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Testicular Cancer

by Viraj A. Master, MD, PhD

Testicular cancer begins as a scrotal mass, which is usually not painful. Diagnosis is by ultrasonography. Treatment is with orchiectomy and sometimes lymph node dissection, radiation therapy, chemotherapy, or a combination, depending on histology and stage.

Testicular cancer is the most common solid cancer in males aged 15 to 35, with about 8000 cases annually, but only about 400 deaths. Incidence is 2.5 to 20 times higher in patients with cryptorchidism. This excess risk is decreased or eliminated if orchiopexy is done before age 10 yr. Cancer can also develop in the contralateral normally descended testis. The cause of testicular cancer is unknown.

Most testicular cancers originate in primordial germ cells. Germ cell tumors are categorized as seminomas (40%) or nonseminomas (tumors containing any nonseminomous elements). Nonseminomas include teratomas, embryonal carcinomas, endodermal sinus tumors (yolk sac tumors), and choriocarcinomas. Histologic combinations are common; eg, teratocarcinoma contains teratoma plus embryonal carcinoma. Functional interstitial cell carcinomas of the testis are rare.

Even patients with apparently localized tumors may have occult nodal or visceral metastases. For example, almost 30% of patients with nonseminomas will relapse with nodal or visceral metastases if they undergo no treatment after orchiectomy. Risk of metastases is highest for choriocarcinoma and lowest for teratoma.

Tumors originating in the epididymis, testicular appendages, and spermatic cord are usually benign fibromas, fibroadenomas, adenomatoid tumors, and lipomas. Sarcomas, most commonly rhabdomyosarcoma, occur occasionally, primarily in children.

Symptoms and Signs

Most patients present with a scrotal mass, which is painless or sometimes associated with dull, aching pain. In a few patients, hemorrhage into the tumor may cause acute local pain and tenderness. Many patients discover the mass themselves after minor scrotal trauma.

Diagnosis

  • Ultrasonography for scrotal masses

  • Exploration if testicular mass is present

  • Staging by abdominal, pelvic, and chest CT as well as tissue examination

Many patients discover the mass themselves during self-examination. Monthly self-examination should be encouraged among young men.

The origin and nature of scrotal masses must be determined accurately because most testicular masses are malignant, but most extratesticular masses are not; distinguishing between the two during physical examination may be difficult. Scrotal ultrasonography can confirm testicular origin. If a testicular mass is confirmed, serum markers α-fetoprotein and β-human chorionic gonadotropin should be measured and a chest x-ray taken. Then, inguinal exploration is indicated; the spermatic cord is exposed and clamped before the abnormal testis is manipulated.

If cancer is confirmed, abdominal, pelvic, and chest CT is needed for clinical staging using the standard TNM (tumor, node, metastasis) system ( AJCC/TNM* Staging of Testicular Cancer and TMN and Serum Marker Definitions for Testicular Cancer). Tissue obtained during treatment (usually radical inguinal orchiectomy) helps provide important histopathologic information, particularly about the proportion of histologic types and presence of intratumoral vascular or lymphatic invasion. Such information can predict the risk of occult lymph node and visceral metastases. Patients with nonseminomas have about a 30% risk of recurrence despite normal x-rays and serum markers and having what appears to be localized disease. Seminomas recur in about 15% of such patients.

AJCC/TNM* Staging of Testicular Cancer

Stage

Tumor

Regional Lymph Node Metastasis

Distant Metastasis

Serum Tumor Markers

0

pTis

N0

M0

S0

I

pT1–pT4

N0

M0

SX

IA

pT1

N0

M0

S0

IB

pT2

N0

M0

S0

pT3

N0

M0

S0

pT4

N0

M0

S0

IS

Any pT/pTX

N0

M0

S1–S3

II

Any pT/pTX

N1–N3

M0

SX

IIA

Any pT/pTX

N1

M0

S0

Any pT/pTX

N1

M0

S1

IIB

Any pT/pTX

N2

M0

S0

Any pT/pTX

N2

M0

S1

IIC

Any pT/pTX

N3

M0

S0

Any pT/pTX

N3

M0

S1

III

Any pT/pTX

Any N

M1

SX

IIIA

Any pTp/TX

Any N

M1a

S0–S1

IIIB

Any pT/pTX

N1–N3

M0

S2

Any pT/pTX

Any N

M1a

S2

IIIC

Any pT/pTX

N1–N3

M0

S3

Any pT/pTX

Any N

M1a

S3

Any pT/pTX

Any N

M1b

Any S

*For AJCC/TNM staging definitions, see Table: TMN and Serum Marker Definitions for Testicular Cancer

Adapted from Edge SB, Byrd DR, Compton CC, et al: AJCC Cancer Staging Manual, 7th edition. New York, Springer, 2010.

TMN and Serum Marker Definitions for Testicular Cancer

Feature

Definition

Tumor

pTX

Not assessable

pT0

No evidence of primary tumor (eg, scar in testis)

pTis

Intratubular germ cell tumors (carcinoma in situ)

pT1

Limited to testis and epididymis without vascular or lymphatic invasion

May invade tunica albuginea but not tunica vaginalis

pT2

Limited to testis and epididymis with vascular or lymphatic invasion, or extends through tunica albuginea and involves tunica vaginalis

pT3

Invades spermatic cord with or without vascular or lymphatic invasion

pT4

Invades scrotum with or without vascular or lymphatic invasion

Regional lymph node metastasis

NX

Not assessable

N0

None

N1

≥ 1 node, all ≤ 2 cm in greatest dimension

N2

≥ 1 node > 2 cm but ≤ 5 cm in greatest dimension, with or without other nodes ≤ 5 cm in greatest dimension

N3

≥ 1 node > 5 cm in greatest dimension

Distant metastasis

M0

None

M1

Present

M1a

Nonregional nodal or lung metastasis

M1b

Distant metastasis other than nonregional lymph nodes or lung

Serum markers

SX

Markers not available or not measured

S0

Levels within normal limits

S1

LDH < 1.5 × the upper limit of normal for the LDH assay and hCG < 5000 mIu/mL and AFP < 1000 ng/mL

S2

LDH = 1.5–10 × upper limit of normal for the LDH assay or hCG 5000–50,000 mIu/mL or AFP 1000–10,000 ng/mL

S3

LDH > 10 × upper limit of normal for the LDH assay or hCG > 50,000 mIu/mL or AFP >10,000 ng/mL

AFP = alpha fetoprotein; AJCC = American Joint Commission on Cancer; hCG = human chorionic gonadotropin; p = pathologic staging; pT = primary tumor; N = regional lymph nodes (assessed clinically); M = distant metastases; S = serum tumor markers.

Data from Edge SB, Byrd DR, Compton CC, et al: AJCC Cancer Staging Manual, 7th edition. New York, Springer, 2010.

Prognosis

Prognosis depends on histology and extent of the tumor. The 5-yr survival rate is > 95% for patients with a seminoma or nonseminoma localized to the testis or with a nonseminoma and low-volume metastases in the retroperitoneum. The 5-yr survival rate for patients with extensive retroperitoneal metastases or with pulmonary or other visceral metastases ranges from 48% (for some nonseminomas) to > 80%, depending on site, volume, and histology of the metastases, but even patients with advanced disease at presentation may be cured.

Treatment

  • Radical inguinal orchiectomy

  • Radiation therapy for seminomas

  • Usually retroperitoneal lymph node dissection for nonseminomas

Radical inguinal orchiectomy is the cornerstone of treatment and helps provide important diagnostic information; it also helps formulate the subsequent treatment plan. A cosmetic testicular prosthesis may be placed during orchiectomy. Silicone prostheses are not widely available because of the problems with silicone breast implants. However, saline implants have been developed. For men who wish to retain reproductive capacity, sperm banking is potentially available in anticipation of radiation therapy or chemotherapy.

Radiation therapy

Standard treatment for seminoma after unilateral orchiectomy is radiation therapy, usually 20 to 40 Gy (higher dose is used for patients with a nodal mass) to the para-aortic regions up to the diaphragm. The ipsilateral ilioinguinal region is no longer routinely treated. Occasionally, the mediastinum and left supraclavicular regions are also irradiated, depending on clinical stage.

Lymph node dissection

For nonseminomas, many experts consider standard treatment to be retroperitoneal lymph node dissection. For clinical stage 1 tumors in patients who have no prognostic factors that predict relapse, an alternative is active surveillance (frequent serum marker measurements, chest x-rays, CT). Intermediate-sized retroperitoneal nodal masses may require retroperitoneal lymph node dissection and chemotherapy (eg, bleomycin, etoposide, cisplatin), but the optimal sequence is undecided.

Lymph node dissection is done laparoscopically at some centers. The most common adverse effect of lymph node dissection overall is failure to ejaculate. However, a nerve-sparing dissection is often possible, particularly for early-stage tumors, which usually preserves ejaculation.

Chemotherapy

Nodal masses > 5 cm, lymph node metastases above the diaphragm, or visceral metastases require initial platinum-based combination chemotherapy followed by surgery for residual masses. Such treatment commonly controls the tumor long term. Fertility is often impaired, but no risk to the fetus has been proved if pregnancy does occur.

Surveillance

Surveillance is appropriate for some patients, although many clinicians do not offer this option because it requires rigorous follow-up protocols and excellent patient adherence to be safe. It is more commonly offered to patients at low risk of relapse. High-risk patients usually get retroperitoneal lymph node dissections or, in some centers, 2 courses of chemotherapy after orchiectomy instead of surgery.

Recurrences

Nonseminoma recurrences are usually treated with chemotherapy, although delayed retroperitoneal lymph node dissection may be appropriate for some patients with nodal relapse and no evidence of visceral metastases. Surveillance is not used as often for seminomas because the morbidity of 2 wk of radiation therapy is so low and the results in preventing late relapse so high that there is less reason to try to avoid treatment.

Key Points

  • Testicular cancer is the most common solid cancer in males aged 15 to 35 but is often curable, particularly seminoma.

  • Assess scrotal masses by ultrasonography and if they are testicular, do a chest x-ray and measure α-fetoprotein and β-human chorionic gonadotropin.

  • Do radical inguinal orchiectomy, usually with radiation therapy (for seminomas) and retroperitoneal lymph node dissection (for nonseminomas).

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