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Testicular cancer, although rare, is the commonest, solid-organ cancer in men aged 15 - 44 years (see below). Fortunately, it is usually eminently treatable, with an overall 5-year survival rate of 97%.

Classically, testicular cancer presents as a painless, rapidly-growing swelling of the testicle, but as many as 20% of patients may experience significant pain, sometimes mis-diagnosed as epididymitis or orchitis. Although early diagnosis is important, the overall prognosis is excellent even after late diagnosis (see the annual statistics below).

Risk factors for testicular cancer

Many risk factors have been suggested, but the major ones are:

  • undescended testis (results in a 4-times increased risk; overall risk 1-2%)
  • subfertility (with abnormal, small, soft testes)
  • family history of testicular cancer (iso-chromosome-12 results in a 10-times increased risk)
  • Caucasian origin
  • previous contra-lateral tumour (results in a 12-times increased risk)

Clinical presentation

Although testicular cancer usually presents as a painless, progressive scrotal swelling (pictured right), it may also present as:

  • a secondary hydrocele
  • a paraneoplastic syndrome
  • non-specific constitutional symptoms (e.g. weight loss, fever, fatigue, chills, night sweats, decreased appetite)
  • symptoms of metastatic disease (e.g. abdominal pain from lymph nodes, haemoptysis from lung metastases, headache due to cerebral metastases)

Click here to view the teaching video (by Mr Duncan Summerton) about scrotal swellings.

Tests & investigations

Any clinically suspicious scrotal swelling warrants urgent investigation, as soon as possible after the initial assessment.  Many urologists run "one-stop" clinics for suspected testicular cancer, from where investigations can be arranged as soon as the patient has been seen. The major investigative steps are: 

Investigation Details


If possible, ultrasound should be arranged directly from the outpatient clinic, so the patient can be reviewed with the result as soon as possible.

Ultrasound usually shows a mass within the testis together with evidence of microcalcification which may be premalignant (pictured right).

It may also be possible to identify enlarged para-aortic nodes with ultrasound if a suspicious mass is found in the testis.


Blood for tumour markers should be taken as a baseline, before any treatment is instigated, including:

  • alpha-fetoprotein (AFP) - raised in the presence of yolk sac elements. Elevated in 50 - 75% of non-seminomatous germ cell tumours (NSGCTs) but not in seminoma. Following treatment, the expected half-life is 5 - 7 days
  • beta-human chorionic gonadotrophin (ß-HCG) - raised in the presence of syncitiotrophoblastic elements. Raised in all choriocarcinomas, 40% of NSGCTs & 10% of seminomas. Following treatment, the expected half-life is 24 - 36 hours
  • lactate dehydrogenase (LDH) - a non-specific marker of the bulk of disease present


Excision-biopsy is usually performed by radical inguinal orchidectomy, removing the testis and spermatic cord together (pictured right). Ideally, this should be scheduled as soon as possible after initial presentation. 

A testicular prosthesis can be inserted at the time of surgery although there is a risk of infection. Some clinicians prefer to defer insertion of a prosthesis until completion of any scheduled chemotherapy or radiotherapy.

Once a cancer has been confirmed, more detailed histological sub-typing is normally performed by the pathologist.


If cancer is confirmed, abdominal, chest & pelvic CT scanning is usually performed to stage the disease more accurately. It may, however, as a matter of convenience, be performed before orchidectomy.

This may reveal significant intra-abdominal lymph node enlargement (pictured right) which cannot always be detected by abdominal palpation or abdominal ultrasound.


95% of testicular tumours are germ cell tumours (GCTs). Other, rarer tumours include lymphomas, which are usually seen in men over the age of 50 years. Germ cell tumours consist of:

  • seminomas (40 to 45%)
  • non-seminomatous germ cell tumours - NSGCTs (55 to 60%). Any combination of teratoma, embryonal carcinoma, choriocarcinoma & yolk sac tumour
  • mixed seminoma / NSGCT (up to 5%)

Primary treatment

Radical inguinal orchidectomy with or without insertion of a testicular prosthesis is the initial treatment for a suspected testicular cancer.

Through a groin incision, the spermatic cord is isolated, mobilised and "soft" clamped to prevent any tumour spread into the circulation.  The testes is delivered through the groin incision and removed, together with the spermatic cord.  The image shown (right) is of a right inguinal orchidectomy. 

By approaching the abnormal testis through an inguinal incision, maximal cord length can be removed with the testis. More importantly, however, the scrotal skin drains via the inguinal lymph nodes, whilst the testis drains directly to para-aortic (intra-abdominal) nodes.  There is, therefore, a potential to disseminate disease into the inguinal nodes if the testis is approached by an incision through the scrotum; by using a groin incision, a second lymphatic field is not breached.

Clinical staging

Clinical staging is completed by histological examination of the excised testis and CT scanning.

In common with most cancers, the clinical stage is described using the TNM staging system ( for Tumour, Nodes & Metastases). The prefix "p" denotes that the stage has been confirmed by pathological analysis (of the testis) or by CT scan (of the nodes). For testicular tumours, an S-stage (for Serum tumour markers) may also be included in the staging process:

TNM + S     Details of classification
(orchidectomy specimen)
pTx Primary tumour cannot be assessed
pT0 No evidence of primary tumour (e.g. histological scar in testis)
pTis Intra-tubular germ cell neoplasia (intra-epithelial neoplasia)
pT1 Tumour limited to testis & epididymis without vascular/lymphatic invasion; tumour may invade tunica albuginea but not tunica vaginalis
pT2 Tumour limited to testis & epididymis with vascular/lymphatic invasion; or tumour extending through tunica albuginea with involvement of tunica vaginalis
pT3 Tumour involving spermatic cord with or without vascular/lymphatic invasion
pT4 Tumour invading scrotum with or without vascular/lymphatic invasion
(CT/PET scanning)
Nx Regional lymph nodes cannot be assessed
pN0 No regional lymph node metastases
pN1 Metastasis in a lymph node mass ≦ 2cm in greatest dimension & 5 or fewer positive nodes, none >2cm in greatest dimension
pN2 Metastasis in a lymph node mass >2cm but <5cm in greatest dimension; or >5 nodes positive, none >5cm; or evidence of extra-nodal extension of tumour
pN3 Metastasis with a lymph node mass >5cm in greatest dimension
(CT/PET scanning)
Mx Distant metastases cannot be assessed
M0 No distant metastases
M1 Distant metastasis
M1a Non-regional lymph node(s) or lung
M1b Metastases in other sites
(blood tests)
Sx Serum tumour markers not available or not performed  
S0 Serum tumour markers within normal limits
  LDH (U/L) ß-HCG (mIU/mL) AFP (ng/mL)
S1 < 1.5-times norm & < 5,000 & < 1,000
S2 1.5-10-times norm or 5,000-50,000 or 1,000-10,000
S3 > 10-times norm or >50,000 or >10,000

Secondary treatment

Although radical orchidectomy alone may cure patients with organ-confined disease, secondary treatment in the form of chemotherapy or radiotherapy is usually offered, depending on CT staging, tumour histology and tumour marker status after orchidectomy. In most hospitals, this takes place under the care of Clinical Oncologists, rather than urologists.

In the event of large-volume retroperitoneal lymph node disease (pictured above), chemotherapy is used as first-line treatment. Residual nodal enlargement (or persistently raised tumour markers suggesting residual tumour) is normally treated by retroperitoneal lymph node dissection & excision.

Details of this, the possible histological findings and subsequent management are beyond the expected level of knowledge for undergraduates.