1. classic seminoma (85%) 2. anaplastic seminoma (10%) - more aggressive with higher metastatic potential 3. spermatocytic seminoma (5%) - classically seen in OLDER patients

Testicular Tumors Flashcards by Kyra Porter

testicular tumors - epidemiology

*most common tumor of young men
*one of the most curable of all cancers
*no clear etiology, but 10% have history of undescended testis
*bilateral in 2-3%
*>50% of patients present with metastatic disease
*“right goes left, but left stays left” (nodal spread)
*distant mets via blood to lung, liver, brain, bones, kidney
*10% present with epididymitis

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testicular malignancies - classifications

germ cell tumors
a. seminoma
b. non seminomas (embryonal carcinoma, yolk sac tumor, choriocarcinoma, teratoma)
non-germ cell tumors
a. sex cord stromal tumors (sertoli cell tumors, leydig cell tumors)
b. secondary malignancies (lymphoma, metastases)

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general considerations of testicular tumors

*typically present as a firm, painless mass (therefore, CANNOT BE TRANSILLUMINATED on physical exam)
*do NOT biopsy (risk of seeding the scrotum)
*typical age of incidence: 15-40 years
*general risk factors:
-cryptorchidism
-Klinefelter syndrome
-Down syndrome
-testicular dysgenesis syndrome

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tumor marker: alpha fetoprotein (AFP)

*elevated in 50-70% of non-seminoma germ cell tumors (NSGCT)
*produced by embryonal carcinoma and yolk sac tumors
*NOT produced in pure choriocarcinoma or seminoma
*half-life of 4-6 days

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tumor marker: human chorionic gonadotropin (hCG)

*elevated in all choriocarcinomas
*elevated in 40-60% of embryonal carcinoma
*elevated in 5-10% of seminomas
*half-life of 24 hrs

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tumor marker: lactase dehydrogenase (LDH)

*non-specific tumor marker
*elevated in about half of the cases of testicular tumors
*attests to tumor burden

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seminoma - overview

*most common germ cell testicular tumor
*originates in the germinal epithelium of the seminiferous tubules
*75% are confined to testis at presentation; 15% involve regional nodes; 10% with distant spread

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seminoma - gross pathologic features

*well-demarcated, homogenous, pale mass
*no hemorrhage
*no necrosis

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seminoma - microscopic pathologic features

*large cells, clear cytoplasm, central nuclei (“fried egg” appearance)
*placental alkaline phosphatase (PLAP) positive in up to 98% of seminomas

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seminoma - 3 types

classic seminoma (85%)
anaplastic seminoma (10%) - more aggressive with higher metastatic potential
spermatocytic seminoma (5%) - classically seen in OLDER patients

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seminoma - clinical presentation

*painless testicular mass (some may present with testicular discomfort or swelling)
*mass CANNOT be transilluminated
*relatively slow growing
*mean age at presentation = 40 years
*6-10x higher incidence among white men
*increased PLAP

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seminoma - tumor markers

*hCG produced in 5-10% of seminomas
*NO pure seminoma produces AFP
*increased placental alkaline phosphatase (PLAP)

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seminoma - therapy considerations

*do NOT perform a biopsy
*discuss sperm banking
*radical inguinal orchiectomy (removal of testicle; confirms diagnosis & helps determine staging)
*management depends on stage
*good prognosis
*does respond to radiation therapy

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embryonal carcinoma testicular tumor - overview

*a non-seminoma germ cell testicular cancer

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embryonal cell testicular tumor - gross pathologic features

*hemorrhagic mass with necrosis
*usually smaller than seminomas (i.e. does not replace the entire testis)

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embryonal cell testicular tumor - microscopic pathologic features

*immature, primitive cells (“embryo-like”) with prominent nucleoli and pleomorphic nuclei
*resemble undifferentiated stem cells
*may form glands

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embryonal cell testicular tumor - clinical presentation

*painless testicular mass
*early hematogenous spread: retroperitoneum, lung, liver
*typically positive for placental alkaline phosphatase (PLAP)

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embryonal cell testicular tumor - tumor markers

*may secrete alpha fetoprotein (AFP) or beta-hCG, but usually BOTH

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embryonal cell testicular tumor - therapy considerations

*do NOT biopsy
*discuss sperm banking
*chemotherapy may lead to differentiation of tumor cell types (resulting in a new, more mature tumor type)

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embryonal cell testicular tumor - prognosis

*determined by clinical stage
*aggressive tumors
*highest rate of lymphovascular invasion & extension into the paratesticular tissue

yolk sac testicular tumor - overview

*a non-seminoma germ cell testicular cancer
*most common testicular tumor in children < 3 years old

yolk sac testicular tumor - gross pathologic features

*solid gray-white tumor
*gelatinous surface
*hemorrhage, necrosis, and cystic changes often present

yolk sac testicular tumor - microscopic pathologic features

*classic histology = Schiller-Duval body
-a central vessel surrounded by tumor cells residing in a cystic space
-exhibits a glomerulus-like structure
-present in 50-75% of cases
*most common pattern is a microcytic pattern

yolk sac testicular tumor - clinical presentation

*painless testicular mass
*the most common testicular tumor during childhood (esp. < 3 years old)
*metastases often via hematogenous spread; most commonly spreads to the lungs
*often good prognosis

yolk sac testicular tumor - tumor marker

*alpha fetoprotein (AFP) is typically elevated

choriocarcinoma testicular tumor - overview

*a **non-seminoma** germ cell testicular cancer *characterized by disordered **syncitiotrophoblastic and cytotrophoblastic elements**

choriocarcinoma testicular tumor - gross pathologic features

*hemorrhagic mass with necrosis

choriocarcinoma testicular tumor - microscopic pathologic features

*malignant tumor of **syncytiotrophoblasts and cytotrophoblasts** *do NOT get villi (as you would have in placental tissue)

choriocarcinoma testicular tumor - clinical presentation

*painless testicular mass ***rapid hematogenous spread** (is placenta-like tissue and "programmed" to find blood vessels) *may secrete **hCG → hyperthyroidism (TSH-like effects) and gynecomastia (LH- and FSH-like effects** *increased risk of **brain metastases** *often involves retroperitoneal lymph nodes *POOR PROGNOSIS due to rapid metastasis

choriocarcinoma testicular tumor - tumor markers

***high hCG ALWAYS present** -alpha subunit of hCG is similar to the alpha subunits of FSH/LH, so may cause gynecomastia and/or hyperthyroidism *pure forms do NOT make AFP

teratoma testicular tumor - overview

*a **non-seminoma** germ cell testicular cancer

teratoma testicular tumor - gross pathologic features

*exhibits **mature fetal tissue (teeth, hair, etc)** *lesions may be well-circumscribed

teratoma testicular tumor - microscopic pathologic features

*histology may reveal a variety of tissues (organized or unorganized presentation) *composed of **cells derived from at least 2 of the 3 embryonic germ layers (endoderm, mesoderm, ectoderm)** *"immature" teratomas have tissue not seen in adult tissue elements

teratoma testicular tumor - clinical presentation

*painless testicular mass ***MALIGNANT in males (benign in females)** but prepubertal are benign and orchiectomy is curative *prognosis depends on tumor stage

teratoma testicular tumor - tumor markers

*pure teratomas do NOT produce hCG or AFP *some tumors, however, may be mixed

mixed germ cell tumors

*the **majority of germ cell tumors are MIXED** (e.g. embryonal carcinoma plus yolk sac tumor plus teratoma) *combinations with SEMINOMAS are **treated as non-seminoma germ-cell tumors** (chemotherapy) *prognosis - based upon the tumor component with the worst prognosis

sex cord stromal tumors - overview

*comprise ~5% of testicular tumors *can be Leydig Cell tumors and Sertoli Cell tumors *usually benign *wide age range (14-87 yrs) *no known risk factors

Leydig Cell tumor - overview

*a **sex cord stromal tumor** *the most common sex cord stromal tumor *more frequently presents in adults (40-50yrs) but can present at any age

Leydig Cell tumor - pathologic features

*gross: golden brown to yellow cut surface *micro: **Leydig cells with abundant pink cytoplasm and REINKE CRYSTALS (pink-staining rod-like cytoplasmic inclusions)**

Leydig Cell tumor - clinical presentation

*painless testicular mass *Leydig cells produce androgens and estrogen, so can result in **precocious puberty (children) or gynecomastia (adults)**

Leydig Cell tumor - management

*radical inguinal **orchiectomy** preferred *prognosis dependent on tumor stage (most are benign)

Sertoli Cell tumor - overview

*a **sex cord stromal tumor** *composed of the **cells that line the seminiferous tubules** *can present at any age (avg. age = 45 yrs)

Sertoli Cell tumor - microscopic pathologic features

*tumor forms tubules *uniform cuboidal or columnar cells with moderate pale or lightly pink cytoplasm *often with prominent cytoplasmic lipid vacuoles

Sertoli Cell tumor - clinical presentation

*painless testicular mass *rarely exhibit gynecomastia or precocious puberty *may be seen in patients with: -Peutz-Jeghers syndrome -Carney syndrome -androgen insensitivity syndrome -testicular feminization syndrome

Sertoli Cell tumor - management

*radical inguinal orchiectomy *prognosis based on tumor stage (only 10% are malignant)

lymphoma testicular cancer - overview

*a **non-germ cell testicular cancer** *comprise 5% of all testicular tumors *may be primary or secondary

lymphoma testicular cancer - microscopic pathologic features

*sheets of malignant lymphoid cells infiltrate between normal testicular structures *most common = **diffuse large B cell lymphoma** *others include: MALT lymphoma, follicular lymphoma, T cell lymphoma, Burkitt lymphoma (in children)

lymphoma testicular cancer - clinical presentation

*painless testicular mass ***most common cause of a testicular mass in older men over 60 yrs** *usually **BILATERAL** *commonly also presents with B symptoms (fever, night sweats, weight loss) *prognosis generally POOR