1202 Testicular Cancer
testis before puberty decreases the risk of • N4: Juxtaregional nodes.
BASIC INFORMATION
DEFINITION
Testicular neoplasms are primary cancers origi-
nating in a testis.
SYNONYMS
Testis tumor
Testicular neoplasms
ICD-9CM CODES
186.9    Testicular neoplasm
M906/3  (seminoma)
M9101/3  (embryonal carcinoma or teratoma)
M9100/3 (choriocarcinoma)
ICD-10CM CODES
C62.1 Malignant neoplasm of unspecified
descended testis
C62.0 Malignant neoplasm of undescended
testis
EPIDEMIOLOGY &
DEMOGRAPHICS
INCIDENCE: 5.4 cases per 100,000 men annu-
ally. White men have the highest incidence at
6.3 cases/100,000 men. Testicular cancer is
the most common cancer diagnosis in men
between 15 and 35 yr. The incidence has been
gradually increasing since 1975.
PREVALENCE: 1% to 2% of all cancers in
males.
PREDOMINANT AGE: Can occur in any age but
most common in young adults; average age for
embryonal cell carcinoma: 30 yr; average age
for seminoma: 36 yr.
PHYSICAL FINDINGS & CLINICAL
PRESENTATION
• Testicular cancer typically presents as a
painless mass in the testis. Any mass within
the testicle should be considered cancer until
proven otherwise. It may be found by the
patient, who brings it to the attention of a
physician, or it may be found by a physician
on a routine examination.
• Symptoms other than scrotal or testicular
swelling are typically absent unless the cancer
has metastasized (10% of patients at diagno-
sis). Occasionally a patient may report scrotal
fullness or heaviness. About 10% of patients
present with acute pain. Back pain secondary
to enlarged retroperitoneal lymph nodes can
occur. Gynecomastia from tumors that secrete
beta-human chorionic gonadotropin (hCG) is
found in 5% of men with testicular cancer.
• Testicular palpation should be performed with
two hands. Transillumination may distinguish
a solid mass (e.g., cancer) and a fluid-filled
lesion (e.g., hydrocele or spermatocele). The
mass is nontender; indeed, it is less sensitive
than a normal testicle.
ETIOLOGY, CLASSIFICATION, &
PATHOLOGY
• 
Cryptorchidism (undescended testes) is a
major risk factor even if corrected by orchio-
pexy; however, treatment of undescended
testicular cancer from fivefold to twofold. • M0: No distant metastases.
Other risk factors are family history (risk is 8 • M1: Distant metastases present.
to 10 times as high in a brother of a person The clinical stages consist of stage I, with tumor
with testicular cancer), genetic disorders confined to the testis; stage II, with positive
(Down’s syndrome, testicular dysgenesis regional lymph nodes; and stage III, with metas-
syndrome), Klinefelter’s syndrome, infertility, tases. Figure T1-9 shows the clinical staging of
tobacco use, and white race (risk is highest testicular cancer.
among whites and lowest among blacks).
• Classification: testicular cancers can be classi-
fied as pure seminomas or nonseminomatous
DIAGNOSIS
germ cell tumors (embryonic carcinoma, cho- DIFFERENTIAL DIAGNOSIS
riocarcinoma, yolk sac carcinoma, teratoma).
• Spermatocele.
• Pathology: germ cell tumors account for
• Varicocele.
>95% of testicular cancers.
• Hydrocele.
• Epididymitis/orchitis.
Cell Type Frequency (%)
• Epidermoid cyst of the testicle.
Seminoma 42 • Epididymis tumors.
Embryonal cell 26 • Inguinal hernia.
carcinoma • Hematocele or testicular rupture.
Teratocarcinoma 26 • Torsion of testicular appendage.
Teratoma 5 • Skin cancer.
Choriocarcinoma 1
WORKUP
• Other rare types: Physical examination, laboratory tests, and
○ Yolk sac carcinoma. imaging studies (see Section III, “Testicular
○ Mixed germ cell tumors. Mass”). A radical inguinal orchiectomy is diag-
○ Carcinoid tumor. nostic and therapeutic. Immunohistochemical
○ Sertoli cell tumors. analysis is used to determine the histologic
○ Leydig cell tumors. composition of the tumor. Staging involves CT of
○ Lymphoma. chest, abdomen, and pelvis and measurement
○ Metastatic cancer to the testes. of beta subunit of human chorionic gonado-
• TNM staging system for testicular cancer tropins (β-hCG), alpha-fetoprotein, and lactate
○ T0: No apparent primary. dehydrogenase.
○ T1: Testis only (excludes rete testis).
○ T2: Beyond the tunica albuginea. LABORATORY TESTS
○ T3: Rete testis or epididymal involvement. • Serum hCG.
○ T4: Spermatic cord. • Serum alpha-fetoprotein (AFP): elevated in
1. Spermatic cord. nonseminoma tumors.
2. Scrotum. One or both of these tumor markers will be
• N0: No nodal involvement. elevated in 70% of cases of testicular cancer.
• N1: Ipsilateral regional nodal involvement. • Serum lactate dehydrogenase (LDH) level:
• N2: Contralateral or bilateral abdominal or elevated with rapid turnover of malignant
groin nodes. cells.
• N3: Palpable abdominal nodes or fixed groin • Testicular biopsy contraindicated.
nodes.
Clinical staging of testicular cancer
Stage
I II III*
• Tumor confined • Retroperitoneal • Visceral disease
to testis adenopathy below diaphragm
• No clinical or (on CT scan) (e.g., liver or bowel
radiographic involvement) or
evidence of cancer any disease above
after orchiectomy diaphragm
*Stage III disease can be subdivided into minimal, moderate, and
high-risk, depending on the location of tumor and the extent
of tumor spread.
FIGURE T1-9  Clinical Staging of Testicular Cancer. The AJCC TNM staging system is less commonly
used, because it is based upon histologic evaluation of the orchidectomy specimen and retroperitoneal peri-
aortic lymph node dissection. Because the latter may not be performed in every patient, the clinical staging
system is generally more practical. (From Skarin AT. Atlas of diagnostic oncology, ed 4, St Louis, 2010, Mosby.)
 Testicular Cancer 1203

IMAGING STUDIES
TABLE T1-3  International Germ Cell Consensus Criteria for Testicular Cancer
• Testicular ultrasound.
• CT scan of chest, pelvis, and abdomen. Nonseminoma Seminoma
T
• MRI of the brain in patients with neurologic
Good Prognosis
symptoms.
• PET scan is not recommended (frequent false Testis/retroperitoneal primary Any primary site
positives). And And
No nonpulmonary visceral metastases No nonpulmonary visceral metastases
TREATMENT And And
Good markers—all of Normal AFP, any hCG, any LDH
• Seminoma • AFP < 1000 ng/mL and
1. Stage I: Most patients with clinical stage • hCG < 5000 IU/L (1000 ng/mL) and

and Disorders
Diseases
1 are cured with orchiectomy. Radical • LDH < 1.5 × upper limit of normal
orchiectomy plus one cycle of single 58% of nonseminomas 90% of seminomas
agent carboplatin chemotherapy or radia- 5-year PFS 89% 5-year PFS 82%
tion therapy (RT) to the paraaortic lymph 5-year survival 92% 5-year survival 86%
nodes was the standard of treatment Intermediate Prognosis
for many years but has been eliminated
I
Testis/retroperitoneal primary Any primary site
in many instances and most patients And And
are treated with active surveillance post No nonpulmonary visceral metastases Nonpulmonary visceral metastases
orchiectomy. More relapses are associ-
And And
ated with surveillance (20% vs. 4% with
Intermediate markers—any of Normal AFP, any hCG, any LDH
radiotherapy or chemotherapy), but long-
• AFP ≥ 1000 and ≤ 10,000 ng/mL or
term survival approaches 100% irrespec- • hCG ≥ 5000 IU/L and ≤ 50,000 IU/L or
tive of initial option chosen.1 • LDH ≥ 1.5 × normal and ≤ 10 × normal
2.  Stage IIA or IIB: RT or cisplatin-based 28% of nonseminomas 10% of seminomas
chemotherapy (e.g., cisplatin, bleomycin,
5-year PFS 75% 5-year PFS 67%
etoposide).
5-year survival 80% 5-year survival 72%
• Nonseminoma
1. Stage IA: radical orchiectomy plus nerve Poor Prognosis
sparing retroperitoneal lymph node dis- Mediastinal primary No patients classified as
section (RPLND). Or poor prognosis
2.  Stage IB: Same as stage IA plus two Nonpulmonary visceral metastases
cycles of chemotherapy (bleomycin, eto-
Or
poside, and cisplatin [BEP]).
3. Advanced stages: cisplatin-based chemo- Poor markers—any of
therapy or RPLND. • AFP > 10,000 ng/mL or
• Posttreatment surveillance for testicular can- • hCG > 50,000 IU/L (10,000 ng/mL) or
cer survivors (annually). • LDH > 10 × upper limit of normal
1. Fertility assessment. 16% of nonseminomas
2. Physical examination and skin examina-
5-year PFS 41%
tion (increased risk of dysplastic nevi).
3. Testicular examination (3% to 4% risk of 5-year survival 48%
second testicular cancer). AFP, α-fetoprotein; hCG, human chorionic gonadotrophin; LDH, lactate dehydrogenase; PFS, progression-free survival.
4. Serum tumor markers (hCG, AFP). From Skarin AT. Atlas of diagnostic oncology, ed 4, St Louis, 2010, Mosby.
5. Abdominal and pelvic CT every 3 to 4
months for 2 years, every 6 to 12 months Prognosis can be determined by criteria
in third and fourth year, and annually established by the International Germ Cell EVIDENCE
thereafter. Consensus Criteria (Table T1-3). Because
Available at www.expertconsult.com
treatment produces favorable outcomes
DISPOSITION
even in advanced stages, the U.S. Preventive SUGGESTED READINGS
• The overall cure for testicular cancer is >95% Services Task Force recommends against
(80% for metastatic disease). Patients with Available at www.expertconsult.com
screening asymptomatic men for testicular
pure seminomas have a better prognosis. cancer. RELATED CONTENT
• Therapeutic radiation and chemotherapy are Testicular Cancer (Patient Information)
1 HannaNH, Einhorn LH: Testicular cancer, discoveries risk factors for cancers of thyroid, lymphoma,
and updates, N Engl J Med 371:2005-2016, 2014. kidney, pancreas, stomach, and leukemia. AUTHOR: FRED F. FERRI, M.D.
Testicular Cancer 1203.e1

EVIDENCE SUGGESTED READINGS

Feldman DR et al.: Medical treatment of advanced testicular cancer, JAMA
Abstract[1] 299(6):672–684, 2008.
Purpose: Lin K, Sharangpani R: Screening for testicular cancer: an evidence review for
To evaluate the prevalence of testicular microlithiasis (TM) in children the U.S. Preventive Services Task Force, Ann Intern Med 153:396–399, 2010.
who have undergone scrotal ultrasonography (US) and their association Petterson A et al.: Age at surgery for undescended testis and risk of testicular
with testicular tumors. cancer, N Engl J Med 356:1835, 2007.
Materials and Methods: Shaw J: Diagnosis and treatment of testicular cancer, Am Fam Physician
This HIPAA-compliant study with waiver of informed consent was 77(4):469–474, 2008.
­approved by the institutional review board. From 2003 to 2012, all
­patients with scrotal US and report mentioning calcifications or micro-
lithiasis and all patients with testicular tumors from pathology database
were identified. US studies were evaluated for the type of TM (classic ≥5
microliths or limited <5 microliths in a single view) and change in follow-
up studies if available. Medical charts were reviewed for US indication,
underlying medical conditions, and pathologic abnormalities, when avail-
able. Fisher exact test was used to analyze the association of testicular
tumors and TM.
Results:
A total of 3370 boys had scrotal US, 83 (2%) of whom had TM or micro-
calcifications in the report. TM was usually bilateral (n = 62, 75%) and
classic (n = 59, 71%) type. TM was significantly less common in those
younger than 2 years of age than in older age groups (0.1% versus 3.1%,
P < 0.0001). The most common indication for US was scrotal pain (40
of 83 patients, 48%), and the most common associated medical condi-
tion was cryptorchidism (nine of 83 patients, 11%). Testicular tumor was
significantly more likely in boys with TM (12% versus 0.3%, P < 0.01).
Five (83%) of six patients with premalignant or benign tumors had a
premalignant condition (cryptochydism in two and Peutz-Jeghers syn-
drome in three). Four patients with TM had malignant testicular tumors,
all diagnosed after the age of 16 years.
Conclusion:
TM has a prevalence of 2% in boys who undergo scrotal US. It is most
commonly bilateral, classic type, and stable at follow-up studies. There
is a significant association of TM and testicular tumors. Malignant tumors
were seen only in adolescent boys.

Evidence-Based Reference
Cooper M, Kaefer M, Fan R, et al.: Testicular microlithiasis in children and associ-
ated testicular cancer, Radiology 270:857–863, 2014.