This document discusses testicular tumors, including their etiology, classification, clinical presentation, diagnosis, staging, and treatment. Some key points:
- Testicular cancer is the most common cancer in men ages 15-35 and has a high cure rate with early detection and treatment.
- Risk factors include cryptorchidism, prior testicular cancer, infertility, and genetic factors. Carcinoma in situ is a precursor to most germ cell tumors.
- Tumors are classified as seminomas or non-seminomas. Staging involves tumor markers, imaging, and pathology to determine extent of disease.
- Treatment involves radical orchidectomy followed by radiotherapy for seminomas or chemotherapy for
2. Importance
⢠Testicular tumors are rare.
⢠1 â 2 % of all malignant tumors.
⢠Most common malignancy in men in the 15 to 35 year age group.
⢠Most curable solid neoplasms and serves as a paradigm for the
multimodal treatment of malignancies.
⢠Seminoma - most common bilateral primary testicular tumour;
Lymphoma - most common bilateral testicular tumour
4. Etiology
⢠Cryptorchidism
⢠Intersex disorder
⢠Testicular atrophy
⢠Chromosomal abnormalities - loss of chromosome 11, 13, 18, abnormal
chromosome 12p.
⢠Exogenous estrogen administration to mother during pregnancy
⢠Carcinoma-in-situ
⢠Previous testicular malignancy
5. Cryptorchidism
⢠7 - 10% patients - history of cryptorchidism
⢠Most common - seminoma
⢠5 - 10% tumors - contralateral testis
⢠Relative risk - Intraabdominal testis (1 in 20) > Intrainguinal
testis (1 in 80)
⢠Orchidopexy - does not alter malignant potential - facilitates
examination & detection
6. ⢠Malignancy due to
⢠Abnormal germ cell morphology.
⢠Elevated temperature - abnormal spermatocyte maturation.
⢠Endocrinal disturbances.
⢠Gonadal dysgenesis.
7. Carcinoma in-situ
⢠Pre malignant precusor of all GCT, except spermatocytic
seminoma.
⢠Incidence - 0.8%.
⢠Testicular CIS develops from fetal gonocytes.
⢠Characterized histologically by seminiferous tubules containing
only Sertoli cells and malignant germ cells.
8. ⢠Risk Factors for CIS:
⢠History of testicular carcinoma (5% to 6%),
⢠Extra gonadalGCT (40%),
⢠Cryptorchidism (3%),
⢠Contralateral testis with unilateral testis cancer (5% to 6%),
⢠Somatosexual ambiguity (25% to 100%)
⢠Atrophic testis 30 %
⢠Infertility (0.4% to 1.1%)
⢠TESTICULAR BIOPSY gold standard for diagnoses of CIS
11. Seminoma
⢠Classical: 80 - 85%
⢠middle age
⢠PLAP & B-hCG - raised
⢠slow growing
⢠good prognosis
⢠Spermatocytic: 5 - 10%
⢠age > 50 years
⢠low metastatic potential
⢠good prognosis
⢠Anaplastic: 5 - 10%
⢠middle age
⢠aggressive
⢠higher local & metastatic potential
⢠high B-hCG production
⢠Inguinal Orchiectomy + Radiation
12. Non-Seminomatous Germ Cell
Tumors
⢠Embryonal Carcinoma
⢠25 - 35 years
⢠3 - 6% testicular tumors
⢠small, rounded, irregular mass
⢠invades tunica albuginea
⢠Yolk Sac Tumor/ Endodermal
Sinus Tumor
⢠most common testicular tumor in
infants & children
⢠raised AFP
⢠histologically - cells demonstrate
vacuolated cytoplasm secondary
to fat and glycogen deposition,
resemble 1 - 2 week old embryos
13. ⢠Teratoma
⢠raised AFP
⢠resistant to both chemotherapy &
radiotherapy
⢠mature teratoma - differentiated
elements from 2-3 embryonic germ cell
layers
⢠immature teratoma - undifferentiated
primitive tissue
⢠malignant teratoma - malignant changes
⢠Chorionic Carcinoma
⢠pure choriocarcinoma - rare
⢠second - third decades
⢠raised PLAP, B-hCG
⢠high incidence of distant metastases
14. ⢠Leydig Cell Tumors
⢠most common non-germ cell cell timor of
testis - 1 - 3% testicular tumours
⢠bimodal age distribution - 5 - 9 years; 25
- 35 years age
⢠25% cases - childhood; bilaterally - 5 -
10% cases
⢠presentation - prepubertal children -
virilization; adults - gynecomastia
⢠elevated serum & urinary 17-
ketosteroids & estrogens
⢠Sertoli Cell Tumors
⢠rare; < 1% testicular tumors
⢠bimodal age distribution - < 1 year; 20 - 45 years
age
⢠presentation - testicular mass; virilization in
children; gynecomastia in adults
⢠Gonadoblastomas
⢠rare
⢠seen in patients with gonadal dysgenesis
⢠age group - 30 years of age
⢠clinical presentation - gonadal dysgenesis
15. Secondary Tumors of Testis
⢠Lymphoma
⢠most common testicular tumour
over age of 50 years
⢠most common secondary
neoplasm of testis
⢠presentation - painless
enlargement of testis,
constitutional symptoms in 25%
patients; bilateral - 50% patients
⢠Leukemic Infiltration of Testis
⢠relapse of children with acute
lymphocytic leukaemia
⢠bilateral - 50% cases
⢠treatment - bilateral testicular
irradiation with 20Gy & reinstitution od
adj chemotherapy
⢠Metastatic Tumor
⢠rare
⢠most common primary - prostate >
lung > gastrointestinal tract >
melanoma > kidney
17. Lymphatic drainage
⢠Right Testis - Inter-aortocaval nodes > Precaval > Preaortic > Right common iliac
> Right external iliac
⢠Left Testis - Left Para-aortic > Preaortic > Left common iliac > Left external iliac
⢠Cross over from right to left possible.
⢠Epididymis - external iliac chain.
⢠Inguinal node metastasis - scrotal involvement by the primary tumor, prior inguinal
or scrotal surgery, or retrograde lymphatic spread secondary to massive
retroperitoneal lymph node deposits.
⢠Testicular cancer spreads in a predictable and stepwise fashion, except
choriocarcinoma.
20. Physical Examination
⢠Firm to hard fixed area within tunica albugenia - suspicious
⢠Seminoma expand within the testis as a painless, rubbery
enlargement.
⢠Embryonal carcinoma or teratocarcinoma may produce an irregular,
rather than discrete mass.
⢠Choriocarcinoma - no testicular enlargement
22. Investigations
⢠All patients with a solid, firm intra-testicular mass that cannot be
transilluminated should be regarded as malignant unless
otherwise proved.
⢠Scrotal Ultrasound -
⢠rapid, reliable technique
⢠hypoechoic area within the tunica albuginea - markedly
suspicious for testicular cancer.
24. Alfa-fetoprotein
⢠NORMAL VALUE < 16 ngm/ml
⢠Raised AFP :
⢠Pure embryonal carcinoma
⢠Teratocarcinoma
⢠Yolk sac Tumor
⢠Combined tumors
⢠AFP not raised in pure choriocarcinoma & pure seminoma
30. Prognostic Grouping
Stage T N M S
Stage 0 Tis N0 M0 S0
Stage 1a T1 N0 M0 S0
Stage 1b T2 - T4 N0 M0 S0
Stage 1c any T N0 M0 S1 - S3
Stage IIa any T N1 M0 S0 - S1
Stage IIb any T N2 M0 S0 - S1
Stage IIc any T N3 M0 S0 - S1
Stage IIIa any T any N M1 S0 - S1
Stage IIIb any T any N M0 - M1 S2
Stage IIIc
any T any N M0 - M1a S3
any T any N M1b any S
31. Treatment
⢠Treatment should be aimed at one stage above clinical stage.
⢠Seminomas - radio-sensitive - treat with radiotherapy.
⢠Non-seminomatous - radio-resistant - surgery.
⢠Advanced diseases/ metastases - chemotherapy.
32. Treatment (Cont.)
⢠RADICAL INGUINAL ORCHIDECTOMY - first line of therapy
⢠Bulky Retroperitoneal Tumours/ Metastatic Tumors - Initially
âDOWN-STAGEDâ with CHEMOTHERAPY
⢠Transscrotal biopsy - 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.
38. Conclusion
⢠Improved Overall Survival of Testicular Tumour due to Better
Understanding of the Disease, Tumour Markers and Cis-platinum
based Chemotherapy.
⢠Current emphasis - diminishing overall morbidity of various
treatment modalities.