TESTICULAR TUMOUR

TESTICULAR TUMOUR 1% of all Malignant Tumour Affects young adults - 20 to 40 yrs - when Testosterone Fluctuations are maximum 90% to 95% of all Testicular tumours from germ cells 99% of all Testicular Tumours are malignant. Causes Psychological & Fertility Problems in young

Survival in Testicular Tumours Improved overall survival in last 15 to 20 years due to - Better understanding of Natural History and Pathogenesis of disease Reliable Tumour Markers Cis-platinum based chemotherapy

CROSS SECTION OF TESTIS Stroma Seminiferous Tubules (200 to 350 tubules) Interstitial Cells Supporting Spermatogonia Leydig or (Androgen) Sertoli Cell

EPIDEMIOLOGY Incidence : 1% of all Malignant Tumor Age : 3 Peaks - 20-40 yrs. Maximum - 0 - 10 yrs. - After - 60 yrs. Bilaterality : 2 to 3% Testicular Tumor

CLASSIFICATION I. Primary Neoplasma of Testis. A. Germ Cell Tumour B. Non-Germ Cell Tumour II. Secondary Neoplasms. III. Paratesticular Tumours.

I. PRIMARY NEOPLASMS OF TESTIS Germinal Neoplasms : (90 - 95 %) 1. Seminomas - 40% (a) Classic Typical Seminoma (b) Anaplastic Seminoma (c) Spermatocytic Seminoma

2. Non seminomatous GCT 1. Embryonal carcinoma- 20-25% 2 2. Non seminomatous GCT 1. Embryonal carcinoma- 20-25% 2. Teratoma- 25-35% (a) mature (b) Immature 3. choriocarcinoma -1% 4. Yolk sac tumor

I. PRIMARY NEOPLASMS OF TESTIS B. Nongerminal Neoplasms : ( 5 to 10% ) 1. Specialized gonadal stromal tumor (a) Leydig cell tumor (b) Other gonadal stromal tumor 2. Gonadoblastoma 3. Miscellaneous Neoplasms (a) Adenocarcinoma of the rete testis (b) Mesenchymal neoplasms (c) Carcinoid (d) Adrenal rest “tumor”

A. Reticuloendothelial Neoplasms B. Metastases II. SECONDARY NEOPLASMS OF TESTIS A. Reticuloendothelial Neoplasms B. Metastases III. PARATESTICULAR NEOPLASMS A. Adenomatoid B. Cystadenoma of Epididymis C. Mesenchymal Neoplasms D. Mesothelioma E. Metastases

AETIOLOGY OF TESTICULAR TUMOUR 1. Cryptorchidism 2. Carcinoma in situ 3. Trauma 4. Atrophy

CRYPTORCHIDISM & TESTICULAR TUMOUR Risk of Carcinoma developing in undescended testis is 14 to 48 times the normal expected incidence

CRYPTORCHIDISM & TESTICULAR TUMOUR The cause for malignancy are as follows: Abnormal Germ Cell Morphology Elevated temperature in abdomen & Inguinal region as opposed to scrotum Endocrinal disturbances Gonadal dysgenesis

A-Seminoma -35% of GCT. -3 types classic, spermaocytic & anaplastic -The classic seminoma is most common(85%) of all seminoma & is most common in the 4th decade of life. -Microscopically monotonous sheets of large cells with clear cytoplasm & densely staining nuclei are seen. -Syncytiotrophoblastic elements are seen in approximately 10-15% of cases, an incidence of hCG production in seminoma.

B-Embryonal cell ca -20% *2 variants of embryonal cell ca are common -adult type & -infantile type (yolk sac tumor) which is the most common testicular tumor of infant & children.

C-Teratoma 5% -May be seen in both adult & children. -They contain more than one germ cell layer in various stages of maturation & differentiation. -Grossly the tumor appears lobulated & contains variable size cysts filled with gelatinous or mucinous material.

Mature teratoma may have elements resembling structures derived from (ectoderm, mesoderm, &endoderm) while immature teratoma consist of undifferentiated primitive tissue. -Mature teratoma doesn’t attain the same degree of differentiation as teratoma of the ovary.

D- Choriocarcinoma <1% -lesions tend to be small within the testis -usually demonstrate central hemorrhage on gross inspection. *Microscopically syncytio & cytotrophoblast must be visualized. *Clinically choriocarcinoma behave in an aggressive fashion characterized by early hematogenous spread. -Paradoxically, small intratesticular lesion can be associated with wide spread metastatic disease.

E- Mixed cell type 40% Within the mixed cell types most are teratocarcinomas about 25% of all testicular tumor. Which are combination of teratoma & embryonal cell ca. Treatment of mixture testicular tumor SGCT & NSGCT similar to that of NSGCT. F- Carcinoma in situ (CIS) CIS is demonstrated in 5.2% of the contralateral testis. If diagnosed CIS is usually treated by external beam radiation therapy.

Pattern of metastatic spread. With the exception of choriocarcinoma which demonstrates early hematogenous spread to the lung, germ cell tumor typically spread in stepwise lymphatic fashion. In paraaortic LN it extend from T1 to L4 but are concentrated at the level of renal hilum because of their common embryologic origin of the kidney.

Certain factors may alter the primary drainage of the testis neoplasm. -Invasion of epididymis or spermatic cord may allow spread to external iliac & obturator LN, -scrotal violation or invasion of tunica albuginea may result in inguinal metastases. -Visceral metastases may be seen in advanced disease. Lung, liver, brain, bone, or adrenal may be involved.

TNM staging of testicular carcinoma TX-Primary tumor cannot be assessed T0-No evidence of primary tumor Tis-Carcinoma in situ T1-Tumor has not spread beyond the testicle and epididymis T2-Tumor has spread to blood vessels, lymphatics, or tunica vaginalis T3-Tumor invades spermatic cord T4-Tumor invades scrotum

NX-Regional nodes cannot be assessed N0-No nodal metastasis N1-Metastasis to single lymph node < 2 cm in greatest diameter N2-Metastasis to single lymph node > 2 cm, but < 5 cm, or multiple nodes < 5 cm N3-At least one node > 5 cm MX-Distant metastasis cannot be assessed M0-No distant metastasis M1-Distant metastasis is present

S1 LDH < 1.5× normal, b-hCG < 5000 mIU/ml, a-FP < 1000 ng/ml S2 LDH 1.5–10× normal, b-hCG 5000–50 000 mIU/ml, a-FP 1000–10 000 ng/ml S3 LDH >10× normal, b-hCG >50 000 mIU/ml, a-FP 10 000 ng/ml

Clinical findings. -Painless testicular swelling is the most common presentation, the enlargement is usually gradual its usually firm & nontender -testicular heaviness is not unusual. -The typical delay of treatment from initial recognition of the lesion by the pt to definitive therapy (orchiectomy) range from 3-6 months. -The length of delay correlate with incidence of metastases.

10% of pt presented with acute testicular pain may be the result of intratesticlar infarction or hemorrhage 10% presented with symptom related to metastatic disease, -back pain (retroperitoneal metastases involving nerve roots) is the most common symptom. -Other symptoms include cough or dyspnea (pulmonary metastases), -anorexia nausea or vomiting (retro duodenal metastases), -bone pain(skeletal metastases), -lower extremity swelling (venacaval obstruction).

10% of pt are asymptomatic at presentation tumor detected incidentally like after trauma. 5-10% of testicular tumor may presented with hydrocele & help to camouflage it. *Gynecomastia present in -5% of all GCT & -30-50% of sertoli& leydig cell tumor due to complex hormonal interaction.

DICTUM FOR ANY SOLID SCROTAL SWELLINGS All patients with a solid, Firm Intratesticular Mass that cannot be Transilluminated should be regarded as Malignant unless otherwise proved

Tumour Markers TWO MAIN CLASSES Onco-fetal Substances : AFP & HCG Cellular Enzymes : LDH & PLAP ( AFP - Trophoblastic Cells HCG - Syncytiotrophoblastic Cells )

AFP –( Alfafetoprotein ) NORMAL VALUE: Below 16 ngm / ml HALF LIFE OF AFP – 5 and 7 days Raised AFP : Pure embryonal carcinoma Teratocarcinoma Yolk sac Tumour Combined Tumour REMEMBER: AFP Not raised is Pure Choriocarcinoma or Pure Seminoma

HCG – ( 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% - Teratocarcinoma 25% - Yolk Cell Tumour 7% - Seminomas

ROLE OF TUMOUR MARKERS Helps in Diagnosis - 80 to 85% of Testicular Tumours have Positive Markers Most of Non-Seminomas have raised markers Only 10 to 15% Non-Seminomas have normal marker level After Orchidectomy if Markers Elevated means Residual Disease or Stage II or III Disease Elevation of Markers after Lymphadenectomy means a STAGE III Disease

ROLE OF TUMOUR MARKERS cont... Degree of Marker Elevation Appears to be Directly Proportional to Tumour Burden Markers indicate Histology of Tumour: If AFP elevated in Seminoma - Means Tumour has Non-Seminomatous elements Negative Tumour Markers becoming positive on follow up usually indicates - Recurrence of Tumour Markers become Positive earlier than X-Ray studies

Imaging Primary testicular tumor can be rapidly & accurately assessed by scrotal ultrasound. This technique can determine -whether the mass is truly intratesticular, -can be used to distinguish the tumor from epididymal pathology, & -may also facilitate testicular examination in the presence of hydrocele.

Once the diagnosis is established by inguinal orchiectomy, -chest x-ray & abdominal CT used to assess the 2 most common sites of metastatic spread ( the lung & retro peritoneum).

Differential diagnosis 1-Epididymoorchitis is the most common misdiagnosis, history of acute onset of symptoms, fever, urethral discharge, & irritative voiding symptoms make the diagnosis of epididymitis more likely.

2-Hydrocele trnsillumination of scrotum readily distinguish between fluid filled hydrocele & solid testicular tumor. Since 5-10% of testicular tumor may be associated with hydrocele ultrasound study of the scrotum is mandatory. 3-Others like spermatocel, hematocele, granulomatous orchitis, most commonly result from tuberculosis.

Treatment Inguinal exploration with cross clamping of the spermatic cord vasculature & delivery of the testis into the field is the main stay of exploration for possible testicular tumor. Scrotal approach & open testicular biopsy should be avoided. Further therapy depend on the histologic characteristic of the tumor as well as the tumor stage. SGCT are radiosensitive & chemosensitive while NSGCT are chemosensitive.