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Testicular Cancers: Presented By: DR Isha Jaiswal Moderator: DR Madhup Rastogi Date:10 September 2014

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0% found this document useful (0 votes)
87 views56 pages

Testicular Cancers: Presented By: DR Isha Jaiswal Moderator: DR Madhup Rastogi Date:10 September 2014

Teste final

Uploaded by

Ivan Vladanov
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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TESTICULAR CANCERS

Presented By: Dr Isha Jaiswal


Moderator: Dr Madhup Rastogi
Date:10th September 2014
Overview

Cancers of testis are relatively rare cancer accounting for approx. 1 % cancer in
males. However it is important in field of oncology as it represents a highly
curable neoplasm & the incidence is focused on young patients at their peak of
productivity
Anatomy
• The testis is the male gonad.
• It is homologous with the ovary in female.
• It lies obliquely within the scrotum suspended by
the spermatic cord
• The left testis is slightly lower than the right
• Shape: Oval
• Size:3.75 cm long, 2.5 cm broad, 1.8 cm thick
• Weight: about 10-15 gm.
• Has 2poles , 2surface, 2 borders
Descent of testis
aMa
Develops at T10-T12 segments in post abdominal wall from genital
ridge & subsequently descend to reach scrotum

8 wMt
f-i.Vmm tnmn nimp:

□ Begin to descend in 2nd month of intrauterine life ABDOMI


NAL
□ 3rd month reach iliac fossa CAVITY

□ 4th -6th month deep inguinal ring


□ 7th month inguinal canal
INGUIN
□ 8th month: superficial inguinal ring AL
CANAL
□ 9th month: scrotum SCROTUM

4 lurvjr iran4h*
1107-mro i rrwvn njropi

Cryptorchidism: one or both testicles fail to reach scrotum before


birth. Most of time it reached scrotum by 1 year of age. If not
orchidopexy need to be done:
8 lurur month*. (26-tttt
cnmn tumpi
Coverings of testis
Internal (deep) ring

□ Skin

□ DARTOS Muscle
□ External Spermatic Fascia
□ Cremastric Muscle External (superficial) ring
Dartos
□ Internal Spermatic Fascia
External spermadic fascia
□ Tunica Vaginalis
Cremaster muscle
□ Tunica Albuginea
Internal spermadic fascia

Tunica vaginalis (parietal)

Tunica vaginalis (visceral)


Structure of testis

200-300 lobules
Each lobule has 2-3 seminiferous tubules

Each seminiferous tubules lined by cell in


different stages of spermatogenesis
Among the seminiferous tubules are Sertoli
cells.
Between the loops of the seminiferous
tubules are interstitial cells, produce
testosterone.
Seminiferous tubules join to form 20-30
straight tubules.
Mediastinum
testis Ductus
Tunica

Ductus
epididymis

Somniferous
tubule Efferent
ductules
Intersbtfum
Tubulus rectus
(straight tubules)

spermatic cord
ductulo&

Rot© lest* within


modiaslinum fostls

Ktane oi sentnn
Lumon of
sominNerous *
tubule
Testis • Basomoni
Sominlefous tubules mamhrano
it tfeistillal cells Spermatozoa
Geimii/d ©pill wlial cels
Rete testis: network of tubules located in the
hilum of the testicle(mediastinum testis) that
carries sperm from the seminiferous tubules to
the efferent ducts

Rete testis give rise to 12-30 efferent ductules

Epididymis: tube about 20 feet (6 m) long that is


coiled on the posterior surface of each testis
connect efferent duct to vas deferens

Ductus deferens rextends from the epididymis in


the scrotum on its own side into the abdominal
cavity through the inguinal canal
deferens
ligamentus remnant. of
processus vaginalis

Head (Caput) of epididymis

Straight tubule
Efferent ductules
Seminiferous
Rete testis in
mediastinum

(Corpus)
Tunica epididymis
vaginali - Parietal
s
.Visceral
Capsule (tunica
albuginea) Tail (Cauda)
of epididymis

Fig. 15.1 Testis surrounding structures in men


Blood Supply
Areterial supply
• The testicular artery branch of abdominal aorta .
• The testis has collateral blood supply from
1. the cremasteric artery
2. artery to the ductus deferens
Venous drainage
• The veins emerge from the back of the testis, and receive
tributaries from the epididymis;
• they unite and form convoluted plexus, called the
pampiniform plexus.
• plexus to form a single vein, which opens, on the right side,
into the inferior vena cava ,on the left side into the left renal
vein
Lymphatic Drainage

Drain into the retroperitoneal lymph glands between the


levels of Til and L4, but they are concentrated at the level of
the LI and L3 vertebrae

Lymph nodes located lateral or anterior to the inferior vena


cava are called paracaval or precaval nodes, respectively.

Interaortocaval nodes are located between the inferior vena


cava and the aorta.

Nodes anterior or lateral to the aorta are preaortic or


paraaortic nodes, respectively
Rotrocaval

Interaortocaval
Precaval
Pre-aorilc

Paracaval

I
□ On the right:
□ Interaortocaval region, followed by the paracaval, preaortic, and
paraaortic lymph nodes.

□ On the left:
□ Preaortic and para-aortic nodes and thence to the interaortocaval

□ Metastatic nodal disease to the common iliac, external iliac, or


inguinal lymph nodes is usually secondary to a large volume of
disease with retrograde spread.
□ If the patient has undergone a herniorrhaphy, vasectomy, or other
transscrotal procedure, metastasis to the pelvic and inguinal lymph
nodes is more likely
□ Through the thoracic duct to lymph nodes in the posterior
mediastinum and supraclavicular fossae and occasionally to the
axillary nodes.

□ Contralateral spread is mainly seen with right-sided tumors.

□ In 15% to 20%, bilateral nodes are involved


Nerve Supply
• Sympathetic nerves arising from segment T10 of the spinal cord.

• Both afferent for testicular sensation and efferent to the blood vessels(vasomotor).
Epidemiology of testicular cancer
INTRODUCTION
> Comprise a morphologically and clinically diverse group of tumors
> Predominantly affects young males
> 1 -2 % of all cancers in USA

> Testicular cancer forms about 1% of all malignancies in males in India.


> Incidence (ASR)- 0.6 per 100000
> Mortality (ASR)- 0.3 per 100000

> 95% are Germ Cell Tumours (GCTs)


> 90% GCT are in testes,2-10% in extra gonadal (eg retropreitoneum, mediastinal)
> Cure rate increased with introduction of platinum based chemotherapy from 10 to 80%
EPIDEMOLOGY OF TESTICULAR CANCER
• Age: for GCT: median age at diagnosis is 34 years, with 50% of
incident cases between 20 and 34 years.
• In a man age: 50 years or older solid testicular mass is usually
lymphoma
• Age - 3 peaks
2 - 4 yrs 20 - 40 yrs above 50 yrs
• Geographic: Highest incidence in Denmark, Norway, and Switzerland
and the lowest in eastern Europe and Asia.
• Race: more common in young white men ,less in African Americans
Predisposing Factors
1. Cryptorchidism
2. Klinefelter syndrome
3. Positive family history
4. Positive personal history
5. Intratubular germ cell neoplasia
6. Trauma
7. Viral infection
8. Hormonal factors
9. Exposure to environmental oestrogen
Undescended Testicles (Cryptorchidism)

Predisposing Factors
1. Cryptorchidism
• For inguinal cryptorchidism odds ratio is
5.3 for seminoma 3 for non seminoma

• This risk is further increased if the testis is intra-abdominal.


• Abdominal testis is more likely to be seminoma, testis brought to scrotum by orchiopexy is
more likely to be NSGCT.
• There is still an increased risk of developing a tumour in the contralateral normally
descended testicle in pt. with cryptorchidism
• GCT develop in 2% of cryptorchids & 5-10% of normally descended testis
• Prepubertal orchidopexy fails to prevent the subsequent development of malignancy
KLINEFELTER SYNDROME
Taller man

• Characterised by: average height

Reduced facial hair

• testicular atrophy
Reduced body hair

• absence of spermatogenesis Breast development


Kjynaecomastin)

• eunuchoid habitus Osteoporosis

remimne fat
distribution
• gynecomastia Small testes
(testicular atrophy)
Karyotype: 47XXY
Pt. are at increased risk of mediastinal GCT
Predisposing Factors

2. Positive family history

❖ Men with first degree relative with testicular cancer


❖ Median age being less by 2-3 yrs
❖ brother of men with testicular tumor: 8-10 times more risk of
developing TGCT
❖ Relative risk to father and sons: 2-4 times
Predisposing Factors

3. Positive personal history

❖ 12 folds increased risk of developing GCT in the contralateral testis


❖ Higher risk for contralateral tumor if
• Younger age
• Seminoma
Predisposing Factors
4. Intratubular Germ Cell Neoplasia (ITGCN)
• Precursor lesion of all types of germ-cell tumors except spermatocytic seminoma
• Originate from primordial germ cells early during embryogenesis, possibly due to an excess of
estrogens.

❖ No spermatogenesis
❖ PLAP positive
❖ Present in adjacent testicular parenchyma in 80% of pt with GCT
❖ 5-9% in unaffected contralateral testis; increases to 36% in atrophy or
cryptorchidism
❖ 50% risk of GCT in 5 yrs, 70% in 7yrs
Pathological classification
l:lntra tubular germ-cell neoplasia(IGCN)

2:GERM CELL TUMORS 95%


Seminoma 40%
Classic type anaplastic Spermatocytic type
Non seminomatous germ-cell tumors 60%
□ Embryonal carcinoma 20-25%
□ Teratoma 25-35%
□ Yolk sac (endodermal sinus) tumor
□ Choriocarcinoma 1%
□ Mixed germ-cell tumor
3:Classification of Sex-Cord Stromal Tumors of the
Testis 2-3%
□ Leydig cell tumor
□ Sertoli cell tumor
□ Granulosa cell tumor
□ Fibroma-thecoma stromal tumor
□ Gonadoblastoma
□ Sex cord-stromal tumor unclassified type

4: others 5%
□ lymphoma

rabdomyosarcoma
□ melanoma
Seminoma
• The commonest variety of testicular tumour
• Adults are the usual target (4th and 5th decade); never seen in infancy
• Right > Left Testis
• Starts in the mediastinum: compresses the surrounding structure.
• Patients present with painless testicular mass
• 30 % have metastases at presentation, but only 3% have symptoms related
to metastases
Seminoma

Serum alpha fetoprotein is normal Beta HCG is elevated


in 30% of patients with Seminoma
Classification
a) classical
b) Anaplastic
c)
Spermatocytic
Seminoma
> Typical/ Classical
> 82% - 85% > Anaplastic
> Middle age
> 5% -10
> PLAP - 90%
> Middle age
> Syncytiotrophoblsts - |Beta HCG(10%)
> Aggressive - lethal
> Very slow growth
> Greater mitotic activity
> Spermatocytic > Higher local invasion
> 2% -12% of seminomas > Higher metastatic potential
> Old age > 50 yr > Higher rate of p-HCG production
> Does not arise from ITGC
> PLAP negative
> Extremely low metastatic potential
> Good prognosis
Embryonal Carcinoma
• 2nd most common germ cell tumor 90% of NSGCT
• Present in majority of mixed germ cell tu mors
• Most men present in their 20s to 30s with a testicular mass
• Highly malignant tumours; may invade the cord stuctures.epidydymis
• High degree of metastasis
• Serum AFP is positive in 33 5, & beta HCG is elevated in 20% of
cases
Yolk Sac Tumour
• Most common germ cell tumor ( & most common testicular tumor) in children,
where it occurs in its pure form.
- 60% of GCT in children. First 2 years of life.
- Pure yolk sac tumor <2% of testicular tumors in adults
- 40% of mixed germ-cell tumors.
- Elevated serum levels of alpha-fetoprotein.
- Microscopically, Schiller-Duval bodies are a characteristic feature
• Testicular mass the most usual presentation.
Choriocarcinoma
• A rare and aggressive tumour (5yrs survival is 5%)
• Typically elevated hCG
• Presents with disseminated disease
• Metastasis to lungs and brain
• Primary is very small and often exhibit NO TESTICULAR
ENLARGEMENT
• Small palpable nodule may be present.
• Prone to hemorrhage, sometimes spontaneous (lungs and brain)
Teratoma
• Teratoma in greek means “monster tumor”
• Contain all three germ layers with varying degree of
diffrentiation
• Occurs in its pure form in pediatric age group with a mean
age of diagnosis at 20 months
• In adults, occur as a component of mixed germ cell tumor &
is identified in > 47 % of mixed tumors.
• Normal serum markers.
◦ Mildly elevated AFP levels
Interstitial cell tumors
1. Leydig cell tumors
❖ May affect 20-60yrs of age
❖A masculinising tumor, produces androgens
❖ No association with crytochordism
❖ Presents with painless testicular mass
❖ Precocious puberty
• Prominent external genitalia
• Deep masculinised voice
• Pubic hair
❖Gynacomastia and decreased libodo due to oestrogen production by
increased peripheral conversion
Interstitial cell tumors

2. Sertoli Cell Tumor


can occur in any age group including infants No
association with crytochordism Excess
estrogen production Gynacomastia in 1/3rd of
cases 10 % are malignant
Interstitial cell tumors
3. Gonadoblastoma
❖ Mixed germ cell/sex cord/stromal tumor
❖ Composed of seminoma like germ cells and Sertoli differentiation
❖ Exclusively in patients with dysgenic gonads and intersex syndromes
❖ 80% are phenotype females with primary amenorrhoea
❖ 20% are males with crytochordism and dysgenic gonads and hypospadias
❖ Considered in-situ malignant form of GCT
❖ Bilateral orchidectomy because of risk of bilateral tumours
Secondary Tumors of Testis

• Lymphoma - most common secondary tumor


- most common testicular tumor in patients above 50 years
- most common variety is histiocytic
• Leukamic Infilteration of testis
-primary site of relapse after ALL remission -occurs mainly in
the interstitial space -Metastases to testis

- rare
Spread Rete Testis
Ductus Deferens

Epididymis

1. Direct Spread: Tunica Albuginea

❖ This spread occurs by invasion.


Seminifer
❖ Whole of testis in involved and restricted ous
Tubules
❖ Tunica albuginea is rarely penetrated
Tunica Vaqinalis
❖ May be crossed by "blunder biopsy"
❖ Scrotal skin involvement
❖ Fungation on the anterior aspect
❖ Spread to spermatic cord and epidedymis
may occur : points towards bad prognosis
Spread
2. Lymphatic spread:
From testis
'Seminoma metastasize exclusively through para-aortic nodes
lymphatics
'They drain primarily to para-aortic lymph nodes
'From RPLN drain into cysterna chili, thoracic duct Inguinal
,posterior mediastinum & left supraclavicular Lymph
' from medial side of testes run along the artery to From scrotal wall
the vas to drain to nodes at the bifurcation of to inguinal nodes
common iliac
'No inguinal nodes until scrotal skin involvement
Spread

3. Blood Spread
❖ NSGCT spread through blood route
❖ Lungs, liver, bones and brain are the usual sites usually involved
Clinical Features

1. Due to primary tumor


a) Painless testicular lump
b) Sensation of heaviness if size > than 2-3 times
c) Rarely dragging pain is complained of (1/3 rd cases)
d) May mimic epidedymo-orchitis
e) Sudden pain and enlargement due to hemorrhage mimicking torsion
f) History of trauma (co-incidental)
DICTUM FOR ANY SOLID SCROTAL SWELLINGS

• All patients with a solid, Firm Intratesticular Mass that


cannot be Trans illuminated should be regarded as
Malignant unless otherwise proved.
Clinical Features

2. Due to metastasis
❖ Abdominal or lumbar pain (lymphatic spread)
❖ Dyspnoea, hemoptysis and chest pain with lung mets
❖ Jaundice with liver mets
❖ Hydronephrosis by para-aortic lymph nodes enlargement
❖ Pedal oedema by IVC obstruction
❖ Troiser's sign
Clinical Features

3. Clinical examination:
a) Enlarged testis (except choriocarcinoma)
b) Nodular testis
c) Firm to hard in consistency
d) Loss of testicular sensation
e) Secondary hydrocele
f) Flat and difficult to feel epididymis
g) General examination for metastasis
Tumor markers
TWO MAIN CLASSES
• Onco-fetal Substances : AFP &
HCG
• AFP -Trophoblastic Cells
HCG - Syncytiotrophoblastic Cells
AFP, BHCG & LDH are included in TNM staging of testicular cancers
Human Chorionic
Gonadotropin
Has a and (3 polypeptide chain

NORMAL VALUE: < 1 ng / ml


HALF LIFE of HCG: 24 to 36 hours

RAISED P HCG -
100 % - Choriocarcinoma 60% -
Embryonal carcinoma
55% - Teratocarcinoma
25% - Yolk Cell Tumour
7% - Seminomas
AFP -Alfa feto protein

normal value: below 16 ngm /

ml half life of AFP - 5 and 7

days
Raised AFP :
Pure embryonal carcinoma Teratocarcinoma
Yolk sac Tumor Combined tumors,
AFP not raised in pure choriocarcinoma & pure
seminoma
Serum Tumor Markers (S)
Beta HCG AFP
LDH
(miu/mi) (ng/mi)

S1 < 1.5 x N <5000 <1000

S2 1.5-10 x N 5000-50000 1000-10000

S3 >10 x N >50000 >10000


ROLE OF TUMOUR MARKERS

• Helps in Diagnosis -80 to 85% of Testicular Tumors have Positive Markers


• Most of Non-Seminomas have raised markers.

• Indicate Histology of Tumor:


If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elements

Degree of Marker Elevation Appears to be Directly Proportional to Tumor Burden


ROLE OF TUMOUR MARKERS
• may predict the responsiveness of nonseminomas to treatment
• The level of beta-HCG should decrease by 90% or more every 21 days with each successful
treatment cycle of chemotherapy.
• The decline of AFP is less predictable

• Normalization of tumor marker after high inguinal orchidectomy does not ensure complete
disease removal however after Orchiectomy if Markers Elevated means Residual Disease

• Negative Tumor Markers becoming positive on follow up usually indicates -Recurrence of


Tumor
• Markers become Positive earlier than radiological studies
Scrotal ultrasound
Ultrasonography of the scrotum (7.5MHZ)
is a rapid, reliable technique to exclude
Testicular and other scrotal swelling
Solid & cystic swelling
Hydrocele & epididymitis.

Ultrasonography of the scrotum is


basically an extension of the physical
examination.
Hypoechoic area within the tunica
albuginea is markedly suspicious
for testicular cancer.
Staging Work Up
• General
History (document cryptorchidism and previous inguinal or scrotal
surgery)
Physical examination
• Laboratory Studies CBC, LFT, RFT, LDH
• Serum assays
Alpha fetoprotein (AFP)
Beta human chorionic gonadotropin
• Diagnostic Radiology
— Chest x-ray films, posterior/anterior and lateral views

- Computed tomography (CT) scan of abdomen and


pelvis

— CT scan of chest for non seminomas and stage


II seminomas

— Ultrasound of contralateral testis


Large left para aortic nodal mass due to GCT
causing hydronephrosis
“I always had the size difference there, but I didn’t
know...I would’ve still been waiting if it hadn’t started
hurting, it just got so painful I couldn’t sit on my bike
anymore.”
_-Lance Armstrong

I want to finish by saying that I intend to be an


avid spokesperson for testicular cancer once I
have beaten the disease... I want this to be a
positive experience and I want to take this
opportunity to help others who might someday
suffer from the same circumstance I face today.
(lance Armstrong)

ixqu*trf.com

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