Testicular cancer refers to a malignancy originating from the testis. It is the most common malignancy to occur in young men (especially ages 20-35). About 50% of testicular cancers happen before 35 years of age. Most other cases happen by/at the age of 55. Despite it being the most common cancer in young men, it is still a rare cancer, accounting for 0.4% of all cancers.
Pathophysiology and classification
We can classify the cancers as either primary neoplasms, secondary neoplasms and paratesticular neoplasms:
All germ cell tumours are believed to occur during development as a foetus. There is a phase where it remains as a carcinoma in situ (intratubular germ cell neoplasia) before turning into a cancerous growth.
- Germ cell tumours - these make up 90-95% of all testicular cancers. These are tumours deriving from the reproductive cells (sperm cells in males and the eggs in females).
- Seminoma - a seminoma is a germ cell tumour of the testicle itself. They are highly sensitive to radiotherapy. They secrete human chorionic gonadotrophin (hCG).
- Non-seminomas:
- Embryonal carcinoma - 20% of testicular cancers.
- Teratoma
- Teratocarcinoma
- Choriocarcinoma
- Yolk sac tumour - predominant in pre-pubertal boys.
- Mixed germ cell tumours - these are techinica
- Non-germ cell tumours:
- Leydig cell - Leydig cells produce testosterone.
- Sertoli cell tumours
- Gonadoblastoma
- Other miscellaneous cancers such as adenocarcinoma of rete testis, carcinoid mesenchymal, adrenal rest tumours.
- Metastases
- Reticuloendothelial tumours - most commonly testicular lymphomas.
Factors that lead to the development of testicular cancers include congenital abnormalities trauma, hormones, atrophy and genetic predisposition all play a role in the development of the cancer.
Carcinomas in situ do not regress but the tunica albugenia provides a barrier to metastasis (and for this reason we should not do a scrotal needle biopsy).
Metastasis does occur via the spermatic cord lymphatic system going to the retroperitoneal lymph node chain (mainly the para-aortic lymph nodes). From there it spreads to the thoracic/mediastinal lymph nodes. For this reason it is considered an emergency as the growth of tumours can compress vital structures. Haematogenous spread can occur via the pampiniform plexus.
The urgent nature of the disease is also due to the rapid progression of the disease. Non-seminomas double in size every 10-30 days. Seminomas are much slower fortunately, however, they may recur 2-10 years after the initial treatment due to its slow progressing nature.
⚠️ Risk factors
- Age - testicular cancer is most common at the age of 20 and 55.
- Cryptorchidism - this leads to distorted differentiation of germ cells which can change the normal development of the primordial germ cell.
- Family history
- Previous diagnosis of testicular cancer
- Testicular atrophy
- White ethnicity
- HIV infection
- Klinefelter syndrome
😷 Presentation
The typical presentation of testicular cancer is a painless lump on the testicle. Sometimes it may also present with testicular pain. It is more common on the right testicle.
The characteristics of the lump are:
- Non-tender
- Arising from the testicle
- Hard
- Irregular
- Non-fluctuant
- Not transilluminable
Seeing as germ cell tumours release hCG, this leads to Leydig cell dysfunction. Leydig cell dysfunction then leads to an increase in both testosterone and oestradiol. However, the relative rise in oestradiol is grater than testosterone. This causes gynaecomastia.
🔢 Staging
The Royal Marsden staging system is used for staging of testicular cancer:
- Stage 1 - confined to the testicle.
- Stage 2 - spread to retroperitoneal lymph nodes below diaphragm.
- Stage 3 - spread to lymph nodes above the diaphragm.
- Stage 4 - metastasised to other organs.
The most common sites for testicular cancer to metastasise are lymphatics, lungs, liver and brain.
🔍 Investigations
A testicular examination and abdominal examination should be done along with taking a clinical history of course.
- 🥇 🏆 Ultrasound with Doppler studies - this evaulates the extent of the testicular mass as well as its nature.
- CTAP - if ultrasound is negative but suspicion remains high. It can also be used to assess extratesticular metastasis.
- CXR - to check for mediastinal nodal spread.
- α-fetoprotein - may be raised in most cases of non-seminomas but not in seminomas and choriocarcinomas.
- hCG - elevated in all cases of choriocarcinoma (non-seminoma) and in 5-10% of seminomas.
- LDH - a non-specific tumour marker for both seminomas and non-seminomas. However, it has a high false positive rate.
💡 As we mentioned previously, scrotal biopsy should not be done as this compromises the tunica albugenia’s ability to prevent the cancer from metastasising. A biopsy should be done during the orchidectomy to determine the histological classification of the tumour.
🧰 Management
If a patient is suspected of having testicular cancer → refer to urology via 2 week wait pathway. Suspicion should be raised if there is a non-painful enlargement or change in shape/texture of the testis.
The management options are dependent on the stage and grade of the cancer. Testicular cancer is a highly treatable form of cancer and often is highly sensitive to radiotherapy.
- Surgery - radical inguinal orchidectomy. This involves removal of the affected testicle along with the epididymis, spermatic fascia, spermatic cord and insertion of a prosthesis.
- Chemotherapy
- Radiotherapy
- Sperm banking - this should be considered prior to any treatment, especially considering the cancer often happens in young men who wish to have children later on.
Follow-up will be done to monitor for reoccurrence. This is done via tumour markers, CT scans or CXRs.
🚨 Complications
The complications mentioned refer to complications of treatments provided for testicular cancer.
- Infertility
- Hypogonadism
- Peripheral neuropathy
- Hair loss
- Kidney, liver and cardiac damage
- Increased risk of cancer in the future