OF TREATMENT
• Treatment should be aimed at one stage
above the clinical stage
• Seminomas - Radio-Sensitive. Treat with
Radiotherapy.
• Non-Seminomas are Radio-Resistant and best
treated by Surgery
• Advanced Disease or Metastasis - Responds
well to Chemotherapy
• Transscrotal biopsy is to be condemned.

• The inguinal approach permits early control of

the vascular and lymphatic supply as well as
en-bloc removal of the testis with all its
tunicae.

• Frozen section in case of dilemma

 Treatment of Seminomas
Stage I, IIA, ?IIB –
Radical Inguinal Orchidectomy followed by radiotherapy to
Ipsilateral Retroperitonium & Ipsilateral Iliac group Lymph
nodes (2500-3500 rads)

Bulky stage II and III Seminomas -

Radical Inguinal Orchidectomy is followed by Chemotherapy
 Testes sparing surgery
•Controversial
•Mass <2cm
•Simultaneous bilateral tumors
•Solitary testicle with normal
testosterone
•Biopsy adjacent parenchyma (80%
ITGCN)
•Can treat remaining testicle with
20Gy of XRT
 Scrotal violation

• Local recurrence higher (2.9% vs 0.4%)

(Capelouto et al. J. Urol. 1995)
• •Seminoma – extend radiation portal to
include groin and scrotum area
• •NSCGT – excise scar and cord remnant
• •Extensive groin resection or
hemiscrotectomy not required especially after
chemo
 Treatment of Non-Seminoma
Stage I and IIA:
RADICAL ORCHIDECTOMY
followed by RETROPERITONEAL LYMPH NODES DISSECTION

Stage IIB:
RPLND with possible ADJUVANT CHEMOTHERAPY

Stage IIC and Stage III Disease:

Initial CHEMOTHERAPY followed by SURGERY for Residual
Disease
Lymph Nodes Dissection For Right & Left Sided Testicular
Tumours
 Lymphatic drainage
• The primary drainage of the right testis is
within the interaortocaval region.

• Left testis drainage , the para-aortic region in

the compartment bounded by the left ureter,
the left renal vein, the aorta, and the origin of
the inferior mesenteric artery.

• Cross over from right to left is possible.

Retroperitoneal lymph node dissection

Rationale for RPLND:

The retroperitoneum is the most common site of occult
metastasis
15-25% of retroperitoneal teratoma, resistant to cheotherapy
Low risk of Abdomino-pelvic recurrence no need for long term
surveillance after bilateral RPLND
Offers high cure rates
The long term survival approaches 100% with RPLND +
adjuvant chemotherapy
Disadvantage:
Experienced surgeon
Major surgical procedure
 STANDARD CHEMOTHERAPY FOR
NON-SEMINOMATOUS GERM CELL
TUMOURS
Chemotherapy Toxicity
BEP -
Bleomycin Pulmonary fibrosis
Etoposide (VP-16) Myelosuppression
Alopecia
Renal insufficiency (mild)
Secondary leukemia
Cis-platin Renal insufficiency
Nausea, vomiting
Neuropathy
 PROGNOSIS
Seminoma Nonseminoma

Stage I 99% 95% to 99%

Stage II 70% to 92% 90%

Stage III 80% to 85% 70% to 80%

 Surveillance
 Rationale for surveillance:
70-80% patients of stage I are cured by orchidectomy
alone
No need of chemotherapy in majority of the patients
 The disadvantages being:
Higher risk of relapse
Need for long term surveillance (>5yrs)
Potential for secondary malignancies by surveillance
CT
More intensive therapy required in cases of relapse
than primary chemotherapy
“I always had the size difference there, but
I didn’t know…I would’ve still been waiting
if it hadn’t started hurting, it just got so
Yuvraj Singh –extra gonadal
painful I couldn’t sit on my bike anymore.” seminoma
-Lance Armstrong