Testicular Cancer - Department of Surgery at SUNY ...Testicular cancer is an uncommon but highly treatable cancer Germ-cell tumors comprise >95% of testicular cancers Tumors with seminoma

Testicular Cancer PATRICIA LEUNG 8.22.13 SUNY DOWNSTATE MEDICAL CENTER

www.downstatesurgery.org

Case Presentation

29 year old male No PMH/PSH CC: 6 weeks of painless swelling left testicle Denied any trauma, fever/chills, family history Exam: HR 70 RR 20 T 97.3 BP 134/79 Left testis enlarged, firm, nontender to palpation; no transillumination; right testis WNL No lymphadenopathy


Labs: CBC, CMP WNL β-hCG 30 AFP negative Imaging - Ultrasound: L testicle - 6.3 x 5.5 x 3.6 cm left testicle almost completely replaced by a large solid heterogeneous mass measuring approximately 5 x 4.5 x 3.1 cm R testicle - 3.9 x 2.1 x 1.8 cm


Left radical orchiectomy Pathology: Seminoma, 6.3 x 5 x4 cm Tumor limited to testis and epididymis without vascular/lymphatic invasion; spermatic cord uninvolved by tumor


Introduction

Testicular cancer is most common among men aged 15 to 35 years Secondary peak in incidence after age 60 Incidence 7.5 cases per 100,000 5-fold higher in whites Highly treatable Mortality rate before 1970s was 50% compared to <5% today Most are germ cell tumors (GCT)


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5% are nongerm call tumors (sertoli cell or leydig)

Anatomy www.downstatesurgery.org

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Tunica albuginea covered by tunica vaginalus Epidydymis connects efferent ducts to vas deferens, stores sperm 2-3 months

Differential Diagnosis

Abdominal hernia Epididymitis Hydrocele Lymphoma Orchitis Spermatocele, varicocele Testicular Torsion


Risk Factors

Undescended testis (cryptorchidism) – 4-8 fold increased risk - Orchiopexy Genetics – Klinefelter syndrome, Down’s syndrome Family history of testis cancer – 1.4% have family history; risk of

testicular cancer increases 4-6 fold in sons and siblings Personal history – 1-2% patients with testicular cancer will develop a

second primary tumor in contralateral testis Environment – DES, Agent Orange, solvents Activities – horseback and motorcycle riding, local trauma, and

increased scrotal temperature (are not)


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Surgical correction of an undescended testis (orchiopexy) before puberty appears to lower risk of testis cancer only slightly (RR 2-3 before 12, 2-6 after 12) Most commonly is seminoma

Types of Testicular Germ Cell Tumors

Seminomas (30-60%) Nonseminomas - Embryonal carcinomas (3-5%) - Teratomas (5-10%) - Yolk sac tumors - Choriocarcinomas (1%) - Mixed (60%) Tumors with a mixture of seminoma and nonseminoma components

are managed as nonseminomas Tumors with seminoma histology but with elevated serum AFP are

treated as nonseminomas


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Focus on GCT as comprise 90-95% of all testicular mass Peak incidence seminomas in 4th decade, nonseminomas in 3rd decade 30-60% Seminoma 3-5% Embryonal Carcinoma in its pure form Present in 40% of NSGCT 5 – 10% Teratoma 1% pure choriocarcinoma Tumors of mixed histology 60% of all GCTs

Seminoma vs. Nonseminoma

Seminoma Less aggressive

Radiosensitive

Diagnosed at earlier stage: CS I, II and III disease is 85%, 10% and 5%

Metastatic seminoma who experience relapse after treatment, 10-15% have NSGCT elements

Nonseminoma CS I, II and III is 33%, 33%, 33%

Higher incidence of occult metastasis

Higher risk of systemic relapse after treatment of retroperitoneum


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At diagnosis the proportion of patients with CS I, II and III is Higher risk of systemic relapse after treatment of retroperitoneum 1-4% after radiotherapy and 10% after RPLND for nonseminoma

Diagnosis

Localized disease Painless swelling or nodule of one testicle Dull ache or heavy sensation Hematoma with trauma

Metastatic disease: Anorexia, nausea, GI symptoms Back pain (retroperitoneal disease) Cough, chest pain, hemoptysis (mediastinal adenopathy or metastatic

lung disease Gynecomastia (hCG) Hyperthyroidism (hCG)


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Should undergo evaluation hCG and TSH have common alpha subunit

Serum tumor markers

Alpha-fetoprotein (AFP) – elevated in 40-60% of men with nonseminomas; seminomas do not produce AFP

β-hCG – elevation seen in 14% of patients with stage I seminoma and 50% of patients with metastatic seminoma; 40-60% of men with nonseminoma have elevated levels

LDH – elevated in both but with less clear prognostic significance Measured before and after surgery


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Liver disease with elevated AFP False positives for hcg in patients who IM inject testosterone should result in normalization of hCG; marijuana use AFP produced by yolk sac cells Hcg – expression of trophoblasts LDH also seems to correlate with concentration proportional to tumor volume

Imaging

Testicular ultrasound – highly specific CT Abdomen/Pelvis Chest XR, +/- CT MRI PET – no role

RadioGraphics March 2004 vol. 24 no. 2 387-404

JUM July 1, 2007 vol. 26no. 7 981-984


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Mri too costly Figure 3b. Testicular seminoma in a 51-year-old man with a palpable mass in the right testis. (a) Axial T2-weighted MR image shows a solid mass in the right testis. The mass has a lobulated margin and uniform signal intensity. Bandlike structures of low signal intensity (arrows), which represent fibrovascular septa, are seen within the mass. (b) Axial contrast material-enhanced MR image shows that the septa (arrows) enhance more than the tumor tissue. This finding indicates that the septa include a large amount of vascular structures. Seminomas appear as well-defined hypoechoic lesions without cystic areas, while nonseminomatous germ cell tumors (NSGCTs) are typically nonhomogeneous hyperechoic lesions with calcifications, cystic areas, and indistinct margins. Ultrasound is not reliable in local tumor staging. Hypoechoic – less reflective – darker gray Hyperechoic more reflective lighter gray

Summary of initial workup

European Association of Urology 2012


Management

NO Transscrotal biopsy – risk of local dissemination of tumor into scrotum

NO Transscrotal approach – increase in risk of local recurrence

YES Radical inguinal orchiectomy with division of spermatic cord at level of internal ring


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Transscrotal approach – 2.7% vs. 0.4 % local recurrence

TNM Classification


Post-orchiectomy


Retroperitoneal Nodes Most common route – to

retroperitoneal lymph nodes Right sided tumors

Interaortocaval

Precaval and paracaval nodes

Left sided tumors Para-aortic and pre-aortic

Interaortocaval

Contralateral spread more common with right sided tumors and associated with large volume disease


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With the exception of choriocarcinoma, the most common route of disease dissemination is via the lymphatic channels from the primary tumor to the retroperitoneal lymph nodes and susbsequently to distant sites. Choriocarcinoma has a propensity for hematogenous dissemination. The retroperitoneum is the initial site of metastatic spread in 70-80% of patients with GCT.


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46 yo M with a right sided GCT with interaortocaval lymph node

Staging



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Stage I - disease confined to the testis, Stage II - retroperitoneal metastases, and Stage III - supradiaphragmatic or visceral metastases.

Simplified Staging

Clinical Stage I No Radiographic Evidence of Metastatic Disease

Elevated STM

Clinical Stage II Retroperitoneal Lymphadenopathy

Clinical Stage III Pulmonary, non-retroperitoneal lymph nodes or visceral metastases

Retroperitoneal nodes with STM levels 2 and 3

NO STAGE IV


Post-orchiectomy management Seminoma


Post-orchiectomy management Seminoma Stage 1

Surveillance Adjuvant treatment with radiation therapy Single cycle of carboplatin chemotherapy

Disease-specific survival – 99% independent of management choice Stage IIA/IIB

Paraaortic and iliac node radiation therapy Chemotherapy Both

Stage IIC/III Chemotherapy


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Retroperitoneal lymph node left vs right Stage IIA/IIB – N1, N2 nodes IIC – N3 nodes, III – M1

Post-orchiectomy management Nonseminoma


Post-orchiectomy management Nonseminoma Stage I

Surveillance (30% relapse) Adjuvant chemotherapy Modified retroperitoneal lymph node dissection (RPLND)

Stage IIA/IIB Bilateral RPLND Multiagent platinum-based chemotherapy – overall cure rate of 85%

Stage IIC/III Chemotherapy


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Approximately 30% of stage I nonseminomatous GCT will relapse, so treating all patients would risk toxicity in 70% cases; vascular and lymphatic invasion most powerful predictors of relapse; important is also presence of undifferentiated cells (relapse rates approach 50% vs 20% without high risk factors 80% of relapses occur within 1st yr after orchiectomy, 90% by year 2, almost all by year 3 Patients with pT2 tumors, more than 80% embryonal component, or lymphovas- cular invasion are considered to have high-risk testis cancer. These patients are not good candidates for surveillance be- cause 35% to 40% of them will have subclinical retroperitoneal disease. Transabdominal or thoracoabdominal The modified right-side RPLND template is bounded superiorly by the right renal artery, medially by the lateral aspect of the aorta, lat- erally by the ipsilateral ureter, and inferiorly by the inferior mesenteric artery and ipsilateral common and external iliac vessels (figure 1). The right-side template focuses on removal of lymph nodes in the interaortocaval, precaval, and preaortic regions. ( NO SUPRAHILAR renal nodes) A modified left-side template RPLND follows the same contralateral boundaries, with the focus on removing lymph nodes in the interaortocaval, left paraortic, and preaortic regions above the inferior mesenteric artery (figure 2). These modified templates have resulted in greater than 90% postoperative ejaculatory emission.4 Further nerve-sparing studies identifying and preserving sympathetic fibers intraoperatively have resulted in greater than 98% postoperative ejaculatory function.8 Benefits of RPLND – cuts surveillance to 2 yrs from 5 yrs Bilateral RPLND – loss of antegrade ejaculation and infertility secondary to damage of sympathetic nerve fibers

Surveillance www.downstatesurgery.org

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Involved process

Summary

Testicular cancer is an uncommon but highly treatable cancer Germ-cell tumors comprise >95% of testicular cancers Tumors with seminoma histology but with elevated AFP are

considered nonseminomas Seminomas are radiosensitive and respond well to platin-based

chemotherapy Most common route of disease dissemination is via the lymphatic

channels from the primary tumor to retroperitoneal lymph nodes Retroperitoneal lymph node dissection is an effective therapy for

patients with high-risk clinical stage I nonseminomatous germ cell cancer.


References NCCN Clinical Practice Guidelines in Oncology 2012

European Association of Urology: Guidelines on Testicular Cancer 2012

Campbell-Walsh Urology 10th edition

Retroperitoneal lymph node dissection in testis cancer, Urology Times: Clinical Edition June 2009

Evaluation of Lymph Node Counts in Primary Retroperitoneal Lymph Node Dissection; Cancer, Nov 2010

Retroperitoneal lymph node dissection for residual masses after chemotherapyin nonseminomatous germ cell testicular tumor, World Journal of Surgical Oncology 2010: 8:97

The Role of Primary Retroperitoneal Lymph Node Dissection in Clinical Stage I Nonseminomatous Germ Cell Testicular Cancer, American Society of Clinical Oncology 2010

Thank you Dr. Mike Tyler and Dr. Brian McNeil


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Presentation Notes

a 45-year-old patient with severe testicular pain and a possible mass revealed the surprising image of a man in distress, urologists at Queen’s University, in Ontario, followed proper scholarly procedure: They submitted it to Urology, the official journal of the International Society of Urology.

Documents

Testicular Cancer - Department of Surgery at SUNY ...Testicular cancer is an uncommon but highly treatable cancer Germ-cell tumors comprise >95% of testicular cancers Tumors with seminoma