TEACHING MBBS CLASS PURPOSE

1. CARCINOMA TESTIS

2. TESTICULAR TUMOUR
1% of all Malignant Tumour
Affects young adults - 20 to 40 yrs - when
Testosterone Fluctuations are maximum
90% to 95% of all Testicular tumours from
germ cells
99% of all Testicular Tumours are malignant.
Causes Psychological & Fertility Problems in
young

3. Survival in Testicular Tumours
Improved overall survival in last 15 to 20 years
due to -
• Better understanding of Natural History and
Pathogenesis of disease
• Reliable Tumor Markers
• Cis-platinum based chemotherapy
• Modification of surgical techniques

4. Anatomy of Testis
 Scrotum: muscular pouch containing testes
 Testis: a network of tightly coiled
seminiferous tubules that converge and
anastamose into efferent tubules
 Encapsulated by tunica albuginea
 Epididymis: a structure formed from merged
efferent tubules, which attaches along the
posterior and upper border of the testis
 Described as having head, body & tail
 Vas deferens: tube arising from tail of
epididymis,
 Passes through inguinal canal and joins
seminal vesicle duct to form ejaculatory
duct, which passes into prostate gland
 Spermatic cord: structure formed by vas
deferens, testicular arteries, and veins

5. CROSS SECTION OF TESTIS

6. LYMPH NODES

7. EPIDEMIOLOGY
• 2-3 new cases / 100,000 male populations
• Life time probability of developing testicular CA –
0.2%
• Most common malignancy of 15-35 yrs male
• Age : 3 Peaks
- 20-40 yrs. Maximum
- 0 - 10 yrs.
- After - 60 yrs.
• Bilaterality : 2 to 3% Testicular Tumour

8. AETIOLOGY OF TESTICULAR TUMOUR
• Cryptorchidism
• Congenital abnormalities
– Testes, penis, or kidneys
– Inguinal hernia
• History of testicular cancer
• Family history (father, brother)
• Genetics: TGCT1 found
• HIV/AIDS
• Body size
• Moles

9. CRYPTORCHIDISM & TESTICULAR TUMOUR
Risk of Carcinoma developing in undescended
testis is
14 to 48 times the normal expected
incidence

10. CRYPTORCHIDISM & TESTICULAR TUMOUR
The cause for malignancy are as follows:
• Abnormal Germ Cell Morphology
• Elevated temperature in abdomen & Inguinal
region as opposed to scrotum
• Endocrinal disturbances
• Gonadal dysgenesis

11. CLASSIFICATION
I. Primary Neoplasma of Testis.
A. Germ Cell Tumour
B. Non-Germ Cell Tumour
II.Secondary Neoplasms.
III.Paratesticular Tumours.

12. I. PRIMARY NEOPLASMS OF TESTIS
A.Germinal Neoplasms : (90 - 95 %)
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

13. I. PRIMARY NEOPLASMS OF TESTIS
B. Nongerminal Neoplasms : ( 5 to 10% )
1. Specialized gonadal stromal tumor
(a) Leydig cell tumor
(b) Other gonadal stromal tumor
2. Gonadoblastoma
3. Miscellaneous Neoplasms
(a) Adenocarcinoma of the rete testis
(b) Mesenchymal neoplasms
(c) Carcinoid
(d) Adrenal rest “tumor”

14. II. SECONDARY NEOPLASMS OF TESTIS
A. Reticuloendothelial Neoplasms
B. Metastases
III. PARATESTICULAR NEOPLASMS
A. Adenomatoid
B. Cystadenoma of Epididymis
C. Mesenchymal Neoplasms
D. Mesothelioma
E. Metastases

16. Pathogenesis & Natural History of Testicular
Tumour
Course of Spread of Germ Cell Tumours are predictible
once histology of Tumour confirmed
Local invasion of epidydimis or spermatic cord is
hindered by tunica albugenia
Lymphatic Spread has a set pattern depending on site
of tumour
Seminoma may have non-seminomatous metastasis
High Grade Tumours spread by both Vascular invasion
& via Lymphatics

17. Pattern of Spread of Germ Cell Tumour
Right sided tumours-
interaortocaval
Left sided tumours – left
paraaortic & preaortic
nodes
Then cephalad to cisterna
chyli, thoracic duct and
supraclavicular (usually
left)
Epidydimis- External iliac
chain

18. CLINICAL FEATURES
• Painless Swelling of One Gonad
• Dull Ache or Heaviness in Lower Abdomen
• 10% - Acute Scrotal Pain
• 10% - Present with Metatstasis
- Neck Mass / Cough / Anorexia / Vomiting / Back
Ache/ Lower limb swelling
• 5% - Gynecomastia
• Rarely - Infertility

19. PHYSICAL EXAMINATION
• Bimanual Palpation of testis and paratesticular
structures
• Abdominal examination
• Lymph nodes
• Chest

20. Tx = Primary tumour cannot be assessed
T0 = No evidence of Tumour
T1s = Intratubular germ cell neoplasia
T1 = Confined to Testis and epididymis without vascular or lymphatic
invasion; tumour may invade tunica albuginea but not the tunica
vaginalis
T2 = Limited to testis and epididymis with vascular/ lymphatic
invasion or tumour extending through Tunica Albuginea with
involvement of tunica vaginalis
T3 = Invades Spermatic Cord with/without vascular/ lymphatic
invasion
T4 = Invades Scrotum with/without vascular/ lymphatic invasion
N1 = Single or multiple < 2 cm
N2 = Multiple < 5 cm / Single 2-5 cm
N3 = Any node > 5 cm
Epididymis or Scrotal skin – Lymph drainage to Inguinal Nodes
TNM Staging of Testicular Tumour

21. LDH hCG AFP
• S0 <N <N <N
• S1 <1.5x N <5000 <1000
• S2 1.5-10x N 5000-50000 1000-10000
• S3 <10 x N > 50000 >10000
TNMS Staging of Testicular Tumour

22. Clinical Staging of Testicular Tumour
• Staging A or I - Tumour
confined to testis.
• Staging B or II - Spread to
Regional nodes.
– IIA - Nodes <2 cm in size or < 6
Positive Nodes
– IIB - 2 to 5 cm in size or > 6
Positive Nodes
– IIC - Large, Bulky, abd.mass
usually > 5 to 10 cm
• Staging C or III- Spread beyond
retroperitoneal
Nodes or Above Diaphragm or
visceral disease(only lungs).
• Staging IV- visceral disease
involving other organs except
lungs.

23. Requirements for staging
To properly Stage Testicular Tumours following are pre-
requisites:
• (a) Pathology of Tumour Specimen
• (b) History
• (c) Clinical Examination
• (d) Radiological procedure - USG / CT / MRI / Bone Scan
• (e) Tumour Markers -  HCG, AFP

24. DICTUM FOR ANY SOLID SCROTAL SWELLINGS
All patients with a solid, Firm
Intratesticular Mass that cannot be
Transilluminated should be
regarded as Malignant unless
otherwise proved

25. Differential Diagnosis
• Metastasis from
prostate, lung, or
melanoma.
• Epididymitis
• Lymphoma
•Spermatocele
•TB, gumma
•Leukemia

26. • 1. Ultrasound - Hypoechoic area
• 2. Chest X-Ray - PA and lateral views
• 3. CT Scan
• 4. Tumour Markers
- AFP
-  HCG
- LDH
- PLAP
Investigation

28. Left Right
Axial CT Section demonstarating - Left Hydronephrosis, due to large Para-Aortic
Nodal Mass from a Germ cell tumour

29. TWO MAIN CLASSES
• Onco-fetal Substances : AFP & HCG
• Cellular Enzymes : LDH & PLAP
( AFP - Trophoblastic Cells
HCG - Syncytiotrophoblastic Cells )
Tumour Markers

30. NORMAL VALUE: Below 16 ngm / ml
HALF LIFE OF AFP – 5 and 7 days
Raised AFP :
• Pure embryonal carcinoma
• Teratocarcinoma
• Yolk sac Tumour
• Combined Tumour
AFP –( Alfafetoprotein )
REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma

31. 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
HCG – ( Human Chorionic Gonadotropin )

32. • Nonspecific tumor marker but is a useful
prognostic indicator
• Indicator of tumor burden
• Determines the rate of proliferation
• Because of its low specificity (high false-
positive rate), serum LDH levels must be
correlated with other clinical findings in
making therapeutic decisions
Lactate Dehydrogenase (LDH)

33. • 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
ROLE OF TUMOUR MARKERS

34. • 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
ROLE OF TUMOUR MARKERS cont...

35. • 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
PRINCIPLES OF TREATMENT

36. • Radical INGUINAL ORCHIDECTOMY is Standard
first line of therapy
• Lymphatic spread initially goes to
RETRO-PERITONEAL NODES
• Early hematogenous spread RARE
• Bulky Retroperitoneal Tumours or Metastatic
Tumors Initially “DOWN-STAGED” with
CHEMOTHERAPY
PRINCIPLES OF TREATMENT

37. Stage I, IIA, IIB –
Radical Inguinal Orichidectomy 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
Treatment of Seminomas

38. 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
Treatment of Non-Seminoma

39. Radical Orchiectomy
• Inguinal approach
• Testicle and spermatic
cord are excised then
sent for pathologic
staging.

40. • RPLND primary treatment (NSGCTs)
• Remove abdominal lymph nodes
• Problems mainly occur with the nerve:
infertility, ejaculation problems
Retroperitoneal Lymph Node Dissection

41. Limits of Lymph Nodes Dissection For Right &
Left Sided Testicular Tumours

42. • BEP: (Bleomycin, Etoposide, Cisplatin)
4 cycles 21d intervals (4 most common)
• EP: (Etoposide, Platinol)
4 cycles 21d intervals
STANDARD CHEMOTHERAPY FOR
NON-SEMINOMATOUS GERM CELL TUMOURS

43. Chemotherapy Toxicity
BEP -
Bleomycin Pulmonary fibrosis
Etoposide (VP-16) Myelosuppression
Alopecia
Renal insufficiency (mild)
Secondary leukemia
Cis-platin Renal insufficiency
Nausea, vomiting
Neuropathy
STANDARD CHEMOTHERAPY FOR
NON-SEMINOMATOUS GERM CELL TUMOURS

44. • No initial complete response
• VIP: (Vinblastin, Ifosamide,Mesna, Platinol)
3-4 cycles 21d intervals
Vinblastine 100mg/m2
I-Ifosfamide* 1200mg/m2
P-Cisplatin 20mg/m2
*Mesna 240mg/m2 every 4 hrs
Salvage Thearpy

45. Stage I, IIA, IIB Stage IIB, IIC, III
B - Bleomycin
Abdominal Radiotherapy E - Etoposide (VP-16)  4 cycles
P - cis-platin
Follow Up Stable/Regress Relapse/Growth
F/U RPLND
Chemotherapy
THERAPY OF PATIENT WITH SEMINOMA

46. Radical Inguinal Orchidectomy
Stage I, II (minimum)
RPLND
Stage I, II B1 Stage II B2
Observe BEP  2 cycles
Bleomycin
Etoposide
Cis-platin
Therapy of Nonseminomatous Germ Cell Testicular Tumours

47. Radical Inguinal Orchidectomy
Stage II C (advanced) / III
BEP  4 cycles
Complete Response Partial Response Progress
Observe RPLND VIP orAutologous
Bone marrow
Transplant
Cancer Teratoma / Fibrosis
V-Vinblastine
I-Ifosfamide OBSERVE
P-cis-platin
Therapy of Nonseminomatous Germ Cell Testicular Tumours

48. – physical examinations, chest radiographs
and serum tumor markers
– CT scans detect recurrence in the
retroperitoneum and chest
– Follow-up protocols vary by institution,
type, stage and treatment
Follow up

49. • Every 2-3 months 1st yr.
• Every 3-6 month 2nd yr.
• Every 6 month remainder 5 yrs.
• CT scans: 3-6 months 1st yr. then annually
• Men at high risk: Annually with self-exam
monthly
Recommended Exams/ Follow Up

50. Nonseminoma
Year 1-Tumor markers and CXR
every month;
CT abdomen every 2
month.
Year 2-Markers and CXR every 2
month;
CT abdomen every 4
month
Years 3-5 –Markers and CXR every 6
month;
CT abdomen every 6
months;
After Year 5-Markers and CXR
yearly
Surveillance
Seminoma
Year 1- Tumor markers and CXR
every 2 months;
CT abdomen every 3
month
Year 2-Markers and CXR every 2
month;
CT abdomen every 4 mo.
Years 3-5 –Markers and CXR every 6
month;
CT abdomen every 6
months
After Year 5-Markers and CXR
yearly

51. Testicular Self Examination
Method of screening
• Screening not
Recommended
• Good survival rate,
even at later stage
• Not cost-effective

52. PROGNOSIS
Seminoma Nonseminoma
Stage I 99% 95% to 99%
Stage II 70% to 92% 90%
Stage III 80% to 85% 70% to 80%

53. CONCLUSION
• Improved Overall Survival of Testicular Tumour
due to Better Understanding of the Disease,
Tumour Markers and Cis-platinum based
Chemotherapy
• Current Emphasis is on Diminishing overall
Morbidity of Various Treatment Modalities

54. Germ Cell Tumors in Infants & Children
• Most common testis tumour in prepubertal
boys.
• Slow growing scrotal mass
• Hydrocele present in 25% cases
• Alpha- Fetoprotein, elevated in > 90%

55. Germ Cell Tumors in Infants & Children
Treatment
Radical inguinal orchidectomy +/- RPLND
Advanced disease: chemotherapy
Radiotherapy used for residual disease
Prognosis is good,
Mean srvival is 87%.

56. THANK YOU!!