1. Dr. Minhajuddin Khurram
Moderator: Dr Sajid A. Mudhol (Prof . And HOD Dept.
Of Surgery)
Al-Ameen Medical College, Bijapur, India.
TESTICULAR TUMOURS

2. IntroductionIntroduction
Comprise a morphologically and clinically
diverse group of tumors
+1-2% of all malignancies
95% are Germ Cell Tumours (GCTs)
Predominantly affects young males

3. EpidemiologyEpidemiology
1 -2 % of all cancers in USA
5 per 1 lac cases
90% GCT are in testes
2-5% in extra gonadal (eg retropreitoneum)
Cure rate increased with introduction of
platinum based chemotherapy from 10 to
80%

4. Predisposing FactorsPredisposing Factors
1. Cryptochordism
2. Positive family history
3. Positive personal history
4. Intratubular germ cell neoplasia
5. Trauma
6. Hormonal factors
7. Exposure to environmental oestrogen and
contaminations

5. Predisposing FactorsPredisposing Factors
1. Cryptochordism
 Most important risk factor
 6 times higher risk1
 Risk reduces to 2-3 times if orchidopexy done
before puberty
 One in five will have tumors in the normally
descended testis
 Probable pathogenesis: Increased
gonadotrophins/ abnormal reaction to
gonatrophins

6. Predisposing FactorsPredisposing Factors
2. Positive family history
Men with first degree relative with testicular
cancer
Median age being less by 2-3 yrs
Affected brother: 8-10 times more
Affected father: 2-4 times

7. Predisposing FactorsPredisposing Factors
3. Positive personal history
12 folds increased risk of developing GCT in
the contralateral testis
Higher risk for contralateral tumor if
 Younger age
 Seminoma

8. Predisposing FactorsPredisposing Factors
4. Intratubular Germ Cell Neoplasia
(ITGCN)
 A precursor lesion
 ITGCN consists of undifferentiated germ cells
having appearance of seminoma located basally
within seminiferous tubules.
 No spermatogenesis
 Present in adjascent testicular parenchyma in 80%
 50% risk of GCT in 5 yrs, 70% in 7yrs
 5-9% in unaffected contralateral testis; increases to
36% in atrophy or cryptochordism

9. Predisposing FactorsPredisposing Factors
5. Trauma
 No link proved yet between trauma and
testicular tumor
 May simply draw the patient’s attention to
the site
 Or may possibly hasten the growth of the
tumor

10. Predisposing FactorsPredisposing Factors
6. Hormonal Factors
 Thought to be a contributing factor
 Peak incidence after puberty
 Tumors are more common in dizygous twin
pregnancies than monozygous : More
maternal oestrogen in dizygous pregnancy!!

11. Predisposing FactorsPredisposing Factors
7. Exposure to environmental oestrogen
and contaminations
Testicular tumors on a rise in the past 30yrs
Synthetic oestrogen in plastics and
detergents
Exposure to DDT
(dichlorodiphenyltrichloroethane):
It is a potent androgen receptor antagonist
Half life 60-100 yrs: trapped in food chain

12. ClassificationClassification
Classified according to predominant
cell type:
1. Germ Cell tumors (95%)
a) Seminoma
b) Embyonal cell carcinoma
c) Choriocarcinoma
d) Yolk sac tumor
e) Teratoma

13. ClassificationClassification
Classified according to predominant cell
type:
2. Non Germ Cell tomors
a) Interstitial Cell Tumors / Sex Cord / Stromal Tumors
 Leydig cell tumors
 Sertoli Cell Tumors
 Gonadoblastoma
 Granulosa Cell tumors
a) Miscellaneous Testicular Neoplasms
 Epidermoid cyst
 Adenocarcinoma of rete testis
a) Secondary Tumors
 Lymphoma
 Leukemic Infiltration
 Metastases

14. ClassificationClassification
Classified according to predominant
cell type:
3. Tumors of the testicular adnexa
a) Adenamatoid Tumor
b) Cystadenoma
c) Mesothelioma

15. WHOClassificationWHOClassification

16. SeminomaSeminoma
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

17. SeminomaSeminoma
Serum alpha fetoprotein is normal
Beta HCG is elevated in 30% of patients
with Seminoma
Classification (of no clinical significance)
a) Typical
b) Anaplastic
c) Spermatocytic

18. SeminomaSeminoma
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

19. SeminomaSeminoma
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)

20. SeminomaSeminoma
Microscopically:

21. Spermatocytic SeminomaSpermatocytic Seminoma
A rare GCT and accounts for less than 1%
It represents a distinct clinicopathological
entity from other GCT
Does not arise from ITGCN
Not associated with crytochordism
Benign tumour; complete cure by
orchidectomy1
Not positive to PLAP

22. Spermatocytic SeminomaSpermatocytic Seminoma
Microscopically:
Three types of cells:
a) Small cells with narrow rim of cytoplasm
resembling secondary spermatocytes
b) Medium sized cells with eosonophilic cytoplasm
c) Scattered Giant cells
No lymphocytic infiltration

23. Embryonal CarcinomaEmbryonal 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

24. Embryonal CarcinomaEmbryonal Carcinoma
Macroscopically:
Tan to yellow neoplasms (fleshy tumor) that
exhibit large areas of hemorrhage and necrosis.
Microscopically:
Undifferentiated malignant cells with crowded
pleomorphic nuclei
Solid sheets,
Papillary
Glandular
Tubular arrangement of cells
• Most undifferentiated; capacity to differentiate
to other NSGCT within primary or mets

25. Embryonal CarcinomaEmbryonal Carcinoma

26. Embryonal CarcinomaEmbryonal Carcinoma

27. ChoriocarcinomaChoriocarcinoma
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;

28. ChoriocarcinomaChoriocarcinoma
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.

29. ChoriocarcinomaChoriocarcinoma

30. Yolk Sac TumourYolk 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

31. Yolk Sac TumourYolk Sac Tumour
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

32. TeratomaTeratoma
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

33. TeratomaTeratoma
Histologically benign, but found at
metastatic sites in NSGCT
Perhaps metastatised as Embryonal cell
ca
They are resistant to chemotherapy1
Surgical resection required post
chemotherapy in 40-50% cases

34. TeratomaTeratoma
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

35. TeratomaTeratoma
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.

36. TeratomaTeratoma

37. SpreadSpread
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

38. SpreadSpread
1. Direct Spread:

39. SpreadSpread
2. Lyphatic 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

40. SpreadSpread
2. Lyphatic spread:

41. SpreadSpread
3. Blood Spread
 NSGCT spread through blood route
 Lungs, liver, bones and brain are the usual
sites usually involved

42. Clinical Features / PresentaionClinical 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)

43. Clinical Features / PresentaionClinical Features / Presentaion
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

44. Clinical Features / PresentaionClinical Features / Presentaion
3. Clinical examination:
a) Enlarged testis (except choriocarcinoma)
b) Nodular testis
c) Firm to hard in consistency
d) Loss of testicular sensation (be gentle)
e) Secondary hydrocele
f) Flat and difficult to feel epidedymis
g) Sign of Vas negetive
h) General examination for mets

45. Clinical Features / PresentaionClinical Features / Presentaion
3. Clinical examination:
a) Enlarged testis (except choriocarcinoma)
b) Nodular testis
c) Firm to hard in consistency
d) Loss of testicular sensation (be gentle)
e) Secondary hydrocele
f) Flat and difficult to feel epidedymis
g) Sign of Vas negetive
h) General examination for mets

46. InvestigationsInvestigations
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

47. Clinical StagingClinical Staging
Stage I – Tumor confined to the testis
Stage II – Nodal disease present but
confined to below the diaphragm
Stage III – Nodal disease above the
diaphragm
Stage IV – Nonlymphatic metastatic
disease

48. AJCC Staging (TNM)AJCC Staging (TNM)
Primary Tumor (pT)
pTx: Primary tumor cannot be assessed
pT0: No evidence of primary tumor
pTis: ITGCN
pT1: Tumor confined to testicle; may invade into
the albuginea but not the tunica vaginalis
pT2: Tumor extending thru tunica albuginea
with involvement of tunica vaginalis or the
presence of angiolymphatic invasion.
pT3: Spermatic cord involvement.
pT4: Scortal involvement

49. AJCC Staging (TNM)AJCC Staging (TNM)
Regional Lymph nodes (by non-invasive
assessment)
Nx: nodal status unknown.
N0: No regional lymph node metastasis.
N1:single or multiple lymph node involved, <
2 cm
N2: single node, 2-5 cm or multiple nodes <
5 cm
N3:any nodes > 5 cm

50. AJCC Staging (TNM)AJCC Staging (TNM)
Distant metastasis (M)
Mx: status of metastases unknown
M0: no distant metastasis
M1: Distant metastasis

51. TreatmentTreatment
1. Inguinal orchidectomy as soon as the
diagnosis is confirmed
2. Then the treatment differs as per the
histological type: seminoma or NSGCT

52. TreatmentTreatment
1. Scrotal exploration and orchidectomy for
suspected testicular tumor
 Orchidectomy undertaken by the inguinal incision
 Spermatic cords are displayed
 A soft clamp applied across the cord
 Mobilise testis to the wound
 If neseccary, bisect the testes along the anterior
convexity to examine
 Take biopsy, send for frozen section
 In case of tumor, double transfix and divide at the
level of the deep ring
 Some advice hemi-scrotectomy along with
orchidectomy

53. TreatmentTreatment
2. Radio/Chemotherapy
A. Stage I tumor:
 Seminomas:
 Radio-sensitive and chemo sensitive (platinum based
regimen)
 Current protocol: radiotherapy is the mainstay of
treatment with CT and tumor marker based surveillance
 In men who demonstrate relapse, chemotherapy to be
applied
 NSGCT
 Not radio-sensitive
 Subjected to BEP (Bleomycin, etoposide and cis-platinum)

54. TreatmentTreatment
2. Radio/Chemotherapy
A. Stage II- IV
 Combination chemotherapy for seminoma and
NSGCT
 RPLND needed in some cases for post
chemotherapy masses in the retroperitoneum

55. TreatmentTreatment
 Radiotherapy:
 Given to para-aortic and ipsilateral lymph
nodes, field extending from D10-11interspace
to the lower border of the obturator foramen
 Anterior and posterior fields are given
alternatively
 Laterally to the hila of the kidneys
 Contralateral testis being protected by thick
lead cups
 High enery Xrays- 6-8MeV with linear
accilerator
 3000 rads delivered in 3-4 wks

56. TreatmentTreatment
 Chemotherapy
Chemotherapy Toxicity
BEP -
Bleomycin Pulmonary fibrosis
Etoposide (VP-16) Myelosuppression
Alopecia
Renal insufficiency(mild)
Secondary leukemia
Cis-platin Renal insufficiency
Nausea, vomiting
Neuropathy

57. TreatmentTreatment
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

58. TreatmentTreatment
Lymph node dissection:

59. SurveillanceSurveillance
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

60. SurveillanceSurveillance
No fixed surveillance protocol
Surveillance imaging and testing intense in
first 2 yrs
Less frequent in 3-5 yrs
Surveillance after 5 yrs for late relapse
Different studies had surveillance CT
scans 2-13 times in 5 yrs

61. Interstitial cell tumorsInterstitial cell tumors
1. Leydig cell tumors
Considered a pre-ubertal tumor
May affect 20-60yrs of age
A masculinising tumor, produces androgens
No association with crytochordism
Presents with painless testicular mass
Precocious puberty
 Prominent external genitalia
 Deep masculinised voice
 Pubic hair
Gynacomastia and decreased libodo due to
oestrogen production by perpheral conversion

62. Interstitial cell tumorsInterstitial cell tumors
1. Leydig cell tumors
10% are malignant
Orchidectomy is te treatment of choice
Regression of symptoms after orchidectomy
may not be complete
Metastasize by blood to lungs and
retroperitoneum
Abdominopelvic CT, chest Xray, RPLND
Insensitive to radiotherapy and chemtherapy

63. Interstitial cell tumorsInterstitial cell tumors
2. Sertoli Cell Tumor
 Considered a post pubertal tumor
 But can occur in any age group including infants
 No association with crytochordism
 Gynacomastia in 1/3rd
of cases
 10 % are malignant
 Inguinal orchidectomy is the treatment
 RPLND
 Radiotherapy and chemotherapy are ineffective

64. Interstitial cell tumorsInterstitial cell tumors
3. Gonadoblastoma
 Mixed germ cell/sex cord/stromal tumor
 Composed of seminoma like germ cells and
Sertoli differentiation
 Exclusively in patients with dysgenic gonads
and intersex syndromes
 80% are phenotype females with primary
amenorrhoea
 20% are males with crytochordism and
dysgenic gonads and hypospadias

65. Interstitial cell tumorsInterstitial cell tumors
3. Gonadoblastoma
 Considered in-situ malignant form of GCT
 Bilateral orchidectomy because of risk of
bilateral tumours

66. Miscellaneous Testicular NeoplasmsMiscellaneous Testicular Neoplasms
1. Epidermoid Cyst
 A rare benign neoplasm
 Mondermally differentiated teratoam
 Resemmbles Dermoid cyst
 Enucleation or orchidectomy
 HPR is must

67. Miscellaneous Testicular NeoplasmsMiscellaneous Testicular Neoplasms
2. Adeno-carcinoma of rete testis
 A rare but highly malignant neoplasm
 Arises from collecting system of testis
 Usual presentation: painless swellinng with
hydrocoele
 More than 50% present with mets
 Mean survival period is 1 yr
 Radiotherapy and chemotherapy are ineffective
 RPLND in cases of limited retroperitoneal mets

68. Secondary tumorsSecondary tumors
1. Lymphoma
 Primary testicular Non-Hodgekin’s lymphoma is
rare
 Mostly involvement of testes by dissemination from
other sites
 Bilateral involvement in 35 % cases
 Presents as painless testicular mass
 25% have systemic symptoms (fever, night sweats
and weight loss)
 10% CNS involvement
 Radical inguinal orchidectomy
 Refer to heamto-oncologist for staging and
subsequent therapy

69. Secondary tumorsSecondary tumors
2. Leukemic Infiltration
 Relapse of ALL in testes
 Diagnosis by biopsy
 No orchidectomy
 Local control with low dose radiotherapy
(20Gy)
 Should include the contralateral testis:
Bilateral involvement

70. Secondary tumorsSecondary tumors
3. Metastases
 Metastases from prostate cancer
 Lung cancer
 Melanoma
 Colon cancer
 Kidney malignancy
 Presents as diffuse metastatic disease

71. Tumours of the Testicular AdnexaTumours of the Testicular Adnexa
1. Adenomatoid
 Most cmmon paratesticular tumour
 Involving the epidedymis mostly
 May arise from spermatic cord
 Presents as small (0.5 to 5cm) painless
paratesticular mass detected on routine
examination
 3rd
to 4th
decade of life
 Benign
 Excision by inguinal route

72. Tumours of the Testicular AdnexaTumours of the Testicular Adnexa
2. Cystadenoma
 Cystadenoma is benign epithelial hyperplasia of
epidedymis
 Multicystic
 Glandular or pappillary configuration
3. Mesothelioma
 Arises from tunica vaginalis
 Painless scrotal mass with hydrocele
 Older adults
 Both Benign and malignant varieties have been identified
 Malignant cases ralted to asbestos exposure
 Radical orchidectomy
 RPLND in malignant cases

73. ReferencesReferences
1. Textbook of Urology 10th
Ed. By
Cambell and Walsh
2. Short practice of surgery, Bailey and
Love
3. A concise textbook of surgery by Dr S.
Das

74. THANK YOU