world cancer report - iarc

Fig. 5.52 Trends in incidence and mortality of testicular cancer in Norway, 1960-1990. Incidence has
increased significantly while mortality has decreased, due to effective chemotherapy.
decade older for testicular seminoma.
Mortality has declined markedly since the
introduction of cisplatin as the basis of
chemotherapy in the mid-1970s.
Etiology
Generally relevant environmental causes
of testicular cancer have not been established.
There is an increased incidence of
the disease in individuals with a history of
an undescended testicle, testicular feminization
and those with a family history of
testicular cancer. In utero exposure to
exogenous estrogens may increase the
risk of testicular cancer as a result of
increased incidence of cryptorchidism and
dysgenesis. A history of maternal exposure
to diethylstilbestrol has been associated
with an increased relative risk of up to 5.3
[13]. Testicular cancer is more common in
higher socioeconomic groups. Hormonal
and genetic factors seem likely to play an
important, but currently unclear, role as
risk factors; other factors may include the
influence of heat [14].
Detection
Most patients with testicular germ cell
tumours present with a painless swelling
212 Human cancers by organ site
or a nodule in the testis. Other common
presentations include back pain, (caused
by retroperitoneal metastasis), haemoptysis
(consequent upon pulmonary metastases)
and gynecomastia (excessive development
of male mammary glands).
Diagnosis is based on physical examination,
ultrasonography and biopsy. In
patients with nonseminoma, serum
tumour markers alpha-fetoprotein and/or
human chorionic gonadotrophin are elevated
in 80% of patients with disseminated
disease and in 50% of patients with early
stage disease. Patients with testicular
seminoma may have modestly elevated
levels of human chorionic gonadotrophin
and of lactic dehydrogenase.
There are no reliable screening tests for
testicular cancer. Due to low incidence and
a high cure rate, advocacy of testicular
self-examination and the impact of selfassessment
are controversial.
Pathology and genetics
About 90% of testicular malignancies
arise from germ cells and these tumours
are classified as seminoma (40%) (Fig.
5.53) or nonseminoma, which includes
embryonal tumours (20-25%) (Fig. 5.54),
Fig. 5.53 Histology of a seminoma with uniform
cells resembling primitive germ cells, large vesicular
nuclei and a glycogen-rich clear cytoplasm.
Note the scattered lymphocytic infiltrates.
Fig. 5.54 Embryonal carcinoma consisting of a
pleiomorphic proliferation containing glandular
structures.
teratoma (25-30%) and choriocarcinoma
(1%). Germ cell tumours can also arise
from extra-gonadal primary sites.
Ovarian germ cell tumours of young
women share clinical features and treatment
approaches with male germ cell
tumours. All germ cell tumours are commonly
associated with the presence of
isochromosome 12p (an abnormal chromosome
12 with two identical short
arms), a region which contains the gene
for cyclin D2 [15]. The initiation of a
germ cell tumour is associated with various
aberrations in the normal developmental
pathway of the germ cell (Fig.
5.55).
Management
Current management of germ cell
tumours should yield average cure rates in
excess of 95%, and even 80% of patients
with metastatic disease respond to
chemotherapy, radiotherapy and surgery
(Fig. 5.56). However, survival in develop-