The Testicular Cancer Awareness Network

testicular cancer current management

Privacy Policy
Americans with Disabilities Act (ADA)
How to Find a Cancer Treatment Trial
Three types of Stages of Testicular Cancer
Alternative treatment:
Justins Page
How can patients and their families cope with testicular cancer
Links & Support Groups
Testicular problems
Sexually Transmitted Diseases
Urinary Tract Infections
Questions to Ask Your Doctor about Cancer Treatment
Chemotherapy Side Effects
The Orchiectomy
Testicular Implants
Clinical trials
testicular cancer current management
Questions and Answers
News Articles Related to Testicular Cancer
TC Dictionary

Epidemiology and Aetiology

The incidence of testicular tumours is approximately 3-4 cases per 1,00,000 males each year. The incidence is believed to be doubling every 30 years for the white males. The incidence is highest in Scandinavia, Switzerland and Germany (5-6 cases per 1,00,000 males annually), intermediate in USA and UK while it is lowest in Asia and Africa (0.8 per 1,00,000 males in Japan annually). [1] At Tata Memorial Hospital about 150-160 cases are seen every year, the commonest age group affected is between 20-35 years. [2]

Testicular cancer is slightly more common on the right than on the left, which parallels the increased incidence of cryptorchidism on the right side. One to 2% of primary testicular tumours are bilateral, and up to half of these tumours have history of unilateral or bilateral cryptorchidism. Tumours may be synchronous or metachronous but they are usually of the same histologic type.

Although the cause of testicular cancer is unknown, both congenital and acquired factors are linked with its development. Cryptorchid tests are at a higher risk for tumour development. Level of descent of the testis appears to be correlated with the risk of tumour development, risk for intra abdominal testis is 1 in 20 and for the inguinal testis 1 in 80. Seminoma is the commonest histologic type. Orchiopexy facilitates the examination of testis but does not alter the risk of tumour development. Current studies have implicated the role of transplacental damage to the foetal gonads by the maternal oestrogen levels. Offsprings of dizygotic twin pregnancies are associated with increased testis cancer risk (odds ratio (OR)1.5) as compared to offsprings from monozygotic twin pregnancies. [3] Similarly, sons born after a pregnancy characterized by severe maternal nausea are associated with increased testis cancer risk. [4] Other acquired factors such as trauma and infection-related testicular atrophy (mumps orchitis) have been found to have weak association with risk of testis cancer development. Recent segregation analysis of Swedish and Norwegian families has suggested a role of a high-frequency recessive gene in familial testis cancer. [5]

Clinico-pathological features

About 95% of testicular tumours are of germ cell origin (GCT), only 5% of tumours are of other histologic types. Current accepted model of testicular tumour development is that totipotential germ cells follow abnormal pathways of differentiation resulting into either seminoma or embryonal carcinoma. Embryonal cells give rise to teratoma by intra-embryonic differentiation while yolk sac tumour or choriocarcinoma are produced by extra-embryonic differentiation. [6,7] Virtually all germ cell tumours of the testis develop from the intratubular germ cell neoplasia (carcinoma in situ, CIS) except spermatocytic seminoma and the rare prepubertal tumours. CIS is usually a diffuse disease, which can be diagnosed with a random testicular biopsy. CIS gives rise to invasive GCT in approximately 50% of cases of cases within 5 years. It is bilateral in 5% of cases and progression to tumour development can be prevented by low dose testicular irradiation (20-25 Gy).

Only 40% of GCT are of one histologic type, while the remaining 60% display mixed histology. Combination of seminoma and one or more non-seminomatous elements is considered as non-seminomatous tumour. Apparently pure seminomas with abnormal AFP (> 10-20 ng/ml) and/or highly elevated hCG (> 200 mIU/ml) are treated as non-semonomatous tumours. Pure seminomas usually spread by lymphatics mainly to paraaortic nodes, sometimes to mediastinal and supraclavicular nodes. Haematigenous spread is extremely rare. Seminoma is extremely sensitive to radiotherapy and to chemotherapy.

Non-seminomatous germ cell tumours (NSGCT) metastasize both to the lymphatics and via the blood stream, especially to the lungs. Embryonal carcinoma is the most undifferentiated tumour and is very responsive to chemotherapy. Teratoma is the tumour that has undergone somatic differentiation. Incomplete differentiation leads to immature teratoma while complete maturation leads to mature teratoma, but mature teratoma is benign only in children. Teratoma is poorly responsive to chemotherapy and to radiotherapy. Yolk sac tumour is the most common tumour in children; it spreads mainly to the lung and can be cured with chemotherapy. Pure choriocarcinoma is extremely rare; it metastasizes diffusely by the blood stream and involves a very poor prognosis. When it is mixed with other histologies, it is potentially curable.

Testicular lymphatics travel along the spermatic cord to the paracaval, paraaortoc and pericaval group nodes. Therefore any suspected testicular tumour should be removed by the inguinal route (high orchidectomy) as scrotal violation leads to altered lymphatic patterns along with some increased risk of local recurrence. Previous orchiopexy also alters lymphatic pathways. These factors need to be considered when planning radiotherapy fields. Testicular tumours (especially NSGCT) have rapid doubling times, hence follow up requires frequent close observation at 2-6 monthly intervals in least first 3 years of follow up.

Clinical Presentation (Symptomatology)

Painless gradual enlargement of the testis is the commonest presentation. Testicular lump may be more or less hard and more or less irregular in contour. Delays in patient seeking definitive treatment after recognition of the initial lesion are frequent (3-6 months) and it correlates with development of metastases. [8] Trauma to the testis (e.g. cricket ball injury) can sometimes lead to confusion in diagnosis. The testicular lump discovered after trivial trauma is erroneously attributed to haematoma with serious consequences. Sometimes even physicians contribute to this delay in definitive diagnosis. Every testicular lump should be assumed to be malignant unless proved otherwise. Availability of scrotal ultrasonography and tumour markers should avoid these diagnostic pitfalls. At least one third of testicular tumour patients seen at Tata Hospital had initial scrotal surgery elsewhere with the diagnosis of either hydrocoele, hematocoele or rarely pyocoele. High index of suspicion and patient education regarding self examination is important. About 10% of testicular tumours present with acute pain which is due to intra-tumoral haemorrhage. Undescended testicular tumours present with suprapubic lump, urinary complaints or bowel complaints. Development of torsion in an undescended testicle can sometimes be the warning sign of testicular tumour. Rarely testiculartumours may present with symptoms of abdominal lump, chronic cough or as a "neck node with unknown primary". Testicular nodule may be preceded by a variably long period of testicular hypersensitivity and hypotrophy. These two signs are characteristic of testicular CIS.

Scrotal ultrasound is an important non-invasive diagnostic tool. GCT of the testis appears as an intratesticular hypo-echoic lesion, irregular in shape and heterogeneous in density. "Burnt out" tumours appear as few microcalcifications in a sclerotic area. Intratesticular microlithiasis represents testicular CIS. FNAC of testicular tumours is generally not recommended as it is useful only if it is positive, exact typing (seminoma versus NSGCT) is not reliable on FNAC and due to the theoretical risk of needle tract recurrence. FNAC is valuable in metastatic sites like retroperitoneum or neck nodes. Any suspected testicular tumour should be explored by inguinal route and if necessary frozen section confirmation or otherwise should be obtained (Chevassue's manoeuvre).

Tumour Markers

Serum beta human chorionic gonadotrophin (bhCG), alpha foeto protein (AFP) and lactate dehydrogenase (LDH) are the most important testicular tumour markers. Elevated bhCG level are seen in 30% of pure seminomas before orchiectomy, while in nonseminoma AFP and/or bhCG are raised in approximately 90% of cases. Following orchiectomy, bhCG is normal in clinical stage I. In comparison, markers remain elevated in 5-10% of clinical stage I NSGCT (occult disease) and only in 40% of patients with histologically documented metastases. In advanced disease (both seminoma and NSGCT), markers remain positive even after orchiectomy. Negative markers do not exclude the diagnosis of germ cell tumour of the testis.

Half-lives of these markers (AFP-5 to 7 days, bhCG-1 to 3 days) are useful in staging as well as prognosis and follow up of these patients. LDH is not a specific marker but is useful in prognostication. AFP and bhCG are measured by radio-immuno assays or monoclonal antibody techniques while LDH is determined by enzymatic assay. Normal values are 10 to 15 ng/ml for AFP and upto 5 mIU/ml for bhCG. Approximately, 1 ng of AFP corresponds to 1 mIU, and 1 ng/ml of bhCG corresponds to 5 mIU/ml. LDH titres are related to upper limit of the normal value (N) of each individual laboratory.

Surgical Treatment (High Orchiectomy/Radical Orchiectomy)

Lymphatic drainage of testis dictates the high "inguinal" route of orchiectomy. The spermatic cord is isolated and divided at the internal inguinal ring. In doubtful cases, a soft non-crushing clamp is applied to the cord, tunica layers of testis are opened after proper isolation of the field, frozen section examination of suspicious areas is done followed by either orchiectomy (if positive for GCT) or else closure and reposition of testis into the scrotum (Chevassue'manoeuvre). The specimen is sent for histological examination. T category is determined by this pathological examination of specimen.

T category : pathologically only

N category : clinical examination and imaging findings

M category : clinical examination, imaging findings and serum tumour markers

TNM Classification of Testicular tumours9 primary tumour
(defined pathologically only)
pTx Radical orchiectomy not performed.
pTO Histological scar or no evidence of primary tumour.
pT is Intratubular germ-cell neoplasia.
pT1 Tumour limited to testis, including epididymis and albuginea.
pT2 Tumour limited to testis with evidence of vascular (Haematic or lymphatic) invasion; or tunica vaginalis involved by tumour.
pT3 Tumour involving spermatic cord with or without vascular invasion.
pT4 Tumour involving scrotum, with or without vascular invasion.

S category : serum tumour markers.

Regional lymph nodes are the bilateral peri-aortocaval nodes, the ipsilateral common iliac nodes and nodes accompanying the spermatic vessels. Pelvic and inguinal nodes are considered regional only following previous inguino-scrotal surgery.


Nx Regional nodes cannot be assessed. Regional nodes cannot be assessed
NO No regional-node metastasis. No regional-nodemetastases
N1 Single or multiple none > 2 cm in thegreatest diameter metastases to 1-5 nodes.metastases, al
l < 2 cm in greatest diameter.
N2 single or multiple extension of the greatest diameter Idem, or extranodalmetastases 2-5 cm
N3 Lymph-node > 5 cm. Lymph-node metastasismetastasis > 5 cm

Distant metastases


Presence of distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
M1a Metastasis to extra-regional lymph-nodes or to the lung.
M2b Distant metastasis in other sites.

Serum tumour markers
Sx Serum tumour markers not available.
S0 Normal serum tumour markers
AFP (ng/ml) hCG (mlU/ml) hCG (mlU/ml)
S1 < 1,000 < 5,000 < 1.5
S2 1,000-10,000 5,000-50,000 1.5-10
S3 > 10,000 > 50,000 > 10