The tumour stage of testicular cancer defines its treatment. If the tumour is localized to the testis, two actions are available to the clinician. The first option for both seminoma and teratoma is observation without further therapy. If this policy is followed in the absence of poor prognosis pathology features, then the likelihood of any further treatment being required is 13% for testicular teratoma and 17% for seminoma. It should be noted that almost all patients who develop progressive disease during the period of observation without treatment are salvageable by chemotherapy. Active surveillance for stage I seminoma and stage I teratoma without lymphovascular invasion or embryonal elements is safe but requires regular follow-up with clinical examination, blood tests and radiology.

In the United Kingdom, many urologists refer patients with stage I seminoma for radiotherapy, following which the prognosis is excellent, with virtually no chance of relapse. The option of single-agent carboplatin is a vastly better alternative. A randomized trial has shown that chemotherapy with carboplatin is as effective as radiation therapy and without the morbidity, two infusions being given at4-weekly intervals in contrast to 3 weeks of daily radiation therapy. Patients with stage I teratoma with high risk features are generally referred for adjuvant chemotherapy using bleomycin, etoposide and cisplatin (BEP) chemotherapy. Treatment in certain circumstances might be modified, dropping bleomycin from the treatment programme to reduce the risk of lung damage.

For stage IIa seminoma, that is, with a nodal mass of less than 2 cm in diameter as defined by CT scanning, many clinicians in the United Kingdom advise treatment with radiotherapy. A consensus of opinion is now emerging, which follows the view that two courses of cytotoxic chemotherapy are equally as effective as radiation treatment in the control of this stage of disease. For stage IIb seminoma, that is, for patients with a disease mass of less than 5 cm, some clinicians, particularly radiotherapists, still treat with radiotherapy, but this is not generally advised in view of the side effects of large field radiotherapy. Chemotherapy should be given using cisplatin based combination chemotherapy.

For all patients with greater than stage IIb disease, whether it is seminoma or teratoma, cytotoxic chemotherapy is given. Before the advent of cytotoxic chemotherapy for teratoma, the disease was invariably fatal. The development of effective chemotherapy programmes has bought about a revolution in the management of patients with malignancy, and now virtually all patients are cured by treatment.

Treatment with cytotoxic agents was originally introduced into medical practice by Li in the early 1960s. As a result, approximately 8% of patients with advanced disease were cured, using a combination of agents that included actinomycin and chlorambucil. In the early 1970s, Samuels treated patients with vinblastine and bleomycin and produced remissions in approximately 50% of men treated. This treatment was of considerable toxicity because of the large dosages of vinblastine and bleomycin used and the relative lack of support programmes for patients with neutropenic sepsis and thrombocytopenia, which occur as a result of the use of these agents. In 1976, Einhorn introduced the bleomycin, vinblastine and cisplatinum (BVP) programme for the treatment of malignant testicular tumours. The introduction of BVP was not in the context of a controlled clinical trial but in a speculative fashion and was found to work. Because BVP turned out to be such an effective regimen, it became widely used even before the results were published. This regimen was enormously successful, and 70% of patients with advanced disease were cured. By substituting etoposide for vinblastine, less toxicity resulted with equivalent effect.

Over the last decade, there have been further refinements in the way that treatment has been given. Drug treatment that initially required six courses of 5-day treatments has now been reduced to four courses of 3-day treatments. The expectation is that 95% of patients with good-prognosis tumour are cured with this regimen and 48% of patients with poor-prognosis disease are cured. Extraordinarily, there has been further change in the collective view with regard to chemotherapy for testicular cancer, and recently many oncologists have reverted to the original 5-day BEP programme. This is based upon analyses of huge numbers of patients and the realization of the superiority of this standard programme.

At the end of treatment, one problem may be that of a persistent mass. By this we mean a residual tumour at the site of the original metastatic disease. The approach to this problem is to proceed to surgery. Surgery may be very extensive and involve both thoracotomy and laparotomy. At surgery, the residual mass of tumour is excised as completely as possible, and this may require dacron grafting of major vessels or removal of a kidney in order to take away the tumour completely. This operative procedure is extremely intricate. Histological examination of the excised mass shows that in one-third of cases there is necrotic tumour, in one-third of cases there is differentiated teratoma and in one-third of cases there is undifferentiated cancer. If necrotic tumour is found, no further action is taken. If undifferentiated tumour is found, further chemotherapy is given and 30–40% of patients will be cured by a combination of chemotherapy and surgery. In those patients who have residual differentiated tumour, it is important to remove the residual mass of the disease because over a 5-year period approximately 50% of differentiated tumours undergo further malignant change, transforming to undifferentiated malignancy.

Unfortunately, a significant number of patients still have progressive or unresponsive tumours and for these patients there is still a possibility of cure, which is in the range of 20–40%. Treatment programmessuch as vinblastine, ifosfamide and cisplatin (VIP), paclitaxel, ifosfamide, cisplatin (TIP) or high-dose therapy with stem cell rescue are used to treat such patients.

The effects of treatment are very closely monitored by measuring changes in the serum levels of the tumour markers AFP and HCG. These are hormones secreted by teratoma and seminoma. If the tumour is being treated effectively, then the levels of these hormones in the blood will decay over a known period: a half-life of 3–5 days for AFP and approximately 12–36 hours for HCG.

There are specific toxicities that relate to treatment. Cisplatin will cause renal damage, deafness and peripheral neuropathy, which may manifest as numbness in the fingers or toes or complete loss of motor and sensory function in the limbs. Bleomycin unfortunately causes pulmonary toxicity, that is, an irreversible and progressive loss of lung function, which is fatal in approximately 2% of patients treated (see Figure 3.13). Bleomycin was omitted from Lance Armstrong’s treatment for metastatic testicular cancer so that he would not lose lung function and of course he went on to win seven consecutive Tour de France titles, albeit with the assistance of doping. Testicular cancer and the drug regimen that is used generally causes sterility; by this we mean loss of functional spermatogenesis. In 80% of patients, however, there is recovery of spermatogenesis, which generally occurs at 18 months from the completion of treatment.