 Testicular tumors: - is the most common cause of firm painless

enlargement of the testis.

The causes remain unknown but
1. cryptorchidism is associated with a four-fold increase in
the risk of cancer.
2. Testicular feminization and Klinefelter also increase the
risk.
3. The risk is increase in siblings of patients with testicular
cancer.
4. The development of cancer in one testis is associated with
marked increase risk of neoplasia in the contralateral
testis.
5. Testicular tumors are more common in white peoples
than the blacks.
Testicular tumors divided into two major 
histogenetic groups:-
Germ cell tumors which represent more than 90% 
1. Seminoma (the neoplastic primitive germ cells may
differentiated along the gonadal lines).
2. Embryonal carcinoma (the primitive germ cells transform
into totipotential cells which largely remain
undifferentiated).
3. Yolk sac tumor (totipotential cells may differentiated into
extraembryonic cell lines).
4. Choriocarcinoma (differentiation of pluripotential
neoplastic germ cells along trophoplastic lines)
5. Teratoma (totipotential cells may differentiated along the
somatic cell lines)
 Gonadal stromal /sex cord tumors.
 Leyding cell tumor
 Sertoli cell tumor
 Seminoma: - it represents about half of all germ cell tumors.
Peak incidence is the fourth decade and it’s of three variants:-
 Classic seminoma:- about 90% of all seminomas. On gross
examination, the tumor is solid, gray-white, poorly
demarcated growth that bulges from the cut surface of the
testis. The tumor may replace the entire testis in more than
half of the cases.
 Histologically: solid nest of proliferating tumor cells in
between there is randomly scattered thin fibrovascular
trabeculea. The tumor cells have well defined borders with
clear cytoplasm. The nuclei show limited pleomorphism and
coarse granular chromatine. Typically there is lymphocytic
infiltration is present in the fibrovascular trabeculea.
Radiotherapy results in 5- years’ survival in 85-90%.
 Spermatocytic seminoma: - about 5% of all seminomas.
It arises in older patients (more than 50 years). On gross
examination the size of the tumor is variable may reach
15 cm. the tumor is poorly demarcated soft yellow gray,
gelatinous with small cystic areas. Histologically:- the
tumor is composed of three population of neoplastic cells
 1) small cells,
 2) intermediate cells which is the most numerous and
similar to tumor cells of classic seminoma,
 3) scattered large cells with clumped coarse chromatin.
All these tumor cells show poor cohesiveness and lack the
lymphocytic infiltration which is characteristic for classic
seminomas.
Siminomas may reach a large size and show late
metastases by lymphatic to iliac and paraortic lymph
nodes, while the other germ cell tumors show an
early metastases even in the absence of palpable
testicular lesion by both lymphatic and
hematogenous routs.
Hematogenous metastases are most common to the
liver and the lung.
Seminoma

Most common type 

Yong men 
Curable 
Arises from sperm 
producing cells
Several histologic 
types.
Lymphocytes 
No markers 
 Seminoma testis gross

A small rim of remaining normal testis appears at the far right. The
tumor is composed of lobulated soft tan to brown tissue.
 Seminoma

Little fried egg looking cells. 

Lymphocytes 
No production of Beta-HCG or Alpha-fetoprotein 
 Seminoma testis mic

Typical seminoma. Lobules of neoplasitic cells have an intervening

stroma with characteristic lymphoid infiltrates. The seminoma cells
are large with vesicular nuclei, and pale watery cytoplasm.
 Anaplastic seminoma: - about 5% of all seminomas.
Has the same gross feature of classic type but
histologically the tumor has more marked nuclear
pleomorphism and increased mitoses. This tumor
tends to be at a high stage than the classic seminoma
at time of diagnosis.
 Embryonal carcinoma:- is the second most common
testicular germ cell tumor, account 15-35% of these
neoplasms. It occurs between 20-35 years. Grossly
appear as ill defined invasive masses containing foci of
hemorrhage and necrosis. The primary lesion is small
even in patient with systemic metastases.
 Histologically the tumor cells are large and primitive
with basophilic cytoplasm, ill defined borders, and large
nuclei with prominent nucleoli. The neoplastic cells may
arrange in solid sheet, glandular structures or irregular
papillae. In most cases neoplastic cells of yolk sac
carcinoma, teratoma, choriocarcinoma mixed with
embryonal areas. Chemotherapy results in cure rate of
95%-98%.
 Embryonal Carcinoma

Aggressive tumor 
20-30 years 
Areas of 
hemorrhage and
necrosis
Two histologically 
distinct cell types.
Markers +/- 
Lance Armstrong 
 Yolk sac tumor (endodermal sinus tumor) :- most
common primary testicular neoplasm in children
younger than 3 years of age, but in adult this tumor are
mostly seen admix with embryonic carcinoma. Grossly
this tumor is typically large and well demarcated.
 Histologically :- show cuboidal or columnar epithelial
cells forming sheets glands, papillae and microcysts
associated with eosinophilic hyaline globules and
forming a characteristic feature is the forming of a
primitive structure similar to the glomeruli (Schiller-
Duvall bodies.)
 By immunohistochemical techniques α- fetoprotein can
be demonstrated in the cytoplasm of the neoplastic cells.
 Choriocarcinoma:- grossly the tumors are very small,
nonpalpable lesion even with extensive systemic
metastases.
 Histologically: the tumor is composed of sheets of small
cuboidal cells irregularly intermingled with or capped by
large eosinophilic syncytial cells containing multiple
dark, pleomorphic nuclei; these represent
cytotrophoblast &syncytiotrophoblastic differentiation
respectively. Well-formed placental villi are not seen.
HCG can be identified by immunohistochemical
techniques in the cytoplasm of the syncytiotrophoblastic
elements.
 Choriocarcinoma

Placental elements 
Synciotrophoblasts 
Make Beta-HCG 
Typically part of a 
‘mixed lineage’ tumor.
Highly aggressive 
This element spreads 
early.
 Teratomas: - grossly firm masses on cut section show multiple
cysts with recognizable areas of cartilage, bone, hair…
 Histologically: three variant of pure teratoma can recognize:
 Mature teratomas: contain fully differentiated tissues from one
or more germ cell layers (e.g. cartilage, neural tissue, adipose tissue,
bone, and epithelium) in a haphazard array.
 Immature teratomas: in contrast, contain immature somatic
elements resemble to those in developing fetal tissue.
 Teratomas with malignant transformation: characterized by
developing of frank malignancy in preexisting teratomatous
elements such squamous cell carcinoma or adenocarcinoma. Most
cases of malignant transformation occur in adult patients while
pure teratomas in prepubertal male are usually benign.
 Mature teratoma testis gross

There are multiple cystic areas, lobules of mature adipose tissue, and
shiny solid nodules corresponding to well-differentiated cartilage.
Teratoma
 Teratoma

Aggressively malignant 
Three germ lines 
Ectoderm 
Endoderm 
Mesoderm 
Makers +/- 
 Mature teratoma testis mic

Large islands of cartilage are seen surrounding well-differentiated

glandular structures.
 Leyding cell tumor: rare neoplasm arises from
interstitial leyding cells of the testis. This tumor is very
interesting because they are functionally active
secreting either testosterone or estrogen or both of
them. It occurs in two age groups: boys older than 4
years and men in their 3th – 6th decades. Although
some boys develope precocious physical and sexual
development ,, feminization with gynecomastia may
observed in adult but still there is no characteristic
clinical pattern of this tumor it’s depend on the its
endocrinal activity. Leyding cell tumors are cured by
orchiectomy.
 Sertoli cell tumor: less frequent than leyding cell
tumor. 20% of sertoli cell tumors are malignant.
Orchiectomy is curative
.