Testis

TESTICULAR TESTIS PATHOLOGY

TESTES

Numbers

4.5cm

20g

Components

Epididymis: pseudostratified with cilia

Rete testis: flat cuboidal

Seminiferous tubules: atypia, lipofushcin

Vas deferens: columnar + lymphocytes

CONGENITAL ANOMALIES

Cryptorchidism

Aplasia (rare)

Fusion of both testes (synorchism)

Developmental cysts

Splenogonadal fusion

 

CRYPTORCHIDISM

How common?

1% of newborns

Etiology

1st:

2nd: trisomy 13, hormonal abnormalities

% bilateral?

25%

Which hormone controls phases of descent?*

First phase: mullerian-inhibiting substance

Second phase: androgen-dependent

Where is it located mostly?

-inguinal canal

When start seeing histologic change

From 2 years

Gross of cryptoid testis

Small

Micro of cryptoid testis?

Spermatogenesis arrest or decrease

Thick and hyalinized seminiferous tubular BM

Interstitial fibrosis but spares Leydig cells (looks prominent)

Good picture below

Can it occur in contralateral descended testis?

Yes

Long-term consequences? How high for tumors? What type of cancer?

Inguinal hernia

Sterility

Cancers: RR=5x, mostly seminomas (85%)

When surgery is done?

At 2 years (spontaneous descent in most within first year)

How can orchiopexy help?

Recover sterility, decrease cancer risk to some extent but not entirely (true for both testes)

Any follow-up? % with ITGCN?

Testicular biopsy controversial

3%

How are cryptorchid-associated tumors compared to sporadic?

Earlier and more bilateral

 

ATROPHY

Etiology

Cryptorchidism

Vascular disease (atherosclerosis, old age)

Inflammatory disorders

Hypopituitarism

Malnutrition or cachexia

Obstruction of semen outflow

High estrogen (prostate cancer treatment, cirrhosis)

High FSH

Exogenous androgenic steroids

Chemoradiation

Klinefelter

Micro

Same as cryptorchidism

 

INFERTILITY

Etiology of decreased fertility with normal histology***

Any obstruction: vas deferens, hypospadia, past paratesticular surgery

Retrograde ejaculation (TURP)

Varicocele

History of mumps or any orchitis

Idiopathic

Immotile cilia syndrome

Chemoradiation

Indications for testicular biopsy in fertility

Azoospermy to differentiate obstructive vs non-obstructive

Unexplained by other tests

Asymmetric testes

Screening for ITGCN in cryptorchid

Histologic patterns

Normal or hypospermatogenesis (all cells present but reduced numbers)

Germ cell arrest (earlier cellular elements of spermatogenesis present but stops at a certain stage, most often at primary spermatocytes)

Sertoli-cell-only syndrome or germ cell aplasia (the tubules contain Sertoli cells but no germ cells)

Hyalinization (cellular elements disappear, leaving thickened seminiferous tubules as in Klinefelter)

Immature testis (no gonadotropin stimulation, prepubertal appearance).

Micro: what do you see in azoospermia?***

-???

 

INFLAMMATION

Which infection starts in testis vs which in epididymis?*

Syphilis starts in testis

TB and gonorrhea start in epididymis

Name some epididymitis/orchitis

Nonspecific epididymitis and orchitis

Granulomatous orchitis: aka AI orchitis

Infectious: gonorrhea, mumps, TB, syphilis

NONSPECIFIC EPIDIDYMITIS AND ORCHITIS

Mechanism?

UTIà retrograde propagation via vas deferens or lymphatics of spermatic cord

Etiology: Age dependent

Kids GNB
Sexually active <35 Chlamydia, gono
Elderly E coli, Pseudomonas

Micro

Interstitial congestion, edema, PMN, macrophages, lymphocytesà abscess with necrosis of epididymisà scarringà sterility but still potent sexually (because Leydig cells spared)

 


GRANULOMATOUS ORCHITIS (AI orchitis)

Classic presentation

Mid-aged men with unilateral large testis of sudden onset

AI vs TB

AI orchitis TB
-Diffuse granulomas 

-Granuloma in seminiferous tubules

No
No AFB, ZN

DDx

Seminoma

Lymphoma

 

INFECTIONS

GONORRHEA

Pathway

Urethraà prostateà seminal vesiclesà epididymis

Micro

Same as nonspecific orchitis

MUMPS

Risk

Sterility (but not common)

Micro: Unilteral, patchy, interstitial inflammation

 

 

TB

Pathway of spread in TB

Always starts from epididymis

SYPHILIS

Pathway of spread in syphilis

Always starts from testis

Micro: Diffuse interstitial inflammation (edema, plasma cells, obliterative endarteritis, perivascular cuffing by lymphocytes) or nodular gummas

 

TORSION

Mechanism

Venous compression

Neonatal: no anatomic defects

Adult: bell-clapper deformity

Micro: Interstitial hemorrhage, hemorrhagic necrosis

 

LESIONS OF TUNICA VAGINALIS

Name a few and explain causes

Hydrocele: serous fluid in tunica vaginalis, due to generalized edema or incomplete closure of processus vaginalis. May be infected secondarily

Hematocele: secondary to trauma, torsion, bleeding disorders, invasion by malignancy

Chylocele: secondary to lymphatic obstruction (elephantiasis)

Spermatocele: local accumulation of semen in spermatic cord, generally in head of epididymis

Varicocele: blood within dilated vein in spermatic cord

 

SPERMATOCELE

Micro
Epididymal cyst filled with spermatozoa and lined by epithelium (flat to pseudostratified)

VASITIS NODOSUM

What is vasitis nodosum?

Occurs in vas deferens in the setting of obstruction

This causes azoospermic infertility

Proliferation of duct structures stuffed with spermatozoa (in the muscular layer of vas)

Obstruction is also associated with sperm granulomas in the vas

INFERTILITY

Types of infertility

Pre-testicular: pituitary/adrenal gl.

Testicular

Post-testicular: (obstructive)

3 causes associated with normal histology

Post-obstructive causes secondary to congenital

Post-surgical

Young’s syndrome (obstructive azoospermia + sinopulmonary infections)

Indications for testicular biopsy

Cryptorchidism to confirm ITGCN

Intersex infertility syndromes (gonadal dysgenesis, androgen insensitivity syndrome)

Previous germ cell tumor


TUMOURS

RF for germ cell neoplasia (not for non-GCT tumors)

Cryptorchidism

Intersex syndromes: gonadal dysgenesis, true hermaphroditism, male pseudohermaphroditism, androgen insensitivity syndrome

Previous testicular GCT

Oligospermic infertility

Family history of GCT

IGCNU (intertubular germ cell neoplasia, unclassified)

Name 3 RF (in particular cytogenetics)*

Cryptorchidism

Family history

Testicular dysgenesis: testicular feminization, Klinefelter

Cytogenetics: i(12p) resulting in gain of copy in 90% testicular GCT (including YST) and ITGCNà number of copies corresponds to aggressiveness

Prior GCT

Is GCT tumor of whites or blacks?

Whites

What are 2 genetic features of most germ cell tumours?

Hyperdiploid

12p amplifications, i(12p)

Give 5 IHC for sex cord-stromal tumors

α-inhibin

Calretinin

MelanA

CD99

S100

Chromogranin

Steroidogenic hormones

Incidence for sex cord-stromal tumors in testis?

Leydig> Sertoli> granulose> pure stromal tumors

AFP-producing tumors

YET

HCG-producing tumors

SEC

Ages with each tumour?

Seminoma: 40

Spermatocytic seminoma: 50-60

EC: 30

Choriocarcinoma: 10-20

YST and teratoma: <3 + adults

Leydig cell and Sertoli: kids to adults

Theory behind totipotent cells and germ cells tumours.

Germ cell tumours thought to derive from totipotent cell to become seminoma or non-seminomatous tumour

Metastases of one germ cell tumour may be different from another. (eg. EC can mets to the lung and show up as a teratomatous met)

Common clinical presentation

Painless enlargement

DDx for enlarged testis

Non-neoplastic (including painful masses!)

Neoplastic: primary vs mets, germ cell vs non,

Why no biopsy?

Will require scrotal skin excision in addition to orchiectomy

Most common spread pathways

LN: retroperitoneal para-aortic (sometimes mediastinal or supraclavicular)

Hemato: lungs, liver, brain, bone (2L2B)

Mets can mature into teratoma

Name tumors with best prognosis

Seminoma (curable for stage 1 and 2)

Teratoma in kids

Which one is bad

Pure choriocarcinoma (not so bad when it’s mixed)

Prognostic difference between histologic types?

Seminomatous better than non-seminomatous

No difference among non-seminomatous

What’s radical orchiectomy?

Testis and tunica vaginalis

Sequence of tumorigenesis. Exceptions?

ITGCNà seminomaà NSGCT

Exceptions: spermatocytic seminoma, pediatric GCT, all teratomas

Value of EM in GCT

Don’t forget this in exam…

Micro for GCT regression

Intratubular hematoxylin-staining bodies (nuclear debris)

Intratubular calcifications

Teratomatous elements

Fibrous scar, macrophages, chronic inflammation

All possible but mostly in choriocarcinoma

Micro for post-chemotherapy effects & relevance

No more chemotherapy Additional chemotherapy needed
Teratoma Residual tumor
Necrosis
Fibrosis
Repair change: foamy macrophages, hemosiderin, FB proliferation, cholesterol clefts

Concept of late recurrence

 

Prognosis***

Staging (serum markers included here)

Histologic type

ITGCN

% in cryptorchid?

3%

Risky for GCT?

50% in 5 years

How often is ITGCN adjacent to invasive GCT?

98%

How should it be called CIS?

Not carcinoma. Seminoma in situ acceptable

Genetics?

i(12p)

In what conditions?

Cryptorchid

Contralateral testis to testis with prior GCT

Infertility

Intersex syndromes

Coexists with most GCT

Micro

Large dark nuclei

Clear cytoplasm

Nucleoli

Mitoses

Sertoli displaced towards lumen

No normal spermatogenesis

Thickened BM

Spread

Pagetoid spread to rete testis common

Variants

Unclassified

Intratubular seminoma

Intratubular embryonal carcinoma

Intratubular YST

What stains (where)? (hint: same as seminoma)*

PAS+: also in normal germ cells

PLAP+: membranous, not in normal germ cells

C-KIT+

OCT3/4+: member of POU transcription factors, “master switch” in differentiation by regulating cells with pluripotent potential

D2-40

Other: ferritin, M2A, 43F

Treatment?

Radiation, orchiectomy

 

SEMINOMA

Peak age compared to NSGCT? Presentation? Can seminoma have AFP?

Peak 40 (10 years later than NSGCT)

Mass (pain only in 1/10), increased hCG (gynecomastia!)

No unless mixed with non-sampled YST

Equivalent in ovary and brain?

Dysgerminoma, germinoma

Gross. Often necrotic and hemorrhagic?

Lobulated bulging creamy white-yellow mass

Not extensive (only syncytiotrophoblastic foci)

Tunica albuginea often intact

 

Micro*

Sheets of large polygonal cells with clear to eosinophilic cytoplasm, slightly “squared” cell borders

Large central nuclei with large 1-2 nucleoli

No nuclear overlapping due to abundant cytoplasm

Fibrous septa containing lymphocyte

Granulomas in 50%à DDx granulomatous orchitis!

Syncytial trophoblasts in 20%à DDx choriocarcinoma

Fibrous scar with calcificationà DDx gonadoblastoma

 

What type of lymphocytes?

T (most lymphomas are B)

IHC*

PAS+ (glycogen)

C-KIT+

PLAP+

HCG+ in syncytiotrophoblast-like cells

CKAE1/3- or weak or focal+: vs strong in NSGCT. Remember seminoma is CK- except CAM5.2 (CK8/18)

EMA-

What’s PLAP?

Placental alkaline phosphatase

Prognosis

Excellent treat with radiation

Spread

Retroperitoneal LN, mediastinum

Name 3 variants

Seminoma with trophoblast giant cells

Mixed

Rare patterns

Cords

Solid tubules

Reticular, cribriform (edema)

Interstitial

Plasmacytoid (atypical seminoma): CK+, CD30+, no difference in therapy

Most important prognosticator

Staging (no1)

Ddx

Granulomatous reaction: PLAP- (useful for identifying residual seminoma)

EM

Glycogen aggregates

Simple cellular organelles…

Seminoma vs embryonal carcinoma

Seminoma Embryonal carcinoma
40 30
Often confined to testis on presentation Often outside of testis on presentationà much more symptomatic
Yellow creamy yellow Hemonecrosis
Pure possible Pure rare
-Distinct borders 

-No nuclear overlap

-Less pleomorphism

-Lymphocytes

-Fibrous septa

-Necrosis less

-Sheets mainly

-Less mitoses

-Clear cytoplasm

-Never glandular

-Indistinct borders 

-Nuclear overlapping

-Pleomorphism

-No lymphocytes

-No fibrous septa

-Necrosis common

-STP patterns

-High mitoses

-Basophilic cytoplasm

-Glandular pattern

No CD30+/CKAE1/3+
OCT3/4+
Radiation Chemotherapy
-HCG-producing ST (gynecomastia) 

-AFP elevation (with mixed with YST)

-PLAP+


Seminoma vs solid YST

Seminoma Solid YST
Single pattern (solid)à edema may mimic microcysts Other patterns (especially microcysts)
Lymphocytes Less
Fibrous septa No
No Extracellular BM deposit
No Hyaline globules
-OCT3/4+ -CK+ 

-AFP+

Seminoma vs choriocarcinoma

Seminoma Choriocarcinoma
No Biphasic
HCG only moderate HCG very high
OCT3/4+ CK+/EMA+

Seminoma vs lymphoma

Seminoma Lymphoma
Younger Older
Interstitial pattern with tubular preservation
Fibrous septa No
Clear cytoplasm No
Distinct Border less distinct
Uniform rounder nuclei Irregular nuclei
ITGCN No
T Mostly B
PLAP+ LCA+

SPERMATOCYTIC SEMINOMA

How much older compared to seminoma?

50-60yrs, 1/10 bilateral

SSx and prognosis

Painless enlargementà usually larger than seminoma

No mets, excellent prog

Origin: Premeiotic

Small (6-8µm) Some 

Resembling secondary spermatocytes (hence spermatocytic)à lymphocyte-like but more cytoplasm

Medium (15-18µmà 2x) Many 

Round nuclei

Filamentous chromatin “spireme”

Giants (50-100µmà 10x size) Scattered 

Can be multinucleated

Sometimes spireme

Nodules of sheets of cells, interrupted by edema

Usually pure, no IGCNU

High mitoses and apoptosis

Uniformly round nuclei, spirene chromatin, inconspicuous nucleoli

Numerous apoptoses

No lymphocytes, no fibrous septa

Variants?

Anaplastic: monomorphic population of intermediate cells

Spread

Intratubular often but never metsà therefore orchiectomy alone curative

When does spermatocytic sarcoma kill?

Sarcomatous differentiation

IHC*

Noneà PLAP-, PAS- (no glycogen), AFP-, HCG-, CK-

Does it occur outside of testis? No

Spermatocytic Seminoma
60 40
Testis only Testis, ovary, mediastinum, pineal, RP
No Cryptorchid
10% bilateral 2%
Never Often mixed
No ITGCN
Rarely sarcomatous differentiation Never
-3 cell types 

-Denser cytoplasm

-Round nuclei

-Interstitial edema common

-Scanty fibrous stroma

-No lymphocytes

-No granulomas

-1 cell type 

-Clear cytoplasm

-Nuclei with squared edges

-No edema

-Fibrous septa common

-Lymphocytes

-Granulomas

No Glycogen
PLAP+, HCG+ (10%)
Never Mets

Anaplastic SS Embryonal carcinoma
-More rounded 

-Foci of typical appearance

-Uglier
No ITGCN
CD30+/CK+/PLAP+/-


EMBRYONAL CARCINOMA

Age compared to seminoma?

-20-30

What can be elevated?

+/- HCG (“SEC”=seminoma, embryonal, choriocarcinoma), AFP (“YET”=YST, embryonal, teratoma)

Gross

Small like seminoma (≈2.5cm)

Not WC

Gray-white with punctuate hemorrhage and necrosis

Micro*

Usually mixedà found in 90% mixed tumors!

STP patterns (solid[1], tubular, papillary, alveolar), double-layered pattern

Indistinct cell borders

Atypical cells, large vesicular nuclei, large nucleoli

Nuclear overlapping

Extensive necrosis

High mitoses

Vascular invasion (important, mostly at periphery)

Can have HCG+ (syncytiotrophoblasts) or AFP+ (syncytial cells) cells or both!*

Intratubular embryonal carcinoma at periphery often

What’s crucial in reporting for embryonal carcinoma?

LVI

% of embryonal carcinoma component

Tumor size

Therefore, sample thoroughly!

IHC*

CD30+

CK+ but EMA-

Patchy PLAP+

OCT3/4+

Focal AFP+ may represent partial YST transformation

DDx

Seminoma:

Carcinoma: CK+, EMA+, CD30-, PLAP-

Solid YST:

Lymphoma (DLBCL): interstitial growth, no ITGCN, PLAP-

Anaplastic spermatocytic seminoma:

 


YST

Incidence? Serum marker?

Pure in kids (#1 testicular tumor <3 yo) vs mixed in adults

Increased serum AFP

Association with cryptorchid?

No

Gross

Yellow-gray myxoid, cystic or hemonecrotic

Name 5 patterns (11 in total)

Microcystic (reticular): most common; prominent cytoplasmic vacuolation confers cystic/lacelike appearance, focal myxoid background. Some microcysts coalesce to become macrocysts

Macrocystic

Solid

Parietal: extensive extracellular deposit of BM between tumor cells

Papillary

Glandular

Hepatoid

Myxomatous: resembling pulmonary edema

Sarcomatoid: RMS

Polyvesicular vitelline (not same as endodermal sinus): regular round vesicle lined by intestinel-type epithetium bulging out from cystic space. Rare…

Endodermal sinus: Schiller-Duval bodies (primitive glomeruli: BVà loose clear stromaà cuboidal epitheliumà spaceà cuboidal epithelium), labyrinth pattern (resembling angiosarcoma)

Relative frequency of each pattern?

Microcystic> macrocystic, solid, parietal> hepatoid, endodermal sinus, polyvesicular vitelline

What else in micro?

Hyaline globules (D-PAS, AFP, AAT+) inside and outside cells, variable size (1-50µm).

Where else can you find hyaline globules?

Rarely in seminoma and embryonal carcinoma

IHC

AFP diffuse+: some may be negative

CK+

A1AT+ in 50%

PLAP+: slightly less than other GCT

EMA-: useful vs carcinoma

OCT3/4-

CD30-

Prognosis

Good <3yo

Mostly mixed in adults

DDx: Seminoma


Solid YST vs embryonal carcinoma

YST Embryonal carcinoma
More patterns
More pleomorphic
Smaller cells
Smaller nuclei, not as crowded Large nuclei and very crowded
Hyaline globules
Extracellular BM deposit
AFP+ CD30+, OCT3/4+

YST vs juvenile granulosa cell tumor

YST JGCT
Solid, cystic, mitoses, atypia
Older kids Neonates, infants
AFP+ Inhibin+, CD99+

 

CHORIOCARCINOMA

Age

20-30

Potential sources?

Ovary, placenta, ectopic germ cell nests in mediastinum or abdomen

Is it common?

Pure very rare (young/prepubertal boys)

Mostly mixed

Ssx (hint=HCG, mets)

Gynecomastia, thyrotoxicosis (HCG mimics TSH), GI bleed, lumbar pain, hemoptysis, neural symptoms

Lab

HCG

Spread

Hematogenous spread to brain

What’s special about size?*

Small even in disseminated cases (so no testicular enlargement or sometimes even atrophic due to HCG), sometimes involuted to scar

Friable, hemorrhagic, solid, necrotic

Micro

Cytotrophoblast 

Intermediate trophoblast

Syncytiotrophoblast
Uniform nuclei Pleomorphic, multinucleated
Clear cytoplasm Amphophilic
Intracytoplasmic lacunae containing RBC
Smudged chromatin
“Caps” CT/IT
Sheets, cords
Remains after chemotherapy (monophasic variant) Rare after chemotherapy

Extensive hemonecrosisà extensive sampling required

Vascular invasion common

ITGCN


IHC

PLAP+ in 50%

HCG+ and inhibin+ in ST only

HPL+ in IT only

CK+

EMA+ (unique) in STà negative in other GCT!

Prognosis

Worse than any other GCT

 

DDx

Embryonal carcinoma (vs monophasic choriocarcinoma): use IHC

Solid YST: AFP+, HCG-

Seminoma with syncytiotrophoblasts: CK-, HPL-

Choriocarcinoma vs torsion-induced hemonecrosis

Choriocarcinoma Torsion
Small painless Painful
HGG elevation No
ITGCN No

IS HE A MAN?

Inhibin

Small

Hemorrhagic, hCG

Extra sections

Angioinvasion, Aggressive

Mononuclear (CT: polygonal cells with clear cytoplasm in cords/nests) and Multinuclear (ST: group of cells with smudged chromatin)

Necrotic Nodule


TERATOMA

Kids vs adults

Infants/kids Adults
<4yo Young
Pure Mixed (present in 50% of GCT); pure form rare
Always mature Mature or immature
Always benign Malignant regardess of maturity*
No ITGCN???
Derives from invasive GCT

Locations

Midlineà brain, neck, mediastinum, retroperitoneal

Gross

Nodular, cystic, cartilage

Lab

Can have AFP elevation in pure teratoma (without YST)

Micro

Mature (differentiated) 3 germ cell layers

Endoderm Gut, bronchial epithelium
Mesoderm Muscle, cartilage, fat
Ectoderm Skin, neural

Immature: immature neuroepithelium, foci resembling Wilms’, immature skeletal muscle

With a malignant component: SCC, neuroblastoma, LMS, chondrosarcoma

Genetics

i(12p)

How to grade?

No need to grade because mets even in mature teratomas (unlike in ovary)

Malignant transformation

Sarcoma (no1 in contrast to ovaries): mostly UPS

Carcinoma: IHC useful (CK+, EMA+, +/-CEA+, PLAP-, AFP-, HCG-)

Wilms

PNET

Treatment for malignant transformation

Surgical as nearly all are chemoresistant

How to differentiate PNET from immature teratomatous focus? How to diagnose epithelial malignancy?

Diagnose as PNET if >1LPF (4x)à concept of GCT overgrowth

Stromal invasion

Peculiar behavior

Pure teratoma can metastasize as non-teratomatous GCT

Prognosis? Tell when it’s critical to find immature component?

Childs: all mature teratomas are benignà critical to find immature elements

Adults: all teratomas (regardless maturity) are considered malignantà not important to find immature elements

Malignant transformation once outside of testis does not respond to chemotherapyà therefore must resect before it spreads

DDx

Epidermoid cyst: squamous epithelium lining cyst with no sebaceous glands, no ITGCN

Dermoid cyst: squamous epithelium lining a cyst with sebaceous glands in the wall, no ITGCNà just like in ovary but very rare in testis, completely benign

Why important to differentiate epidermoid and dermoid cysts from teratomas?

2 cysts are benign

Monodermal variants

Carcinoid: considered to be monodermal teratomas

PNET: considered to be monodermal teratomas

CARCINOID

Can they have carcinoid syndrome?

Yes, 10%

Most important ddx?

Metastatic carcinoid

Primary Metastatic
Teratomatous component Bilateral, multifocal
LVI

PNET

Diagnosis

->1LPF of immature neuroepithelium

IHC

-CD99+

-NE markers+

 

 

MIXED TUMORS* (more common than pure)

Name a few common combos

YET (YST, embryonal, teratoma): with HCG-containing giantsà YST confers slightly better prognosis

ET (embryonal, teratoma): aka teratocarcinoma, lower metastatic rate than embryonal carcinoma alone (remember embryonal carcinoma tends to differentiate into teratoma)

Less common for seminomas, never for spermatocytic seminoma

Why grossing important?

To get all components!

Significance of having YST, EC, CC?

YST associated with decreased relapses when confined to testis whereas EC and CC correlated with aggressiveness. However, YST less sensitive to chemotherapy than EC

POLYEMBRYOMA

Embryoid bodies (resembling developing yolk sacs)

 

 

LEYDIG CELL TUMOURS (interstitial)

Demo and presentation

-Peak 20-40

-Can elaborate androgen, estrogens or CTSDà sexual precocity in kids, gynecomastia in adults

Gross

-WC, homogeneous gold brown, with fibrous bands, buldging

Micro

-Sheets and cords

-Polygonal, central nuclei, nucleoli, abundant granular eosinophilic cytoplasm, indistinct cell bordersà hepatocyte-like

-Inclusions: lipofuscin, lipid vacuoles, Renke crystalloids and eosinophilic globoid inclusions (Renke precursors)

-Mitoses present but rare

 

 

Benign? What are malignant criteria?

No, 10% mets. How to tell?

>5 cm, >3 MF/10 HPF, atypical mitoses, nuclear pleomorphism, necrosis, vascular invasion, infiltrative margins, metastasis

IHC (hint: “MIC”)

CK ?

Calretinin+

Inhibin+

MelanA+

EM

SER

Intracytoplasmic droplets

SERTOLI CELL TUMOURS

Demo and presentation

Anyone under 40

Can elaborate androgens and estrogens but often insufficient to masculinize or feminize

Gross

WC, white homogeneous

Micro

Numerous hollow tubules (trying to recapitulate seminiferous tubules), lined by tall columnar cells

Benign? What are malignant features?

10% mets

Size>5cm, necrosis, moderate-severe atypia, vascular invasion, >5/10 mitoses

IHC

Calretinin

Inhibin

EM

SER

Intracytoplasmic droplets

Variants (2)

Sclerosing: abundant dense stromal tissue distorting sertoli tubules

Large cell calcifying: focal ossification + sertoli tubulesà Carney’s complex (acromegaly, pituitary gigantism, hypercortisolemia, sexual precocity, spotty skin pigmentation, sudden death) (pituitary GH adenomas, bilateral black adrenals, testicular LCCSCT, cardiac myxomas, skin lentigines and psammomatous melanotic schwannoma)

 

 


Name 3 syndromic associations

Androgen insensitivity

Carney’s: LCCSCT (50 cases reported…)

Peutz-Jeghers: LCCSCT

 

GRANULOSA CELL TUMOR

Incidence

Very rare

Adult Juvenile
No1 tumor for infants <6m
Gynecomastic in 20% Often cystic
10% malignant All benign

LYMPHOMA

Demo

>60yo*, can be bilateral

Gross

Diffuse tan involvement (looks like seminoma)

Commonest type

DLBCL

 

 

 

CLASSIFY TESTICULAR TUMOURS

GCT (95%)

Precursor

Intratubular Germ Cell Neoplasia ITGCN

Seminomatous GCTà more pure

Seminoma: 40

With syncytiotrophoblast cells

Spermatocytic seminoma: 50-60

With sarcomatous component

NSGCTà often mixed

Embryonal carcinoma: 30

Yolk sac tumour: <3 and adults

Teratoma: <3 and adults?

Mature

Immature

With malignant transformation

Monodermal variants: (struma ovarii, struma carcinoid, PNET)

Dermoid cyst

Epidermoid cyst

Choriocarcinoma: 10-20

Mixed

Mixed (60% of GCT)

Polyembryoma


NON-GCT

Sex-cord stromal tumours

Sertoli cell

Typical

Sclerosing

Large cell calcifying

Peutz-Jeghers syndrome associated

Carney Complex associated

Leydig

Sertoli-Leydig

Granulosa

Juvenile

Adult

Mixed germ cell/sex cord

Gonadoblastoma

 

Possible cell types in sex cord-stromal tumors

Sertoli

Leydig

Granulosa

Theca

FB

Name 6 major categories of sex cord-stromal tumors

Leydig

Sertoli

SLCT

Granulosa

Fibroma of gonadal stromal origin

Sex cord-stromal tumors of mixed type or indeterminate origin

TESTIS STAGING

Tis ICGNU

T1[2] Testis or epdydimis or TA (but not TV!)

T2 Testis or epdydimis+LVI or TV invasion

T3 Spermatic cord

T4 Scrotum

N0

N1 <2cm in up to 5 nodes

N2 2-5cm, or greater than 5 nodes or extranodal

N3 >5cm in any

M0

M1 Distant

M1a Non-regional nodes or lung “L”

M1b Other than above

S0 Normal markers

S1-3 LDH, HCG, AFP

When to upstage? Is epididymis considered part of testis?

LVI, TV invasionà T2

Spermatic cordà T3

Scrotumà T4

Size and number of LNà N2-3

LDH, HCG, AFP are parts of staging!

Epididymis and TA are parts of testisà therefore T1

Clinical stages

1: Confined to testis

2: Mets limited to retroperitoneal LN below diaphragm

3: Mets outside retroperitoneal LN or above diaphragm

Name 4 uses of serum markers (LDH, AFP, HCG)

Evaluate testicular mass as workup

Stage germ cell tumor

Asses tumor burden

Monitor response

 

SGCT more likely to met. via lymphatics

NSCGT mets via blood

TESTIS GROSSING

Submit cord margin prior to opening testisà need margin, mid section and peri-testicular

Sample necrotic areas and tumourà bisect testis in long axis across head of epididymisà take photos, sample for EM or othersà serial sections at 3mmà record relationship with TA and hilumà cut epididymis longitudinally (not cross-sections)

Vessels

Normal testis

RPLND GROSSING

-Sample thoroughly

-Done when persistently elevated serum markers after radical orchiectomy and chemotherapy

-Can be done for advanced stage tumors (III)

-May include other organs (vertebra)

 

ORCHIECTOMY REPORTING

Size

% of different tumor types

LVI

Tunica invasion

Spermatic cord

ITGCN

DIFFERENTIALS

What are the tumours of the rete testes?

Cystic dysplasia

Adenomatous HP

Adenocarcinoma

 

MESOTHELIUM

PARATESTICULAR TUMOURS

Classification

Primary

Mesothelial origin

Surface epithelial tumors of ovary

Metastatic extension from testes

ADENOMATOID TUMOUR

Clin: 35yrs

Gross: well-circ tan nodule

Micro

Angulated glands

Large signet ring vacuoles

Fibrous stroma

May look infiltrative microscopically

Why important?

Urologist may order FS and this diagnosis can spare patient from orchiectomy!

IHC

Calretinin

Hale’s colloid iron

DSRCT

t(11;22) but CD99-

 

 

 

 

DIFFERENTIALS

Paratesticular masses

Lipoma: often just herniated retroperitoneal fat

Mesothelioma

Adenomatoid tumor: upper pole of epididymis

Mesothelial HP

DSRCT

Sarcoma

4 mesothelial derived tumours in testes?

Adenomatoidà paratesticular

2. DSRCTà paratesticular (???)

3. Mesothelial HP

4. Mesotheliomaà tunica vaginalis

 

Most common benign and malignant paratesticular tumors

Benign: adenomatoid tumor

Malignant: RMS in kids, LPS in adults


 


[1] Higher grade areas more solid*

[2] No LVI

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