This document discusses testicular cancer, including its etiology, classification, clinical features, diagnosis, and treatment. It notes that testicular cancer most commonly affects younger men aged 15-49 and the main symptom is a painless lump in the testicle. The majority (90-95%) are germ cell tumors, classified into seminomas, teratomas, embryonal carcinomas, and other subtypes. Workup involves tumor marker tests, imaging like CT/MRI to stage the cancer and check for metastases. Treatment is based on the stage, with orchidectomy and chemotherapy or radiation typically used.

1. NILOY SHARMA SHUVO
Faridpur medical college, Bangladesh

2.  Introduction
 Etiology
 Classification
 Pathophysiology
 Clinical Feature
 Investigation
 Differential Diagnosis
 Treatment

3.  Although rare, is the most common
malignancy in men in 15-35 yr age group
 Delayed diagnosis
 Has become one of the most curable solid
tumour
 Associated with accurate tumour markers
 Origin in germ cells
 Capacity to differentiate into histologically more
benign forms
 Predictable, systematic pattern of spread
 Occurrence in young individuals

4.  Cancer of the testicles, also known
as testicular cancer, is one of the less
common cancers. It usually affects younger
men between the ages of 15 and 49. The most
common symptom is a painless lump or
swelling in the testicles.

5.  The exact cause of most cases of testicular tumour is
not known.
 Congenital Causes:
Cryptorchidism
Klinefelter’s syndrome
 Age: 20-35 years highest risk group
 Hormones
Maternal hormone ingestion during pregnancy
 History of mumps orchitis, inguinal hernia, hydrocele
in childhood - Atrophy
 High socioeconomic status
 Testicular cancer contralateral testis
 HIV positive.

6.  I. Primary Neoplasma of Testis
 A.Germ Cell Tumour (90-95%)
 B.Non-Germ Cell Tumour
 (5-10%)
 II.Secondary Neoplasms.
 III. Paratesticular Tumours.

7. Germinal Neoplasms : (90 - 95 %)
 Seminomas - 40%
 (a) Classic Typical Seminoma
 (b) Anaplastic Seminoma
 (c) Spermatocytic Seminoma
 Teratoma - 25 - 35%
 (a) Mature
 (b) Immature
 Embryonal Carcinoma - 20 - 25%
 Choriocarcinoma - 1%
 Yolk Sac Tumour

8.  Specialized gonadal stromal tumor
 (a) Leydig cell tumor
 (b) Sertoli’s cell tumour
 (c) Granulosa cell tumour
 (b) Other gonadal stromal tumor
 Gonadoblastoma
 Miscellaneous Neoplasms
 (a) Adenocarcinoma of the rete testis
 (b) Mesenchymal neoplasms
 (c) Carcinoid

9.  Typical : 82-85%
Thirties
Slow growth
 Anaplastic: 5-10%
More aggressive, potentially more lethal
Greater metastatic potential
 Spermatocytic Seminoma: 2-12 %
Cells closely resemble different phases of
maturing spermatogonia
B/L tumours have been reported
Extremely low metastatic potential
Favourable prognosis

11.  Contains more than one germ cell layers in various
stages of maturation and differentiation
 Grosssly large, lobulated, nonhomogenous tumours
 Microscopically, cystic & solid componenets

12.  The malignant transformation of carcinoma in
situ is characterised by growth beyond the
basement membrane, eventually replacing
most of the testicular parenchyma.
Spontaneous regression is rare; therefore, any
growth of the testis should be regarded as
malignant and managed accordingly. The
tunica albugenia is a natural barrier to local
metastasis so it should not be compromised by
direct diagnostic scrotal needle biopsy.

13.  Lymphatic spread is the most common cause of
metastasis and commonly occurs through spermatic cord
lymphatics to the retroperitoneal lymph node chain. One
exception is pure choriocarcinoma, which may
disseminate more frequently through vascular invasion.
On rare occasions a direct communication exists between
testicular lymphatics and the thoracic duct, causing a
thoracic (sternal) metastasis without retroperitoneal
involvement. Scrotal invasion may present with inguinal
metastasis. Germ cell cancers may also present with
extranodal distant metastasis following direct vascular
invasion or tumour embolisation through lymphatico-
venous communications. This accounts for most regional
treatment failures despite radical orchiectomy and
retroperitoneal surgical clearance.

14.  Non-seminoma doubling time ranges from 10
to 30 days. This is reflected by alterations in the
serum tumour markers. Most treatment failure
cases followed by mortality occur within the
first 2 to 3 years of diagnosis. Seminoma
usually has a much slower doubling time and
may recur 2 to 10 years after initial treatment
because of its indolent course. Based on the
natural history of the disease, curability after
multimodality treatment regimens is often
declared after 5 years. However, relapse has
been reported 10 years after treatment.

15.  Nodule/Painless Swelling of One Gonad
 Dull Ache or Heaviness in Lower Abdomen
 10% - Acute Scrotal Pain
 10% - Present with Metatstasis
- Neck Mass / Cough / Anorexia / Back Ache
 5% - Gynecomastia
 Infertility

16.  Ultrasound - Hypoechoic area
 Chest X-Ray - PA and lateral views
 CT Scan
 MRI
 4. Tumour Markers
 - AFP
 -  HCG
 - LDH
 - PLAP(placental alkaline
phosphatase)

17.  Stage 1-Testis lesion-No spread
 Stage 2-Nodes below the Diaphragm only
 Stage 3-Nodes above the diaphragm
 Stage 4-Pulmonary or Hepatic metastases

18.  Torsion
 Epididymitis
 Epididimo-orchitis
 Hydrocele
 Hernia
 Haematoma
 Spermatocele
 Syphilitic gumma

19.  Staging is an essential step in planning treatment
 Blood is collected to enable the levels of tumours
markers (HCG,Alpha fetoprotein and LDH) to be
measured. Tumour marker level can be used to
monitor the response to treatment.
 A chest radiograph shows whether there are
pulmonary deposit.
 Orchidectomy is essential to remove the primary
tumour and to obtain histology
 Computerised tomography (CT) and MRI are the
most useful means of detecting secondary and for
monitoring the response to therapy