non seminoma, germ cell tumor, nonseminoma, chorio, teratoma, pranaya,

2. INTRODUCTION
 Testicular cancer represents around 1–1.5
per cent of male neoplasms.
 Vast majority are germ cell tumours.
 Risk factors include
1. A history of testicular maldescent,
2. A history of a contralateral testicular
tumour,
3. Klinefelter’s syndrome.

3. Classification
 Tumours of the testis are classified according to their
predominant cellular type.
 GERM CELL TUMOURS
(90–95%)
 INTERSTITIAL TUMOURS
(1–2%)
 LYMPHOMA
(3–7%)
 OTHER TUMOURS
(1–2%)

4. Germ Cell Tumours(GCT)
Seminoma (52%-56% of GCT)
Embryonal cell carcinoma,
Yolk sac tumor,
Teratoma,
Choriocarcinoma.
NSGCT
(44-48%
0F GCT)

5. NON-SEMINOMATOUS
GERM CELL TUMOURS (NSGCT)
Embryonal cell carcinoma,
Yolk sac tumor,
Teratoma,
Choriocarcinoma.

6. Seminoma
 On average, seminomas occur at an older
average age than NSGCTs, with most cases
diagnosed in the fourth or fifth decade of
life .
 Seminoma typically has a cut surface which is
homogeneous and pinkish cream in colour.
 Compress neighbouring testicular tissue.

8. NORMAL TESTIS ON LEFT SIDE AND
SEMINOMA ON RIGHT

9.  Two histological variants--
1. More anaplastic appearance
(Syncytiotrophoblasts)
2. Cells which closely resemble different phases
of maturing spermatogonia (spermatocytic
seminoma
 Seminoma arises from ITGCN and is
considered to be the common precursor for
the other NSGCT subtypes.
 This ability of seminoma to transform into NSGCT
elements has important therapeutic implications
for the management of seminoma

10. CONTD…
 Seminomas metastasise mainly via the
lymphatics, haematogenous spread is
uncommon.
 Lymphatic drainage of the testes is to the para-
aortic lymph nodes near the origin of the
gonadal vessels.
 The contralateral para-aortic lymph nodes are
sometimes involved by tumour spread.
 the inguinal lymph nodes are affected only if
the scrotal skin is involved.

11. Non-Seminomatous Germ Cell
Tumours
(NSGCT)
 Tumours may be tiny but can reach the size of a
coconut.
 The smaller tumours may not even distort the tunica
albuginea.
 Most NSGCTs are mixed tumors that are composed
of two or more GCT subtypes.
Yolk sac tumour. Tumours with this component
secrete alpha fetoprotein (AFP).
Otherwise Endodermal sinus tumors- Schiller-Duval
body present in hp study
Yolk sac tumors almost always produce AFP but not
hCG.

12. Schiller duval body
Yolk sac tumor gross

13. Embryonal carcinoma
 Highly malignant tumours that occasionally
invade cord structures.
 EC is the most undifferentiated cell type of
NSGCT, with totipotential capacity to
differentiate to other NSGCT cell types
(including teratoma) within the primary tumor
or at metastatic sites

14. Embryonal
carcinoma

15. Choriocarcinoma-
Often produces human chorionic
gonadotrophin (HCG).
This is a highly malignant tumour that
metastasizes early via both the
lymphatics and the bloodstream.
Choriocarcinoma commonly spreads
by hematogenous routes,
And common sites of metastases
include lungs and brain >> eye,skin

18. Teratoma-
These tumours contain more than
one cell type with components
derived from ectoderm, endoderm,
and mesoderm.
Tumours may range from ‘mature’
with well-differentiated tissue
elements to ‘immature’ with
undifferentiated primitive tissues.
All can metastasise.

19. Contd…
 Mature teratomas may include elements of mature
bone, cartilage, teeth, hair, and squamous
epithelium, a fact that most likely explains the
name teratoma, which roughly means “monster
tumor,” in Greek.
 may cause mildly elevated serum AFP levels.
 Teratoma is resistant to chemotherapy.
 require consolidative surgical resection because
40% to 50% will have residual teratoma.
 Teratomas may grow uncontrollably, invade
surrounding structures,and become unresectable
(known as growing teratoma syndrome)

22. Interstitial cell tumours (1-
2%)
 Tumours arise from leydig or sertoli cells.
 Leydig cell tumour masculinises.
 Sertoli cell tumour feminises.
 Typically small well circumscribed tumours with
a yellow cut surface.
 Most prepubertal tumours (~25 %) produce
androgens, which cause sexual precocity
including prominent external genitalia,
suprapubic hair growth and a deep
masculinised voice

23. Contd..
 Most post-pubertal interstitial cell tumours
produce feminising hormones leading to
gynaecomastia,erectile dysfunction, loss of
libido and azoospermia.

24. Campbell urology 10th edition

25. Intratubular Germ Cell
Neoplasia(ITGCN)
 With the exception of spermatocytic
seminoma, all adult invasive GCTs arise
from ITGCN.
 ITGCN consists of undifferentiated germ cells
that have the appearance of seminoma that are
located basally within the seminiferous tubules.
 tubule usually shows decreased or absent
spermatogenesis, and normal constituents are
replaced by ITGCN

26. Initial Presentation
 most common presentation of testicular cancer is
a painless testicular mass.
 Pain is more commonly associated with NSGCT,
because these tumors tend to be more vascular and
exhibit more rapid growth compared with seminomas.
 Regional or distant metastasis at diagnosis
is present in approximately two thirds of
NSGCTs &15% of pure seminomas
 symptoms related to metastatic disease are
the presenting complaint in 10% to 20% of
patients.

27.  retroperitoneal metastasis may cause a palpable
mass,abdominal pain, flank pain due to ureteral
obstruction.
 Pulmonary metastasis may present as dyspnea,
chest pain, cough, or hemoptysis
 Metastasis to supraclavicular lymph nodes may
present as a neck mass
 A hydrocele may accompany a testicular cancer
and impair the examiner’s ability to evaluate the
testis.( USG is I/C)

28. Differential diagnosis
Testicular mass D/d includes -
1. Epididymoorchitis,
2. Torsion,
3. Hematoma
4. Paratesticular neoplasm (benign or
malignant
5. Hernia varicocele or spermatocele

29. A firm intratesticular mass should be
considered cancer until proven
otherwise and should be evaluated
further with scrotal ultrasonography.
In patients with a presumptive diagnosis
of epididymo-orchitis, patients should
be reevaluated within 2 to 4 weeks of
completion of an appropriate course of
oral antibiotics. A persistent mass or
pain should be evaluated further with
scrotal ultrasonography

30. Diagnostic Delay
 Testicular cancer patients are typically young and
may be less inclined to seek medical evaluation
for symptoms due to denial, ignorance, or limited
access.
 Longest period of delay has been attributed to the
physician in up to two thirds of cases.
 Prior studies show that up to one third of
testicular tumors are initially misdiagnosed as
epididymitis or hydrocele

31.  interval of delay is associated with advanced
clinical stage, suboptimal response to
chemotherapy, and diminished survival

32. Diagnostic Testing
Scrotal Ultrasonography
Serum Tumor Markers
Metastatic workup

33. Scrotal ultrasonography
 should be considered an extension of the
physical examination because it is widely
available, inexpensive, and noninvasive.
 both testes should be evaluated
ultrasonographically,- 2% of GCT are B/L
 With high-frequency transducers (5 to 10
MHz),intratesticular lesions as small as a few
millimeters can be identified and readily distinguished
from an extratesticular pathologic process.
 GCT --hypoechoic and two or more discrete
lesions may be identified.
 NSGCT- Heterogeneous echotexture within a
lesion

35. the homogeneous tissue of the testicular teratoma on the
left of the image produces multiple ultrasound reflections.

36. Serum Tumor Markers
AFP, LDH and hCG., PLAP(Placental Alkaline
Phosphatase)
 At diagnosis, AFP levels are elevated in 50% to
70% of low-stage (CS I, IIA, IIB) NSGCT and
60% to 80% of advanced (CS IIC, III) NSGCT.
 EC and yolk sac tumors secrete AFP.
 Choriocarcinomas and seminomas do not
produce AFP
 Patients with pure seminoma in the primary
tumor with an elevated serum AFP value are
considered to have NSGCT.
 The half-life of AFP is 5 to 7 days

38. AFP levels may also be raised in patients with
 hepatocellular carcinoma and
 cancers of the stomach, pancreas, biliary tract,
and lung.
 Ataxic telangiectasia -MCQ
 Hereditary tyrosinemia.-MCQ
hCG levels are elevated in 20% to 40% of
low-stage NSGCT and 40% to 60% of advanced
NSGCT.

39.  hCG is also secreted by choriocarcinoma and
EC.
 Levels >>5000 IU/L are usually associated with
NSGCT.
 The half-life of hCG is 24 to 36 hours.
 LDH levels are elevated in approximately 20%
of lowstage GCTs and 20% to 60% of advanced
GCTs.
 LDH-1 is the most frequently elevated isoenzyme
in GCT

41. CHEST IMAGING
 chest radiographs at the time of diagnosis as an
initial staging study, and
 CT should be performed in patients with elevated
postorchiectomy levels of serum tumor markers,
evidence of metastatic disease by physical
examination, equivocal findings on chest
radiography.

43.  As such there is no role for routine bone
scintigraphy or brain CT at the time of
diagnosis.
 A notable exception to this is brain CT for
patients with a highly elevated hCG
value(>10,000 IU/L).
 Because these levels are often
associated with metastatic
choriocarcinoma, which has a propensity
for brain metastases.

44. CT Brain In Metastatic Choriocarcinoma,

45. TNM Staging of Testicular Tumor
T
extent of primary tumor is usually classified after
radical orchidectomy and, for this reason, a
pathologic stage is assigned for T
N
CLINICAL-as determined by noninvasive staging
PATHOLOGIC (pN) -as determined by pathologic findings
of RPLND without prior chemotherapy or radiotherapy

46. S
Serum Tumor Markers
M
Distant Metastasis

47. Scrotal exploration and orchidectomy for
suspected testicular tumour
 The orchidectomy is undertaken via an inguinal
incision.
 The spermatic cord is displayed by dividing the
external oblique aponeurosis and a soft clamp is
placed across the cord to stop dissemination of
malignant cells as the testis is mobilised into the
wound.
 If necessary, the testis should be bisected along
its anterior convexity to examine its internal
structure.
 If there is a tumour, the cord should be double
transfixed and divided at the level of the internal
inguinal ring and the testis removed.

49. PATHOLOGICAL(p) PRIMARY
TUMOR
pTX Primary tumor cannot be assessed
pT0
No evidence of primary tumor (e.g., histologic scar
in testis)
pTis
Intratubular germ cell neoplasia (carcinoma in situ)
pT1
Tumor limited to the testis and epididymis without
vascular/lymphatic invasion;
tumor may invade into the tunica albuginea but not
the tunica vaginalis
pT2
with vascular/lymphatic invasion;
With involvement of the tunica vaginalis
pT3
invades the spermatic cord with or without
vascular/lymphatic invasion
pT4
invades the scrotum with or without vascular/lymphatic
invasion

50. Regional Lymph Nodes (N)-
clinicalNx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis with a lymph node mass 2 cm or less in greatest dimension;
or multiple lymph nodes, none more than 2 cm in greatest
dimension
N2 Metastasis with a lymph node mass >2cm & <5 cm in
greatest dimension; or multiple lymph nodes, any
one mass >2cm & <5 cm greatest dimension
N3 Metastasis with a lymph node mass more than 5 cm in
greatest dimension

51. N PATHOLOGICAL
pNX Regional lymph nodes cannot be assessed
pN0 No regional lymph node metastasis
pN1 Metastasis with a lymph node mass 2 cm or less in greatest dimension
and less than or equal to five nodes positive, none more than
2 cm in greatest dimension
pN2 Metastasis with a lymph node mass more than 2 cm but not more than 5
cm in greatest dimension; or more than 5 nodes positive,
none more than 5 cm; or evidence of extranodal extension of tumor
pN3 Metastasis with a lymph node mass more than 5 cm in greatest
dimension

52. Distant Metastasis (M)
MX Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
M1a Nonregional nodal or pulmonary metastasis
M1b Distant metastasis at site other than nonregional lymph nodes or
lung

53. Serum Tumor Markers (S)
SX Marker studies not available or not performed
S0 Marker study levels within normal limits
S1 LDH < 1.5 × N† and
hCG (MIU/mL) <5000 and
AFP (ng/mL) <1000
S2 LDH 1.5-10 × N or
hCG (MIU/mL) 5000-50,000 or
AFP (ng/mL) 1000-10,000
S3 LDH >10 × N or
hcG (MIU/mL) >50,000 or
AFP (ng/mL) >10,000

54.  Stage 0 pTis N0 M0 S0
 Stage I pT1-4 N0 M0 SX
 Stage IA pT1 N0 M0 S0
 Stage IB pT2 N0 M0 S0
• pT3 N0 M0 S0
• pT4 N0 M0 S0
 Stage IS Any pT/Tx N0 M0 S1-3
 Stage II Any pT/Tx N 1-3 M0 SX
 Stage IIA Any pT/Tx N1 M0 S0
Any pT/Tx N1 M0 S1
 Stage IIB Any pT/Tx N2 M0 S0
▪Any pT/Tx N2 M0 S1

55.  Stage III Any pT/Tx Any N M1 SX
 Stage IIIA Any pT/Tx Any N M1a S0
▪Any pT/Tx Any N M1a S1
 Stage IIIB Any pT/Tx N1-3 M0 S2
▪Any pT/Tx Any N M1a S2
 Stage IIIC Any pT/Tx N1-3 M0 S3
•Any pT/Tx Any N M1a S3
•Any pT/Tx Any N M1b Any S

56. MANAGEMENT OF NSGCT
 Clinical Stage I NSGCT
optimal management of CS I NSGCT is
controversial.Surveillance, primary RPLND, and
primary chemotherapy with BEP×2 are accepted
treatment options, with long-term survival rates
approaching 100% for each
Clinical Stage IS NSGCT
 CS IS is defined as the presence of elevated
postorchiectomy serum tumor markers
without clinical or radiographic evidence of
metastatic disease

57.  these patients should be treated similar to
those with CS IIC-III and receive induction
chemotherapy
 Clinical Stage IIA and IIB NSGCT
RPLND (±adjuvant chemotherapy )and
induction chemotherapy (±
postchemotherapy RPLND)
Arguments in favor of RPLND for CS IIA-B
are-
 13% to 35% of patients have pathologically
negative lymph nodes and thus avoid
chemotherapy.

58. 2. long-term cancer-specific survival is 98% to 100%
with RPLND ―
 The disadvantages of RPLND are –
1. additional therapy is required in 48% or more of
patients.
2. 13% to 15% have persistence of disease after
RPLND and require a full induction chemotherapy
regimen
3. high-quality RPLND may not be deliverable at all
institutions
 there is consensus that CS IIA-B NSGCT
patients with elevated AFP or hCG or bulky
lymph nodes (>3 cm) should receive induction
chemotherapy

59. Clinical Stage IIC and III NSGCT.
 Induction chemotherapy with cisplatin-based
multiagent regimens is the initial approach
used for the treatment
 induction chemotherapy is also the preferred
approach for CS IS and CS IIA-B with elevated
postorchiectomyAFP and Hcg
 specific regimen and number of cycles is based on
the IGCCCG risk stratification
(International Germ Cell Consensus Classification,
1997)
 BEP×4(bleomycin-etoposide-cisplatin) is
adopted as the standard regimen

60. For NSGCT, IGCCCG risk is
assigned based on the postorchiectomy
serum tumor marker levels,
mediastinal primary tumor,
and the presence of nonpulmonary
visceral metastase

61.  Postchemotherapy resection of all residual
masses is based on the incidence of residual
cancer (either viable malignancy or teratoma) in
50% or more of patients
 standard approach to patients who experience
relapse within 2 years after first-line chemotherapy
in conventional dose, second-line chemotherapy
with ifosfamide-containing regimens.
 standard approach to patients with relapse 2 years
or more after initial therapy is surgical resection of
all sites of disease if feasible.

62.  NSGCTs are not radiosensitive, but they are highly
sensitive to combination chemotherapy with
bleomycin, etoposide and cis-platinum (so called
BEP chemotherapy).
 Some good prognosis NSGCTs can be managed
by surveillance protocols (using regular CT
scanning and tumour marker measurement) with
the more high risk cases receiving chemotherapy

63. Retroperitoneal Lymph Node
Dissection( RPLND )
 Either a transabdominal or thoracoabdominal
approach to
 the retroperitoneum for lymph node dissection
may be used
 most consistent long-term morbidity of a
standard
 bilateral RPLND has been the loss of
antegrade
 ejaculation and, consequently, potential
infertility,
 owing to damage of sympathetic nerve
fibers

65.  Therefore patients are advised to complete
sperm banking before the surgery.The
sympathetic chain, the paravertebral
sympathetic ganglia, and postganglionic
sympathetic fibers T2 to L4 and their
convergence at the hypogastric plexus are
most crucial in the preservation of antegrade
ejaculation.
 Narayan and colleagues (1982) first reported
that modification of surgical boundaries
resulted in spontaneous return of ejaculation at
3 years.

66.  Exposing the Retroperitoneum—
1. Transabdominal
2. thoracoabdominal approach
 Setting Up the Dissection
 Lymphadenectomy

67. Thoracoabdominal
Approach Main advantages of this approach are to allow
easier visualization and dissection of the
suprahilar lymphatic tissues and less risk of
postoperative small bowel obstruction. In addition,
simultaneous thoracic procedures can be
performed through the same incision.
 Incision starts obliquely over the eighth or ninth rib
and curves downward ,paramedian toward the
pubic ramus. A subperiosteal rib resection is
performed and the ipsilateral rectus muscle is
divided.

69. Transabdominal Approach
 A midline incision is made from the xiphicostal
junction to a point 2 cm above the symphysis
pubis
 Careful inspection of the abdomen,
retroperitoneum, and pelvis is then carried out to
assess resectability and the presence of
metastatic disease. The greater omentum and the
transverse colon are then displaced superiorly.
 The small bowel is reflected to the right, and an
incision is made in the posterior peritoneum
medial to the inferior mesenteric vein

70.  This incision is continued cephalad to the ligament
of Treitz and is extended superiorly and medially
to the duodenojejunal flexure, allowing for superior
mobilization of the fourth portion of the duodenum
and pancreas

71.  The retroperitoneal space has been exposed. The duodenum
has been kocherized; its second, third, and fourth portions
have been reflected superiorly along with the pancreas and
superior mesenteric artery. The entire right colon has been
mobilized and exteriorized.

72. Prognosis

The prognosis of testicular tumours depends
on several factorS including the histological
type and the stage at presentation.
 For NSGCTs, a five-year survival rate of more
than 90 per cent is achievable in patients with
good prognosis tumours while for more
advanced tumours the five-year survival rate is
about 60 per cent

73. Sperm cryopreservation should
be offered to all patients
before RPLND,
chemotherapy, or radiation
therapy owing to the potential
effects of these treatments on
fertility.

74. Cisplatin-based chemotherapy
is associated with numerous
early complications and side
effects, including Fatigue,
myelosuppression, infection,
peripheral
neuropathy,hearing loss,
diminished renal function.

75. THANK
YOU…