Testicular tumors

TESTICULAR
TUMORS
Dr Pankaj Bharadva

INTRODUCTIONINTRODUCTION
Most common malignancy in the age group of 15-
35 males.
Improved survival due to variety of reasons.
- accurate tumor markers
- improved diagnostic techniques
- effective chemotherapy
- well defined tumor biology

More common in higher
socioeconomic classes.
More common on Right side than left
(cryptorchidism --- Rt > Lt).
In primary testicular tumors, 1-2%
bilateral.
Seminoma most common GCT in B/L
primary testicular tumors.
Malignant lymphoma most common B/L
tumor of testis.

They are divided into two major categories:
1)Germ cell tumors → Approximately 95% of
testicular tumors
2)Sex cord– stromal tumors
Most germ cell tumors are aggressive
cancers → capable of rapid & wide
dissemination, although → current therapy
most can be cured
In contrast → Sex cord–stromal tumors are
generally benign

RISK FACTORSRISK FACTORS
Congenital:
Cryptorchidism
 7-10% of all testicular tumors, 3-14 times
 Relative risk : intraabdominal highest 1 in20,
inguinal lowest 1 in 80
 Seminoma is the commonest tumor in this
group.

Acquired :
 Trauma
 Exogenous estrogens (mother while pregnancy)
 Infection related testicular atrophy

Family predispositionFamily predisposition
 Development of testicular germ cell tumors → strong
family predisposition
 The relative risk of development of these tumors in
fathers & sons → 4 times higher than normal, and 8-10
times higher between brothers
 Genetic polymorphisms at Xq27 locus → may
be responsible for this susceptibility
7

CLASSIFICATIONCLASSIFICATION
1. WHO CLASSIFICATION.
 Germ cell tumors:90-95%
* Pure forms.
- Seminoma
- Embryonal Carcinoma
- Yolk sac tumors
- Trophoblastic tumors
- Teratoma
* Mixed forms

 Gonadal stromal tumors
- leydig cell tumor
- sertoli cell tumor
 Both germ cell and stromal elements
- Gonadoblastoma

2. ACCORDING TO CELL TYPE
 Seminoma
 Teratoma
differetiated.(TD)
intermediate(MTI)
anaplastic (MTA): embryonal carcinoma
trophoblastic(MTT):choriocarcinoma

 Secondary tumors
 Lymphoid and hemopoietic tumors
- lymhoma
- leukemia
 Tumors of collecting ducts and rete
 Tumors of tunica,epididymis,cord and appendices
 Soft tissue tumors
 Tumors like lesions
-orchitis
-epidermal cyst
-sperm granuloma

Germ Cell TumorsGerm Cell Tumors
 Incidence of testicular tumors in the USA 6 per→
100,000 → 300 deaths per year
 For unexplained reasons → worldwide increase in the
incidence
 In the 15- to 34-year age group, they constitute the
most common tumor of men → 10% of all cancer
deaths
 In the USA → much more common in whites
than in blacks
12

TUMORIGENIC MODEL FOR GCTTUMORIGENIC MODEL FOR GCT
C h o rio c a rc in o m a
( T ro p h b la s tic p a th w a y s )
Y o lk s a c tu m o r
(Y o lk s a c p a th w a y )
E x tra e m b ry o n ic d iffe re n tia tio n
T e ra to m a
In tra e m b ro y o n ic d iffe re n tia tio n
E m b ry o n a l c a rc in o m a
( T o tip o te n t tu m o r c e ll)
T o tip o te n t g e rm c e ll s e m in o m a
N o rm a l s p e rm a to c y te

PathogenesisPathogenesis
Most testicular germ cell tumors originate from
lesions called intratubular germ cell neoplasia
(ITGCN or IGCN) or ITGCN unclassified (ITGCNU
or IGCNU)
 However, ITGCN has not been implicated as a precursor
lesion of pediatric yolk sac tumors and teratomas, or of
adult spermatocytic seminoma.
 ITGCN is believed to occur → in utero and stay dormant
until puberty
14

ITGCNITGCN
 The lesion consists of:
 Atypical Primodal Germ Cells with large nuclei and
clear cytoplasm → twice the size of normal germ cells.
 Retain the expression of OCT3/4 and NANOG,
which are associated with pluripontentiality
 50% → develop invasive germ cell tumors within five
years after diagnosis → practically all patients with
ITGCN eventually develop invasive tumors.
 ITGCN is essentially a type of carcinoma in situ (CIS),
although the term CIS is not frequently used to refer to
this lesion.
15

ITGCNITGCN
 ITGCN share some of the genetic alterations found in germ cell
tumors such as the gain of additional copies of the short arm of
chromosome 12 (12p) in the form of an isochromosome of
its short arm, i(12p).
 This change is invariably found in invasive tumors regardless of
histological type.
 Activating mutations of c-KIT, which may be present in
seminomas, are also present in ITGCN.
16

SeminomaSeminoma
 Most common type of germ cell tumor (50%)
 Peak incidence → 3rd
decade & almost never
occur in infants
 Identical tumor in ovary → dysgerminoma
 Seminomas contain → an isochromosome 12p and
express OCT3/4 & NANOG
25% of these tumors → c-KIT activating mutations
 c-KIT amplification has also been repeated, but
increased c-KIT expression may occur without
genetic defects.
17

MorphologyMorphology
 Seminoma → uniform population of cells
 Spermatocytic seminoma → nosologic similarity →
a distinct tumor
 Seminomas → produce bulky masses, sometimes 10
times the size of the normal testis.
 Typical seminoma:
 Homogeneous, gray-white, lobulated cut surface
 Devoid of hemorrhage or necrosis
 Generally Tunica albuginea → not penetrated → but
occasionally extension to the epididymis, spermatic
cord, or scrotal sac
18

Fairly well-circumscribed, pale, fleshy, homogeneous massFairly well-circumscribed, pale, fleshy, homogeneous mass
19

MicroscopyMicroscopy
 Sheets of uniform cells divided into poorly demarcated
lobules by delicate septa of fibrous tissue containing a
moderate amount of lymphocytes.
 Seminoma cell → large and round to polyhedral, distinct
cell membrane, clear or watery-appearing cytoplasm, a
large central nucleus with 1-2 prominent nucleoli
 Mitoses vary in frequency.
 The cytoplasm contains varying amounts of glycogen.
 Seminoma cells → diffusely positive for c-KIT , (regardless of c-
KIT mutational status) OCT4, and placental alkaline
phosphatase (PLAP), with sometimes scattered keratin-
positive cells.
20

(a) Clear seminoma cells divided into poorly demarcated lobules by(a) Clear seminoma cells divided into poorly demarcated lobules by
delicate septa.delicate septa.
(b) Large cells with distinct cell borders, pale nuclei, prominent nucleoli,(b) Large cells with distinct cell borders, pale nuclei, prominent nucleoli,
and a sparse lymphocytic infiltrate.and a sparse lymphocytic infiltrate.
21

 15% → contain syncytiotrophoblasts → elevated serum
HCG → though not to the extent seen in patients with
choriocarcinoma
 May also be accompanied by an ill-defined
granulomatous reaction, in contrast to the well-
formed discrete granulomas seen with tuberculosis.
22

PATHOLOGYPATHOLOGY
CHARACTERISTIC
TYPICAL/CLASSIC
SEMINOMA
ANAPLASTC
SEMINOMA
SPERMATOCYTIC
INCIDENCE 82-85% 5-10% 2-12%
AGE 35-39 yrs 35-39 yrs >65 yrs
HISTOLOGY Large cells with distinct
borders, pale nuclei and
prominent nucleoli;
syncitiotrophoblast
Lymphocitic infiltrate
Increased
mitotic activity,
nuclear
pleomorphism
and anaplasia
Same as typical
seminoma, cells
may resemble
spermatogonia
METASTATIC
POTENTIAL
Slow growing, not
aggresive
Aggressive
locally as well as
systemically
Low and thus
favourable
prognosis
 SEMINOMATOUS GCT ( 35%)

Anaplastic seminomaAnaplastic seminoma
 Indicates greater cellular and nuclear irregularity
with more frequent giant cells & many mitoses.
 Is not associated with a worse prognosis & is not
treated differently
 Most authorities do not recognize anaplastic seminoma as
a distinct entity.
24

Spermatocytic SeminomaSpermatocytic Seminoma
 Uncommon tumor → 1-2% of all testicular germ cell
neoplasms
 Age of involvement → much later than for most
testicular tumors → generally over age of 65 years
 In contrast to classic seminoma → slow-growing, does
not produce metastases → prognosis is excellent
 In contrast to typical seminomas → lack lymphocytes,
granulomas, syncytiotrophoblasts, extra-testicular
sites of origin, admixture with other germ cell
tumors, and association with ITGCN 25

Embryonal CarcinomaEmbryonal Carcinoma
 Occur mostly in the 20- to 30-year age group.
 More aggressive than seminomas.
 Share some markers with seminomas → OCT 3/4 & PLAP,
but positive for cytokeratin & CD30, and negative for c-
KIT
 90% elaborate hCG or AFP
Morphology
 Smaller than seminoma → usually does not replace the entire
testis.
 On cut surfaces:
 Often variegated, poorly demarcated at the margins, and
punctuated by foci of hemorrhage or necrosis
 Extension through the tunica albuginea → into the
epididymis or cord frequently occurs. 26

In contrast to the seminoma, the embryonal carcinoma is aIn contrast to the seminoma, the embryonal carcinoma is a
Hemorrhagic mass.Hemorrhagic mass.
27

Cells grow in alveolar or tubular patterns,
sometimes with papillary convolutions.
Lack well-formed glands with basally
situated nuclei and apical cytoplasm seen in
teratomas.
More undifferentiated lesions → may display
sheets of cells
28

Neoplastic cells → epithelial appearance,
are large & anaplastic, have hyperchromatic
nuclei with prominent nucleoli.
In contrast to seminoma → cell borders are
usually indistinct, there is considerable
variation in cell and nuclear size and shape.
Mitotic figures and tumor giant cells are
frequently seen.

Sheets of undifferentiated cells as well as primitive glandularSheets of undifferentiated cells as well as primitive glandular
differentiation. The nuclei are large and hyperchromatic.differentiation. The nuclei are large and hyperchromatic.
30

The entire tumor is composed of undifferentiated cells that haveThe entire tumor is composed of undifferentiated cells that have
overlapping nuclei and scant cytoplasm. Tumor cells form solid nestsoverlapping nuclei and scant cytoplasm. Tumor cells form solid nests
with some slit spaces, allowing for the focal formation of shortwith some slit spaces, allowing for the focal formation of short
papillae.papillae.
31

Yolk Sac TumorYolk Sac Tumor
 Also known as endodermal sinus tumor , yolk sac
tumor is of interest because it is the most common
testicular tumor in infants and children up to 3
years of age.
 In this age group it has a very good prognosis.
 In adults → pure form is rare → frequently occurs in
combination with embryonal carcinoma.
32

 Non-encapsulated, homogeneous, yellow-white,
mucinous appearance.
 MICROSCOPIC:
 Lacelike (reticular) network of medium-sized cuboidal or
flattened cells.
 Papillary structures, solid cords of cells, and a multitude
of other less common patterns
33

50% → endodermal sinuses (Schiller-Duval
bodies) → consist of a mesodermal core
with central capillary and visceral and
parietal layer of cells resembling primitive
glomeruli.
Within and outside cytoplasm →
eosinophilic, hyaline-like globules with -α
fetoprotein (AFP) & α1-antitrypsin activity.
AFP → highly characteristic → underscores
differentiation to yolk sac cells.

An endodermal sinus pattern is composed of complex cords and solid groupsAn endodermal sinus pattern is composed of complex cords and solid groups
of cuboidal cells focally forming glomeruloid Schiller–Duval bodies (arrows).of cuboidal cells focally forming glomeruloid Schiller–Duval bodies (arrows).
Also present are a fibrous stroma and eosinophilic globules (asterisk).Also present are a fibrous stroma and eosinophilic globules (asterisk).
35

ChoriocarcinomaChoriocarcinoma
 Highly malignant form of testicular tumor
 In its “pure” → rare → less than 1% of all germ cell
tumors
Morphology
 Often → no testicular enlargement → are detected
only as a small palpable nodule .
 Typically → small → rarely larger than 5 cm in diameter.
 Hemorrhage & necrosis → extremely common.
36

 Contain two cell types:
1. Syncytiotrophoblastic → large and have many irregular
or lobular hyperchromatic nuclei and an abundant
eosinophilic vacuolated cytoplasm → HCG can be readily
demonstrated in the cytoplasm
2. Cytotrophoblastic → more regular and tend to be
polygonal, with distinct borders and clear cytoplasm →
grow in cords or masses and have a single, fairly uniform
nucleus
37

Clear cytotrophoblastic cells (arrowhead) with central nuclei andClear cytotrophoblastic cells (arrowhead) with central nuclei and
syncytiotrophoblastic cells (arrow) with multiple dark nucleisyncytiotrophoblastic cells (arrow) with multiple dark nuclei
embedded in eosinophilic cytoplasm. Hemorrhage and necrosis areembedded in eosinophilic cytoplasm. Hemorrhage and necrosis are
seen in the upper right field .seen in the upper right field .
38

TeratomaTeratoma
 Group of complex testicular tumors having various
cellular or organoid components reminiscent of
normal derivatives from more than one germ layer.
 Occur at any age from infancy to adult life.
 Pure forms → fairly common in infants & children,
second in frequency only to yolk sac tumors.
 In adults → pure teratomas are rare → 2-3% of germ
cell tumors
 Frequency of teratomas mixed with other germ cell
tumors → 45%.
39

Usually large, ranging from 5-10 cm in diameter
Because they are composed of various tissues →
gross appearance is heterogeneous: solid,
sometimes cartilaginous, and cystic areas.
Hemorrhage & necrosis → usually indicate
admixture with embryonal carcinoma,
choriocarcinoma, or both.
40

 Composed of:
 Heterogeneous, helter-skelter collection of
differentiated cells or organoid structures ((e.g. neural
tissue, muscle bundles, islands of cartilage, clusters of
squamous epithelium, structures reminiscent of thyroid
gland, bronchial or bronchiolar epithelium, and bits of
intestinal wall or brain substance, all embedded in a fibrous
or myxoid stroma))
 Elements may be mature (resembling various adult
tissues) or immature (sharing histologic features with
fetal or embryonal tissue)
 Common form in ovary → dermoid cysts and epidermoid
cysts (with benign behavior) → but rare in testis.
41

The variegated cut surface with cysts reflects the multiplicity of tissueThe variegated cut surface with cysts reflects the multiplicity of tissue
found histologically.found histologically.
42

Teratoma of the testis consisting of a disorganized collection of lands,Teratoma of the testis consisting of a disorganized collection of lands,
cartilage, smooth muscle, and immature stroma.cartilage, smooth muscle, and immature stroma.
43

This tumor is composed of mature somatic tissue, including squamousThis tumor is composed of mature somatic tissue, including squamous
epithelium, fat, and bone.epithelium, fat, and bone.
44

Immature teratoma. This tumor contains numerous immature nerveImmature teratoma. This tumor contains numerous immature nerve
cell precursors arranged in neuroblastic tubelike rosettes and nests.cell precursors arranged in neuroblastic tubelike rosettes and nests.
45

Teratoma with malignantTeratoma with malignant
transformationtransformation
 Rare → when malignancy exists in derivatives of one
or more germ cell layers → thus → there may be a focus
of squamous cell carcinoma, mucin-secreting
adenocarcinoma, or sarcoma
Importance of recognizing non–germ cell
malignancy arising in a teratoma → non–germ cell
component does not respond to
chemotherapy when it spreads outside of the
testis
The only hope → resectability of tumor
 Have an isochromosome 12p → similar to the germ cell
46

Mixed TumorsMixed Tumors
 60% of testicular tumors → composed of more than one
of the “pure” patterns.
 Common mixtures include:
 Teratoma + embryonal carcinoma + yolk sac
tumor; seminoma + embryonal carcinoma; and
embryonal carcinoma + teratoma (teratocarcinoma)
 In most instances → prognosis is worsened by
inclusion of the more aggressive element.
47

Seminomas Vs. NSGCTsSeminomas Vs. NSGCTs
 Seminomas → tend to remain localized to testis for a
long time → 70% present in clinical stage I.
 In contrast → 60% of NSGCTs → advanced clinical
disease (stages II and III).
 Metastases from seminomas → typically lymph nodes
→ hematogenous spread occurs later in the course of
dissemination.
 NSGCTs not only metastasize earlier → also use
hematogenous route more frequently.
 From a therapeutic viewpoint:
Seminomas → extremely radiosensitive,
whereas NSGCTs → relatively radioresistant →
poorer prognosis
48

NON GERM CELLNON GERM CELL
TUMORS OF TESTISTUMORS OF TESTIS
LEYDIG CELL TUMORS:
 Commonest non germ cell tumor of testis.
 1-3% of all testicular tumors.
 Bimodal age distribution: 5-9 yrs. And 25-35.
 Reinke’s crystals– fusiform shaped cytoplasmic inclusions

 Clinical features:
prepubertal- precocious puberty;tumors are
usually benign in this age group
adults may present with gynecomastia and
impotence;10% of tumors may be malignant.
 Lab. Findings: increased 17-ketosteroids(10 to
30 times elevation may be found in malignancy.)
and increased estrogens.
 Treatment: radical inguinal orchidectomy f/b
RPLND if malignant

 Constitute < 1% of all testicular tumors.
 Bimodal age distribution: <1 yr and 20-25 yrs.
 Clinical features:
Testicualr mass usually associated with
feminisation(gynecomastia)
 Treatment:
Radical inguinal orchidectomy f/b RPLND if
malignant(10% of tumors are malignant)
SERTOLI CELL TUMOR:SERTOLI CELL TUMOR:

SECONDARY TUMORS OFSECONDARY TUMORS OF
TESTISTESTIS
LYMPHOMA:
 Commonest secondary tumor and also commonest
tumor in pt. Over the age of 50 yrs.(5% of all testicular
tumors)
 Commonest b/l tumor-50% of cases but ususally
asynchronously
 Pathology: diffuse histiocytic lymphoma is
commonest.
 Clinical features: painless enlargement of testis,
constitutional symptoms.(25% of pt)
 Treatment: radical orchidectomy f/b treatment
according to stage of dz.

LEUKEMIC INFILTRATION:
 Usually presents as a relapse in children with diagnosed
acute lymphocytic leukemia.B/l involvement in 50% of
cases.
 Testicular biopsy rather than orchiectomy should be
performed.
 Treatment: b/l testicular irradiation with 20 Gy and
adjuvant chemotherapy.
METASTASIS:
 Very rare;usually are incidental findings at autopsy.
 Commonest site is prostate f/b lung,git,melanoma and
kidney.

PATHOGENESIS ANDPATHOGENESIS AND
NATURAL HISTORYNATURAL HISTORY
NATURAL HISTORY: short in fast growing
tumors like NSGCT.
SPREAD: predictable and stepwise
1.LOCAL: tunica albugenia is a natural barrier to
local invasion
2.HEMATOGENOUS: especially in choriocarcinoma
lung,liver,brain,bone adrenal,git.
Lymph nodes of the testes extend from T1 to L4 but are
concentrated at the level of the renal hilum because of their
common embryologic origin with the kidney.

PATHOGENESIS AND NATURALPATHOGENESIS AND NATURAL
HISTORYHISTORY
3.LYMPHATIC:
 Rt.testes:
interaortocavalprecavalpreaortic
paracaval f/b retrograde spread
 Lt.testes:
paraaorticpreaortic f/b retrograde
spread(common– ext.iliac)
 cross over from Rt to left may occur
 Inv.of scrotum or tunica
albugeniainguinal mets
 Inv.of epididymis or cord Distal
ext.ernal iliac & obturator mets
 Utimately spread to blood stream
occur through cisterna chyli and
thoracic duct

SYMPTOMSSYMPTOMS
Painless lump more common on the Rt., may be
bilateral(2-3%)
Pain: dull ache or heavy sensation in scrotum (30-40%)
 acute (10%) because of infarction or hemorrhage.
Due to metastasis (10%)
Rarely gynecomastia (1-5%, mainly in Teratomas)
or infertility
Asymptomatic: may be detected incidentally following
trauma or by the sexual partner.

Atypical cases-
- may simulate epididymo-orchitis / a
urinary infection.
- all testicular swellings should be treated
with suspicion & failure to respond to
antibiotics should raise the possibility
of a testicular tumor.

SIGNSSIGNS
 LOCAL EXAMINATION:
 Firm, nontender, heavy testes with loss of sensation
 Look for scrotal and epididymal involvement ( initially epididymis is
normal but later difficult to feel as incorporated by the growth).
 Thickened spermatic cord due to cremastric hypertrophy &
enlargement of testicular vessels.
 Vas is never thickened
 Prostate & Seminal vesicles are normal on P/R.
 Lax secondary hydrocele may be present (10%).
 Illac and inguinal lymphadenopathy.

 PER ABDOMEN:
 Enlarged retroperitoneal lymph nodes.
 Hepatomegaly
 Supraclavicular lymphadenopathy(Virchow’s node.)
SIGNSSIGNS

Clinical stagesClinical stages
 BODEN AND GIBB(1971)
 Stage I: tumor confined to testis, epididymis, or
spermatic cord.
 Stage II: distant spread confined to retroperitoneal
nodes below diaphragm.
 Stage III: metastases outside retroperitoneal nodes
or above diaphragm.
60

STAGINGSTAGING
TNM CLASSIFICATION: (AJCC 1996)
 Tx :cannot be assessed.
 To:no evidence of primary tumor.
 Tis:intratubular cancer(carcinoma in situ)
 T1:tumor limited to the testis and epididymis and no vascular
invasion.
 T2:tumor limited to the testis and epididimis with vascular
/lympatic invasion or tumor extending through the tunica
albuginea with involvement of tunica vaginalis
 T3:tumor invades the spermatic cord
 T4:tumor invades the scrotum

STAGING (CONT.)STAGING (CONT.)
REGIONAL LYMPH NODES
 Nx:regional lymph nodes cannot be assessed.
 N0:no regional lymph node metastasis.
 N1:lymph node mass 2 cm or less,or multiple lymph node
masses (</=6) none >2cm
 N2:lymph node mass > 2 cm but <5 cm in >6 nodes
 N3:lymph node mass >5 cm
DISTANT METASTASIS(M):
 Mo:no evidence of distant metastasis
 M1:non regional nodal or pulmonary mets
 M2:non pulmonary visceral masses

SERUM TUMOR MARKERS(S)SERUM TUMOR MARKERS(S)
LDH hCG(mIU/ml) AFP(ng/ml)
So </= N
and
</= N
and
</= N
S1 < 1.5 x N
and
< 5000
and
< 1000
S2 1.5-10 x N
or
5000-50000
or
1000-10000
S3 > 10 x N
or
>50000
or
>10000

STAGE GROUPINGSTAGE GROUPING
STAGE 1: T1-T4 No Mo So
STAGE 2 : Any T N1,N2,N3, Mo So/S1
a b c
STAGE 3 : Any T, any N, Mo M1
S2/S3 any S

TUMOR MARKERSTUMOR MARKERS
CHARACTERISTC
AFP hCG LDH
CHEMICALLY Single chain
glycoprotein
Glycoprotein
composed of alpha
and B chains
Cellular enzyme
T half 5-7 days 24-36 hrs variable
TUMORS
PRODUCING
Pure embryonic
carcinoma, terato
ca.,yolk sac tumor, not
by pure choriocarcinoma
or pure seminoma
Choriocarcinoma,
embryonal
carcinoma(40-
60%),seminoma(5-
10%)
Advanced GCT
especially
seminoma
FALSE +VE Malignancies,(liver,
pancreas,stomach,lung),
benign liver dz.,ataxia
telengectesia
Malignancies(liver,
pancreas,stomach,
lung,breast),
hypogonadism
Found in
smooth,cardiac
and skeletal
muscle ,liver
COMMENTS Normal levels: < 10
ng/ml
Alpha subunit cross
reacts with
LH,FSH,TSH
non specific.
But is a marker
of tumor burden
and recurr.

TUMOR MARKERS(CONT.)TUMOR MARKERS(CONT.)
 NORMAL LEVELS: A preop baseline level
must be done
AFP: < 10 ng/ml
hCG: < 4mIU/ml
LDH: < 1.5 times reference range

 CLINICAL SIGNIFICANCE:
1. Reflect the amount of tumor burden:
persistant elevation following an
orchiectomy suggests a metastatic
disease rather than a tumor confined to
retroperitoneum.
2. Monitoring therapeutic response:
failure to decline proportional to half
life indicates an incomplete response.
3. Prediction of histologic subtype:
4. Prognostic value:

INVESTIGATIONSINVESTIGATIONS
FOR DIAGNOSIS:
1)USG scrotum: hypocehoic
testicular mass is s/o
malignancy. calcification and
cysts may be found in non
seminomas.
2)FNAC: previously
contraindicated ,recently
shown that there is no scrotal
violation
3)Biopsy: rarely requre and
should be performed through
inguinal route.

INVESTIGATIONS(CONT.)INVESTIGATIONS(CONT.)
 FOR STAGING :
1. Chest X-ray : P/A and lateral view
2. CT scan: abdomen to detect retroperitoneal
lymphadenopathy.Chest CT may be done if abnormal
abdominal CT .Per se chest CT is non specific for
detecting pulmonary mets in absence of negetive abd.
CT
3. MRI: no added advantage over CT. tumors are
hypointense on T2 weighted and show brisk
enhancement with gadolinium.
4. Tumor markers:

TREATMENT OF GCTTREATMENT OF GCT
PRINCIPLES:
1. Radical inguinal
orchiectomy with
clamping of cord at deep
ring is the first and the
essential step in
treatment.
2. Histological diagnosis of
the tumor is mandatory
to plan adjuvant therapy.

TREATMENT(CONT.)TREATMENT(CONT.)

TREATMENT OF SEMINOMATREATMENT OF SEMINOMA
LOW STAGELOW STAGE
S P E R M A T O C Y T IC
n o a d ju v a n t th e r a p y
S U R V E IL L A N C E
r e lia b le a n d m o tiv a te d p t.
N O R IS K F A C T O R S
R A D IA T IO N L O W D O S E
a b d o m in a l a n d p e lv ic
C H E M O T H E R A P Y
s in g le a g e n t c a r b o p la tin
R IS K F A C T O R S P R E S E N T
T Y P IC A L A N D A N A P L A S T IC
l/f r is k fa c to r s
-tu m o r > 6 c m
-v a s c u la r o r ly m p h a tic in v a s io n
S T A G E 1 S E M IN O M A
T 1 -3 N o M o S o
S T A G E 1 S E M IN O M A
R A D IA T IO N - A B D O M IN A L &
P E L V IC
If ly m p h n o d e s c lo s to k id n e y
S T A G E 2 A A N D 2 B S E M IN O M A
T 1 -3 N 1 M o S o /S 1 a n d T 1 -3 N 2 M o S 0 /S 1
S E M IN O M A

RADIOTHERAPY INRADIOTHERAPY IN SEMINOMASEMINOMA
STAGE FIELD OF EBRT DOSE RELAPSES
1-2A Para aortic and ipsilateral renal hilar
(previously pelvic nodes were
included)
25 Gy over 3
wks.@
150 cGy/day
2-4%
2B Ipsilateral pelvic( but B/L common
illac),para aortic,para caval-hockey
stick field
Shield the kidney.
H/o herniorraphy or orchidopexy
contralat.inguinal region to be
included with sheilding of testis.
35 Gy
Conventional
fractionation
used
4%

RADIOTHERAPY(CONT.)RADIOTHERAPY(CONT.)
 FIELDS OF RADIOTHERAPY:
1. PARA AORTIC: boundaries : superiorly T10/11 at
the origin of thoracic duct and laterally upto internal
inguinal ring.The contralateral nodes are treated on
individual basis.
2. PELVIC : L4 vertebra to inguinal ligament including the
orchiectomy scar.
 LIMITED FIELD(limited to retroperitoneum)
 To decrease the chronic complications
 Used only in stage 1 disease.
 Mediastinal irradiation is no longer
recommended.

RADIOTHERAPY(CONT.)RADIOTHERAPY(CONT.)
COMPLICATIONS:
 ACUTE: nausea
dry squamation and erythema of skin
transient decrease in spermatogenesis
 CHRONIC: temporary decrease in spermatogenesis
secondary malignancies(e.g.leukemia.)
gastrointestinal complications
 SURVIVAL RATES:
STAGE 1: >95%
STAGE 2: 80%(70-92%)

TREATMENT OF ADVANCEDTREATMENT OF ADVANCED
SEMINOMA(STAGE 2C AND 3)SEMINOMA(STAGE 2C AND 3)
d i f f u s e d e s m o p l a s t i c r e a c t i o n :
O B S E R V A T I O N
O b s e r v a t i o n
3 m t h ly / 1 y r
6 m t h l y /5 y r
H i s t o lo g y :
f ib r o s i s / n e c r o s is
S a l v a g e c h e m o t h e r a p y
V I C
H i s t o l o g y :
G C T
D is c r e t e w e l l d e l i n e a t e d m a s s > 3 c m :
S U R G I C A L R E S E C T I O N
R e s i d u a l r e t r o p e r i t o n e a l m a s s
( o n C T )
C i s p la t i n b a s e d c h e m o t h e r a p y
S T A G E 2 C ( T 1 - 4 N 3 M 0 S 0 / S 1 ) A N D S T A G E 3 S E M IN O M A ( T 1 - 4 N O - 3 M 1 - 2 S 0 - 3 )

TREATMENT OF STAGE 1TREATMENT OF STAGE 1
NSGCTNSGCT
S U R V E I L L E N C E
in m o t iv a t e d r e lia b le p t .
r is k fa c t o r s a b s e n t
s t a g e N 0 : / N 1 ( < 2 c m )
O B S E R V A T I O N
s t a g e N 2 ( > 2 c m )
A D J U V A N T C H E M O T H E R A P Y
B E P 2 c y c le s
M O D I F I E D
R P L N D
P R I M A R Y C H E M O T H E R A P Y
B E P - 3 C Y C L E S
r is k fa c t o r s p r e s e n t
R I S K F A C T O R S
T 2 o r h ig h e r
e m b r y o n a l > 4 0 %
v a s c u la r / ly m p h a t ic in v a s io n
S T A G E 1 S
p e r s is t e n t t u m o r m a r k e r e le v a t io n
a n d n o r a d io lo g ic d z .
S T A G E 1
T 1 - 4 N 0 M 0 S 0

SURVEILLANCE IN STAGE 1SURVEILLANCE IN STAGE 1
NSGCTNSGCT
 INDICATIONS:
 Risk factors for relapse
 Pt is motivated and reliable for regular follow up.
 PROTOCOL:
1. History examination 2m/1st
2yr
CBC,LFT,tumor markers 4m/3-4yr
Chest x-ray 6m/5yr
2. CT scan 4m,6m,12m respectively
 TOTAL PERIOD: 5yrs

TREATMENT OF STAGE 2ATREATMENT OF STAGE 2A
AND 2B NSGCTAND 2B NSGCT
n o a d ju v a n t c h e m o th e r a p y
m in im a l n o d a l in v o lv e m e n t
< 2 c m
a d ju v a n t c h e m o th e r a p y
B E P 2 C y c le s
n o d a l in v o lv e m e n t
> 2 c m
R P L N D -b ila te r a l P R IM A R Y C H E M O T H E R A P Y
B E P 3 c y c le s if
s u p r a h ila r ,p e lv ic o r in g u in a l L N
b a c k a c h e o r c o n tr a la te r a l d z .
S T A G E 2 A (T 1 -4 N 1 M O S O /S 1 )
S T A G E 2 B (T 1 -4 N 2 M 0 S 0 /S 1 )

RETROPERITONEAL LYMPHRETROPERITONEAL LYMPH
NODE DISSECTIONNODE DISSECTION
RATIONALE:
 Retroperiteoneal nodes are usually and often the
only site of metastatic disease.
 15-40% of the pts.are understaged even with the
most sophisticated imaging modalities
 Untreated retroperitoneal nodal metastasis are
usually fatal.
APPROACHES:Thoracoabdominal and midline
abdominal.Recently lap.methods

RPLND(CONT.)RPLND(CONT.)
 BOUNDARIES:
 STANDARD RPLND:
 Indications:
 non bulky stage 2
disease.(2A and 2B)
 Boundaries are renal
hilum superiorly, upto
the bifurcation of
common illac vessels
inferiorly removing all
nodal tissue betweeen
the ureters

MODIFIED RPLNDMODIFIED RPLND
 INDICATIONS:stage 1
disease only.
 Boundaries :resect all
interaortocaval and ipsilateral
nodes between the renal
hilum and the bifurcation of
common illac and minimise
contralateral dissection
below the level of IMA.
 Avoid suprahilar dissections.
 Advantages: less chances of
retrograde ejaculation bcoz
important symp. fibres from
opp. side are preserved.

LAPAROSCOPIC RPLNDLAPAROSCOPIC RPLND
Port placement for
laparoscopic
retroperitoneal
lymph node
dissection.
Four 10/12-mm
equally spaced
trocars are placed
in the midline.

RPLNDRPLND-- COMPLICATIONSCOMPLICATIONS
 LYMPHATIC: chylous ascites (2-3%); symptomatic cases
require therapeautic paracentesis.
 PULMONARY: Atelectesis
pneumonia
ARDS
Judicious monitoring of peri operative fluid administration is
essential esp.in pts. Treated with Bleomycin.
 WOUND INFECTIONS:

 VASCULAR INJURIES(INTRA-OP.) renovascular
injury can cause postop. Hypertension and bleeding
intraoperatively.
 GASTROINTESTINAL:
prolonged ileus
pancreatitis
gastrointestinal bleeding
duodenal hematomas and lacerations.
 ERECTILE & EJACULATORY DISTURBANCES

ROLE OF RADIOTHERAPYROLE OF RADIOTHERAPY
IN NSGCTIN NSGCT
◦ DISADVANTAGES OF RADIOTHERAPY:
 Many stage 2 bulky tumors have spread beyond the
retroperitoneum
 Does not provide pathological staging.
 Lack of comparable survival data.(24% relapse.)
 Post irradiation relapse: surgery and chemotherapy are
ineffective/not possible or cumulative toxicity precludes their
use.
 Complications of radiotherapy.

CHEMOTHERAPYCHEMOTHERAPY
INDICATIONS:
 Stage 2 bulky(2c) and 3-all GCTs.
 Stage 2 nonbulky(2a and 2b) NSGCT as an alternative to
RPLND(esp. in suprahilar disease)
 PROTOCOLS:
 CURATIVE INTENT:in good risk patients-3 cycles of BEP
every 21 days or 4 cycles of PE
 SALVAGE/POOR RISK:
• 4 cycles of BEP
• VIP –more toxic
• ABMT with high dose:4 cycles of BEP f/b 2 EP
 RESPONSE RATES: 70-80%

CHEMOTHERAPY (CONT.)CHEMOTHERAPY (CONT.)
DRUG DOSE ADR COMMENTS
BLEOMYCIN 30 U IV
on day
2,9,16
Fever, chills,
Pulmonary
fibrosis
Be careful with
FiO2 and Iv
fluids postop
ETOPOSIDE 100
mg/sq.m
IV days
1-5
myelosupression
CISPLATIN 20
mg/sq.m
Days 1-5
Renal
insufficiency
peripheral
neuropathy,mye
losupression
Monitor renal
function

TREATMENT OF HIGHTREATMENT OF HIGH
STAGE NSGCTSTAGE NSGCT
R E C U R R A N C E
g o fo r S A L V A G E C H E M O .
O B S E R V A T IO N
R E S O L U T IO N
N s.m a rk e rs,N C T sc a n
O B S E R V A T IO N
H isto lo g y - n e c ro sis,fib ro sis
te ra to m a
S A L V A G E C H E M O T H E R A P Y
V IP
G E R M C E L L T U M O R
R E S ID U A L R P M A S S
g o fo r b /l R P L N D
E X C L U D E F A L S E P O S IT IV E
P E R S IS T E N T T U M O R M A R K E R
E L E V A T IO N
B E P 3 C Y C L E S
G O O D R IS K D Z .
P O O R R E S P O N S E
g o fo r S A L V A G E C H E M O T H E R A P Y
1 . Ifo sfa m id e re p la c e s e to p o sid e
2 .h ig h d o se c h e m o w ith A B M T
P O O R R IS K D Z .
S T A G E 2 C A N D S T A G E 3

PROGNOSTIC CLASSIFICATIONPROGNOSTIC CLASSIFICATION
 GOOD RISK DISEASE:(NSGCT)
 Testis or retroperitoneal primary
 No nonpulmonary ,visceral metastasis
 S1 or S2 disease.
 POOR PROGNOSIS:
 Mediastinal primary
 Non pulmonary visceral metastasis
 S3 disease

PROGNOSISPROGNOSIS
SGCT:
 STAGE 1: 98%
 STAGE 2 nonbulky: 92-94%
 STAGE 2 bulky and 3: 35-75%
NSGCT:
 STAGE 1: 96-100%
 STAGE 2 non bulky: 90%
 STAGE 2 bulky and 3: 55-80%

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