Testicular tumours are one of the most common cancers in men in the 15 to 35 age group. Approximately 5500 new cases in the United States and 500 new cases in Great Britain occur every year. The highest incidence is in Scandinavia and New Zealand with the lowest incidence in Africa and Asia. It has become one of the most curable solid tumours with a mortality rate that has fallen from 50 per cent before 1970 to less than 10 per cent in 1990.

Most testicular cancers (90–95 per cent) arise from the germ cells (spermatogenic cells). They are often characterized by two types of primitive cells, trophoblast or yolk-sac cells. When trophoblast is present &bgr;-human chorionic gonadotrophin (&bgr;-hCG) is produced and this is one of the tumour markers that can be detected in the serum of the patient. Yolk sac tumours produce alpha-fetoprotein which can also be detected in the serum and both of these provide good tumour markers the level of which depends on the amount of tumour in the body. Serial determinations of alpha-fetoprotein and &bgr;-hCG after surgery closely reflect the effectiveness of treatment and allow a reliable means of determining distant recurrence.

Classically testicular tumours have been divided into seminomas and teratomas; seminomas appear in older men with a peak incidence of 34 to 40 years of age while the teratomas appear in younger men, age 25 to 35. However, it is now clear that there is often a spectrum of different malignant tissues in each tumour, which are often partly seminoma and partly teratoma. The earlier classification of testicular tumour is now largely superseded by systems which attempt to quantify how much of each tissue is present. The presence of yolk sac or trophoblastic tissue in the tumour tends to be associated with a worse prognosis than the presence of differentiated tissue. The British Testicular Tumour Panel formalized the British version of testicular tumour nomenclature and this can be compared (Table 1) 473 with that of the World Health Organization who modified the earlier North American Classification of Mostofi and Price.

Evidence supports the importance of congenital factors. Some 7 to 10 per cent of patients with testicular tumours have a history of cryptorchidism. The estimated risk of a tumour in patients with an associated history of maldescent is now thought to be between 3 and 14 times the normal incidence.

A variety of clinical staging systems have been devised for testicular tumours, e.g. the tumour node metastases (TNM) system. The testicle itself is classified T1 to T4 depending on the spread through the testicle. Lymph node involvement is either N1, involving the para-aortic nodes, or N2 involving nodes in the pelvis or mediastinum. M signifies blood-borne metastases in lung, liver, or brain. Computerized tomography scanning is one of the most effective ways of demonstrating spread of testicular tumours. Testicular tumours spread locally into the epididymis and spermatic cord, and by lymphatic invasion along the lymphatics to retroperitoneal para-aortic lymph nodes.

The majority of patients with testicular tumours present with a painless lump in the testicle (Fig. 1) 1609 although up to 30 per cent are first diagnosed as a result of presentation with metastatic disease. Examination discloses a lump in the testis and not separate from it. A testicular carcinoma is a tumour which is often detected by self-examination.

Ultrasound scan, while not essential, will often confirm the clinical diagnosis. Blood should be sent for tumour markers (alpha-fetoprotein and &bgr;-hCG). This should be done both pre- and postoperatively.

Orchidectomy should be performed through an inguinal approach with a clamp placed on the spermatic cord which theoretically prevents dislodgement of tumour during manipulation of the testicle (Figs. 2, 3) 1610,1611. A frozen section biopsy examination can be carried out if there is any doubt as to the diagnosis but this is not normally necessary and the cord is transfixed and ligated at the internal inguinal ring and the testicle removed. Computerized tomography scans allow clinical staging of the disease.

Subsequent treatment depends on the histology and staging of the tumour. A seminoma with negative markers after orchidectomy and without any detectable metastasis may be treated by radiotherapy of 3000 Gy to the retroperitoneal lymph nodes. Survival following this is almost 100 per cent. Recently it has been suggested that equally good prophylaxis may be obtained with a short course of carboplatinum.

In other non-seminomatous germ cell tumours with no evidence of spread and normal tumour markers, the options are either to keep the patient under surveillance with 3-monthly markers and CT scans, or to perform a radical retroperitoneal lymph node dissection. The latter is the favourite option in North America although with surveillance 80 per cent of patients need no treatment and 20 per cent who show relapse may be treated with chemotherapy at that stage.

Regardless of the original histology, if there is evidence of retroperitoneal node disease combination chemotherapy is given and the patient is followed by regular measurement of tumour markers and CT scans. When the tumour bulk is small the masses will usually disappear completely with survival rate of almost 100 per cent. When the tumour bulk is large, a mass may remain after chemotherapy which may contain active tumour. In these cases a retroperitoneal lymph node dissection is performed surgically so that the tissue can be examined and if tumour is present further chemotherapy may be given. Cisplatin is one of the most active agents in the treatment of testicular cancer and various drug regimens have been advocated including this agent. One of the more commonly used regimens for advanced non-seminiferous germ cell tumours involves four cycles of bleomycin, etoposide, and cisplatin.

Other tumours are rare, constituting between 5 and 10 per cent of all testis tumours, and include Leydig cell tumours and Sertoli cell tumours, both of which have a good prognosis.

Lymphoma of the testis accounts for 5 per cent of testicular tumours and is the most frequent tumour in men over 50. The testis is diffusely enlarged to 5 cm diameter or more. Survival is poor in patients with bilateral disease or with lymphoma at other sites but is better if the disease is confined to the testis.

Metastatic spread of other tumours to the testis is very rare.

Testicular cancer has become one of the most curable of solid neoplasms and serves as an excellent demonstration of the success of a multidisciplinary approach to the treatment of malignant disease.

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