TESTICULAR CANCERS

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TESTICULAR CANCERS Presented By: Dr Isha Jaiswal Moderator: Dr Madhup Rastogi Date:10 th September 2014

description

testicular cancer:anatomy of testis epidemiology,risk factors and spread of testicular cancer clinical presentation tumor markers AFP,BHCG,LDH

Transcript of TESTICULAR CANCERS

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TESTICULAR CANCERS

Presented By: Dr Isha Jaiswal

Moderator: Dr Madhup Rastogi

Date:10th September 2014

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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

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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

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Descent of testis

Develops at T10-T12 segments in post abdominal wall from genital ridge & subsequently descend to reach scrotum

Begin to descend in 2nd month of intrauterine life 3rd month reach iliac fossa 4th -6th month deep inguinal ring 7th month inguinal canal 8th month: superficial inguinal ring 9th month: scrotum

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:

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Skin DARTOS Muscle External Spermatic Fascia Cremastric Muscle Internal Spermatic Fascia Tunica Vaginalis Tunica Albuginea

Coverings of testis

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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.

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• 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 :extends from the epididymis in the scrotum on its own side into the abdominal cavity through the inguinal canal

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Blood Supply

Areterial supply• The testicular artery branch of abdominal aorta . • The testis has collateral blood supply from 1. the cremasteric artery2. 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

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Lymphatic Drainage

Drain into the retroperitoneal lymph glands between the levels of T11 and L4, but they are concentrated at the level of the L1 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 para-aortic nodes, respectively

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On the right: Interaortocaval region, followed by the paracaval, preaortic, and para-aortic

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

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Nerve Supply

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

• Both afferent for testicular sensation and efferent to the blood vessels(vasomotor).

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Epidemiology of testicular cancer

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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%

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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

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Predisposing Factors

1. Cryptorchidism 2. Klinefelter syndrome3. Positive family history4. Positive personal history5. Intratubular germ cell neoplasia6. Trauma7. Viral infection8. Hormonal factors9. Exposure to environmental oestrogen

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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

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KLINEFELTER SYNDROME

• Characterised by: • testicular atrophy• absence of spermatogenesis• eunuchoid habitus• gynecomastia

Karyotype: 47XXYPt. are at increased risk of mediastinal GCT

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Predisposing Factors

2. Positive family history

Men with first degree relative with testicular cancerMedian age being less by 2-3 yrs brother of men with testicular tumor: 8-10 times more risk of

developing TGCTRelative risk to father and sons: 2-4 times

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Predisposing Factors

3. Positive personal history

12 folds increased risk of developing GCT in the contralateral testisHigher risk for contralateral tumor if

• Younger age• Seminoma

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Predisposing Factors4. 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

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Pathological classification

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

1:Intra 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

4: others 5% lymphoma rabdomyosarcoma melanoma

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SeminomaThe commonest variety of testicular tumourAdults are the usual target (4th and 5th decade); never seen in infancyRight > Left TestisStarts 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

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Seminoma

• Serum alpha fetoprotein is normal• Beta HCG is elevated in 30% of patients with Seminoma• Classification

a) classical

b) Anaplastic

c) Spermatocytic

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Seminoma Anaplastic

5% - 10 Middle age Aggressive - lethal Greater mitotic activity Higher local invasion Higher metastatic potential Higher rate of β-HCG production

Typical/ Classical 82% - 85% Middle age PLAP – 90% Syncytiotrophoblsts – ↑Beta HCG(10%) Very slow growth

Spermatocytic 2% - 12% of seminomas Old age > 50 yr Does not arise from ITGC PLAP negative Extremely low metastatic potential Good prognosis

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Embryonal Carcinoma2nd most common germ cell tumor 90% of NSGCTPresent 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.epidydymisHigh degree of metastasisSerum AFP is positive in 33 5, & beta HCG is elevated in 20% of cases

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Yolk Sac TumourMost 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.

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ChoriocarcinomaA rare and aggressive tumour (5yrs survival is 5%)Typically elevated hCGPresents with disseminated diseaseMetastasis to lungs and brainPrimary is very small and often exhibit NO TESTICULAR

ENLARGEMENTSmall palpable nodule may be present.Prone to hemorrhage, sometimes spontaneous (lungs and brain)

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Teratoma

Teratoma in greek means “monster tumor”Contain all three germ layers with varying degree of

diffrentiationOccurs in its pure form in pediatric age group with a mean age

of diagnosis at 20 monthsIn adults, occur as a component of mixed germ cell tumor & is

identified in > 47 % of mixed tumors.Normal serum markers.

◦ Mildly elevated AFP levels

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Interstitial cell tumors

1. Leydig cell tumorsMay affect 20-60yrs of ageA masculinising tumor, produces androgensNo association with crytochordismPresents with painless testicular massPrecocious puberty

Prominent external genitalia Deep masculinised voice Pubic hair

Gynacomastia and decreased libodo due to oestrogen production by increased peripheral conversion

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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

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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

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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

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Spread

1. Direct Spread: This spread occurs by invasion. Whole of testis in involved and restricted Tunica albuginea is rarely penetrated 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

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Spread2. Lymphatic spread:

Seminoma metastasize exclusively through lymphatics

They drain primarily to para-aortic lymph nodes From RPLN drain into cysterna chili, thoracic

duct ,posterior mediastinum & left supraclavicular Lymph

from medial side of testes run along the artery to the vas to drain to nodes at the bifurcation of common iliac

No inguinal nodes until scrotal skin involvement

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Spread

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

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Clinical Features

1. Due to primary tumora) Painless testicular lumpb) Sensation of heaviness if size > than 2-3 timesc) Rarely dragging pain is complained of (1/3rd cases)d) May mimic epidedymo-orchitise) Sudden pain and enlargement due to hemorrhage mimicking torsionf) History of trauma (co-incidental)

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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.

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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

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Clinical Features

3. Clinical examination:a) Enlarged testis (except choriocarcinoma)b) Nodular testisc) Firm to hard in consistencyd) Loss of testicular sensatione) Secondary hydrocelef) Flat and difficult to feel epididymisg) General examination for metastasis

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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

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Human Chorionic Gonadotropin

Has and polypeptide chain

NORMAL VALUE: < 1 ng / ml HALF LIFE of HCG: 24 to 36 hours

RAISED HCG - 100 % - Choriocarcinoma 60% - Embryonal carcinoma 55% - Teratocarcinoma25% - Yolk Cell Tumour7% - Seminomas

normal value: below 16 ngm / ml

half life of AFP – 5 and 7 days

Raised AFP : Pure embryonal carcinomaTeratocarcinoma Yolk sac Tumor Combined tumors,AFP not raised in pure choriocarcinoma & in pure seminoma

AFP –Alfa feto protein

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LDH Beta HCG(mIu/ml)

AFP(ng/ml)

S1 < 1.5 x N <5000 <1000

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

S3 >10 x N >50000 >10000

Serum Tumor Markers (S)

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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

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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

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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.

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Staging Work Up

• GeneralHistory (document cryptorchidism and previous inguinal or scrotal surgery)Physical examination

• Laboratory StudiesCBC, LFT, RFT, LDH

• Serum assaysAlpha fetoprotein (AFP)Beta human chorionic gonadotropin

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• 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

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Large left para aortic nodal mass due to GCT causing hydronephrosis

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“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 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 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