Germ cell tumors account for 95 % of testicular cancers and are divided into seminomatous or nonseminomatous subtypes, each comprising approximately 40–45 % of germ cell tumors, with the remaining being mixed [2]. Nonseminomatous tumors usually contain more than one cell type and may include seminoma mixed with other germ cell neoplasms such as embryonal cell carcinoma, choriocarcinoma, yolk sac tumor, and teratoma. Serum alpha fetoprotein (AFP) can help distinguish patients with pure seminoma from those with mixed tumors as it is only secreted by nonseminomatous tumors. AFP levels are elevated in 20 % of patients with clinical stage I disease and in more than 50 % of patients with metastases [1]. Human chorionic gonadotropin (hCG) is less specific as it can be elevated in both seminomatous and nonseminomatous tumors. Lactate dehydrogenase (LDH) levels are used in both tumor types as a marker of disease burden, as it is elevated in more than 50 % of patients with advanced disease. Non-germ cell tumors of the testis include lymphoma, Sertoli, and Leydig cell tumors [2]. Tumor histology is determined by radical orchiectomy, which involves resecting the testis and ligating the spermatic cord at the inguinal ring (see Table 6.2).

Testicular cancer staging is based on local tumor extent, presence and size of regional nodes, serum tumor marker levels, and distant metastases (see Table 6.3) [1]. Local disease is divided as limited to testis and epididymis (T1), involving testis and epididymis with vascular/lymphatic invasion or tumor extension through the tunica albuginea to tunica vaginalis (T2), tumor invading spermatic cord (T3), and tumor invading scrotum (T4) [1]. Stage I tumors can range from T1 (stage Ia disease) to T4 (stage Ib or Is) but have no nodal or distant metastases. Stage Ib tumors have negative serum tumor markers whereas stage Is tumors are positive. These serum markers are also classified according to the degree of elevation of LDH, hCG, and AFP with S0 referring to normal markers, and S1, S2, and S3 are for increasing serum levels of these proteins. Regional nodes are staged both clinically and pathologically using size cutoffs of 2 and 5 cm. For clinical evaluation, regional nodes less than or equal to 2 cm are N1 disease, those greater than 2 cm but less than 5 cm are N2 disease, whereas nodes greater than 5 cm are N3 disease [1]. Pathologic assessment includes the number of positive nodes. Patients with stage II testicular cancer have retroperitoneal spread with stages IIa, IIb, and IIc having N1, N2, and N3 nodal disease, respectively. Distant metastases are stage III and are either M1a with nonregional (nonretroperitoneal) nodes or pulmonary spread, or M1b with nonpulmonary visceral metastases such as to the brain, bones, and liver. Staging of nodal and distant disease is typically performed with computed tomography (CT).

Regional nodes for testicular cancer are in the retroperitoneum following the primary drainage pathway of each testis. These sites are precaval, paracaval, and interaortocaval nodes for right-sided testicular tumors, and paraaortic and preaortic nodes for left-sided tumors [1, 2]. Contralateral nodes are usually seen with large volume disease and right-sided tumors but are rare without ipsilateral adenopathy. Metastatic nodes are of soft tissue density or are heterogeneous with mixed solid and cystic components, the latter usually seen with nonseminomatous tumors. Progressive spread occurs to retrocrural, subcarinal, and supraclavicular nodes. Pelvic nodes can become enlarged secondary to lymphatic obstruction by bulky abdominal adenopathy [2]. Inguinal adenopathy can also occur when the primary tumor involves the scrotal wall. Although a short axis diameter of 10 mm is typically used to assess nodes, smaller nodes in expected sites of lymphatic drainage can harbor metastases [5].

The management of retroperitoneal nodes in early-stage testicular cancer differs for seminomatous and nonseminomatous tumors, both at initial presentation and after treatment (see Table 6.4). Retroperitoneal node dissection is not performed in early-stage seminoma but can be considered in nonseminomatous tumors. Seminoma is radiosensitive, unlike nonseminomatous tumors, and patients with clinical stage I disease may receive radiation to the retroperitoneum or surveillance for recurrence, which typically occurs at a median of 15 months in 15 % of patients [1]. For patients with nonseminomatous tumors, approximately 30 % of those with clinical stage I disease have occult nodal metastases, and options include retroperitoneal node dissection, chemotherapy, or surveillance for recurrence, which typically occurs in the first year [1, 2]. Node dissection is considered in particular for patients with risk factors such as lymphovascular invasion, embryonal carcinoma, or scrotal extension of tumor [1].

Retroperitoneal lymph node dissection has been modified over time by limiting it to infrarenal nodes in low stage disease, as well as performing a unilateral dissection. The aim is to maximize the likelihood of resecting metastatic nodes while minimizing morbidity. If feasible, the sympathetic nerves are spared to preserve antegrade ejaculation. Based on studies mapping nodal stations, there are several side-specific templates for guiding dissection. For right-sided tumors, the precaval, paracaval, interaortocaval, and hilar gonadal vein nodes are resected and, in some templates, the preaortic and ipsilateral iliac nodes may also be included [6, 7]. For left-sided tumors, the preaortic, paraaortic, and hilar gonadal vein nodes are resected and the interaortocaval and ipsilateral iliac nodes may also be included depending on the template [6, 7].

Surveillance is included as a clinical option in patients with early-stage testicular cancer to avoid the complications of lymphadenectomy and the morbidity of radiation and chemotherapy, which carry the risk of long-term cardiovascular complications and second malignancy [8]. Patients are monitored by checking serum tumor markers, chest radiography or CT, and abdominal CT and this regimen is most intensive in the first year after treatment. Magnetic resonance imaging (MRI) is a nonradiation alternative to CT for surveillance of the retroperitoneum [9]. Chemotherapy is administered for advanced stages of both seminomatous and nonseminomatous tumors (see Table 6.5).

Once retroperitoneal nodes have been nonsurgically treated with radiation or chemotherapy, residual masses can be seen at imaging in up to 70 % of patients [10]. The majority of these masses in patients with seminoma consist of fibrotic tissue without active tumor or teratoma and are therefore observed [2]. Surgery is considered for masses larger than 3 cm with increased activity on positron emission tomography (PET) scans but complete resection can be challenging due to an appreciable desmoplastic reaction [1]. In contrast to seminoma, residual masses larger than 1 cm in patients with nonseminomatous tumors are resected as they have teratoma in 40 % of cases and viable tumor in 10 % [10]. Teratoma is seen either due to persistence of the original teratomatous component or due to transformation of the tumor with chemotherapy [3]. Change in the appearance of the mass to a simple-appearing cyst is seen with evolution to a differentiated mature teratoma. This is resected, as there is potential for growth with mass effect or malignant trans­formation in approximately 5 % of patients [1, 2, 8, 11]. A residual nodal mass with mixed solid and cystic appearance is also resected, as this can be seen with fibrosis, tumor, and/or necrosis. Increased ¹⁸F-fluorodeoxyglucose (FDG) activity in the residual mass on PET imaging suggests viable tumor [12, 13].

Although metastases from testicular tumors are typically by the lymphatic route, hematogenous spread can also occur. This is more common with nonseminomatous tumors and is seen in the lungs, liver, brain, and bones. Late relapse of testicular cancer is defined as a recurrence occurring more than 2 years after completing initial therapy. It occurs in 2–6 % of patients at a median interval of 6 years at sites such as the retroperitoneum, lungs, and mediastinum [1, 14]. Prognostic indicators for patients with germ cell tumors at presentation are serum tumor marker levels, primary tumor location, and visceral metastases. Seminoma patients without nonpulmonary visceral metastases are considered at good risk, regardless of the primary tumor site or serum tumor marker levels. However, seminoma patients with nonpulmonary metastases are at intermediate risk [1]. For patients with nonseminomatous tumors, the presence of a gonadal or retroperitoneal primary tumor, absence of nonpulmonary visceral metastases, and normal or stage 1 elevation of tumor markers are considered good risk features. Stage 2 serum tumor markers put the patient at intermediate risk and presence of a mediastinal primary tumor or nonpulmonary visceral metastases are poor risk factors.

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