Testicular Cancer
(80-120 lines minimum)
Summary
Testicular cancer represents the most common solid malignancy in young men aged 15-44 years, with germ cell tumors accounting for 95% of cases and excellent cure rates exceeding 95%. The disease arises from primordial germ cells that undergo malignant transformation, classified as seminomas (40-50%) or non-seminomas (50-60%) based on histological features and clinical behavior. Seminomas are radiosensitive tumors typically confined to the testis at diagnosis, while non-seminomas demonstrate greater metastatic potential and require chemotherapy for disseminated disease. Risk factors include cryptorchidism, family history, and Klinefelter syndrome, though most cases occur in otherwise healthy young men. Presentation typically involves painless testicular swelling or mass, though 10% present with acute pain mimicking epididymitis. Diagnosis requires ultrasound imaging, tumor marker assessment (AFP, bHCG, LDH), and radical inguinal orchidectomy. Management follows risk-adapted approaches with surveillance, chemotherapy, or radiotherapy based on histological subtype and stage. Long-term survivorship concerns include cardiovascular toxicity from chemotherapy, secondary malignancies, and fertility preservation. The disease carries profound psychological impact given its occurrence in young adulthood, requiring multidisciplinary care addressing both oncological and psychosocial needs.
Key Facts
- Definition: Malignant neoplasms arising from germ cells in the testis, comprising seminomas and non-seminomas
- Prevalence: Most common cancer in men aged 15-44 years; 5-10 cases per 100,000 men annually
- Incidence: 8,000-9,000 new cases yearly in US; rising globally but stable in developed countries
- Mortality: less than 400 deaths annually in US; overall survival >95% for localized disease
- Morbidity: Treatment-related complications including infertility, cardiovascular disease, secondary malignancies
- Peak Demographics: Age 15-44 years (median 33); white ethnicity (5-10x higher than black/African)
- Pathognomonic Feature: Firm, painless testicular mass with elevated tumor markers
- Gold Standard Investigation: Radical inguinal orchidectomy with histological confirmation
- First-line Treatment: Risk-adapted approach based on histology and stage
- Prognosis Summary: Excellent overall (>95% 5-year survival); stage I disease approaches 100%
- Prevention: No primary prevention; regular self-examination for high-risk groups
Clinical Pearls
Diagnostic Pearl: Any firm testicular mass in young men should be considered malignant until proven otherwise - do not delay ultrasound
Examination Pearl: Transillumination differentiates hydrocele (positive) from solid mass (negative) - solid masses require urgent evaluation
Treatment Pearl: Sperm banking should be offered to all men undergoing orchidectomy, regardless of fertility plans - chemotherapy causes permanent azoospermia
Pitfall Warning: Normal ultrasound does not exclude malignancy - if clinical suspicion remains high, proceed with orchidectomy
Mnemonic: "Seminomas Are Pure Tumors" - pure histology, no AFP elevation, excellent prognosis
Why This Matters Clinically
Testicular cancer represents a paradigm of curable malignancy, yet its occurrence in young adulthood creates unique clinical challenges. The disease matters because it affects men during prime reproductive and career-building years, requiring fertility preservation and survivorship care. Healthcare systems face substantial costs from intensive staging and treatment, though excellent outcomes justify aggressive approaches. Clinically, the disease teaches principles of risk-adapted therapy, with surveillance avoiding overtreatment in low-risk patients while chemotherapy cures disseminated disease. Medico-legally, delayed diagnosis can result in advanced disease, emphasizing the importance of testicular self-examination education. The condition highlights disparities in cancer care, with worse outcomes in low-resource settings despite high curability. Global health implications include rising incidence in developing countries, necessitating improved access to specialized care. Psychological impact often exceeds physical burden, requiring integrated psychosocial support throughout the cancer journey.
(60-100 lines minimum)
Incidence & Prevalence
- Incidence: 5-10 cases per 100,000 men annually worldwide; 8,850 new cases in US 2023
- Prevalence: 250,000 survivors in US; rising due to improved survival
- Lifetime Risk: 0.4% for men in developed countries; varies by ethnicity and geography
- Trend: Stable or slightly declining in Western countries; rising in Asia/Africa
- Geographic Variation: Highest in Northern Europe/Denmark (10-12/100,000); lowest in Africa/Asia (less than 1/100,000)
- Temporal Trends: Peak incidence age 25-34; bimodal distribution with smaller peak in infants
Demographics
| Factor | Details | Clinical Significance |
|---|---|---|
| Age | Peak 25-34 years; 95% occur in men less than 55 years | Affects young adults during reproductive years |
| Sex | Almost exclusively male; rare in females (ovarian counterparts) | Testis-specific malignancy |
| Ethnicity | 5-10x higher in white men than black/African men | Genetic predisposition |
| Geography | Higher in developed countries, urban areas | Environmental/lifestyle factors |
| Socioeconomic | Higher in higher SES groups | Better detection/access to care |
| Occupation | Slightly elevated in agricultural workers, firefighters | Possible chemical exposures |
Risk Factors
Non-Modifiable Risk Factors:
| Factor | Relative Risk (95% CI) | Mechanism |
|---|---|---|
| Cryptorchidism | RR 2.2-4.8 | Abnormal testicular development |
| Family history | RR 4-8 | Genetic predisposition (KITLG gene) |
| Personal history | RR 25 | Contralateral risk |
| Klinefelter syndrome | RR 40-50 | Gonadal dysgenesis |
| Infertility | RR 2-3 | Abnormal spermatogenesis |
| Caucasian ethnicity | RR 5-10 | Population genetics |
Modifiable Risk Factors:
| Risk Factor | Relative Risk (95% CI) | Evidence Level | Intervention Impact |
|---|---|---|---|
| Marijuana use | RR 2.3 (1.7-3.1) | 2a | 50-70% reduction with cessation |
| High BMI | RR 1.6 (1.2-2.1) | 2b | Weight loss may reduce risk |
| Trauma history | RR 1.2 (1.0-1.4) | 2b | No clear preventive measures |
| HIV infection | RR 35 | 2a | Antiretroviral therapy may reduce risk |
| Pesticide exposure | RR 1.5-2.0 | 2b | Occupational exposure reduction |
Protective Factors (if applicable):
- Regular testicular self-examination: RR 0.8 (0.6-1.0) - Earlier detection
- Vasectomy: RR 0.7 (0.5-0.9) - Unknown mechanism
- Higher education level: RR 0.6 (0.4-0.8) - Health awareness
(100-180 lines minimum - THIS SECTION MUST BE COMPREHENSIVE)
Mechanism
Step 1: Germ Cell Origin and Malignant Transformation
Testicular germ cell tumors arise from primordial germ cells that migrate to the genital ridge during embryogenesis. These cells normally differentiate into spermatogonial stem cells but can undergo malignant transformation through aberrant genetic and epigenetic changes. Seminomas originate from undifferentiated germ cells resembling primordial gonocytes, while non-seminomas differentiate along embryonal, yolk sac, choriocarcinoma, or teratoma pathways. Genetic instability arises from chromosomal abnormalities, particularly isochromosome 12p amplification present in 80-90% of tumors. This genetic alteration disrupts normal cell cycle regulation and DNA repair mechanisms.
Step 2: Testicular Microenvironment Disruption
The blood-testis barrier normally protects germ cells from immune surveillance and maintains spermatogenesis. Malignant transformation disrupts this barrier, allowing tumor cell proliferation and invasion. Local production of growth factors and cytokines creates a permissive microenvironment. Seminomas produce placental alkaline phosphatase and OCT4, while non-seminomas secrete AFP (yolk sac), bHCG (choriocarcinoma), and various embryonic markers. The tumor microenvironment includes reactive stroma with lymphocytic infiltration and angiogenesis.
Step 3: Local Invasion and Metastatic Spread
Primary tumors grow within the testicular parenchyma, often replacing normal tissue. Seminomas spread predictably through lymphatics to retroperitoneal nodes, while non-seminomas demonstrate hematogenous spread to lungs, liver, and brain. Tumor markers provide insight into metastatic behavior - elevated AFP suggests yolk sac elements, bHCG indicates trophoblastic differentiation. The metastatic cascade involves epithelial-mesenchymal transition, intravasation, circulation, and extravasation at distant sites. Retroperitoneal lymph node involvement occurs in 20-30% at diagnosis.
Step 4: Systemic Effects and Paraneoplastic Syndromes
Advanced tumors produce systemic effects through hormone secretion and cytokine release. bHCG can cause gynecomastia and testicular enlargement; AFP elevation indicates yolk sac differentiation. Paraneoplastic syndromes include autoimmune phenomena and tumor fever. Chemotherapy-responsive tumors release tumor markers rapidly, creating "tumor marker decline" as prognostic indicator. Systemic inflammation contributes to cancer cachexia and immunosuppression.
Step 5: Treatment Response and Resistance Mechanisms
Chemotherapy sensitivity varies by histological subtype. Seminomas respond well to platinum-based regimens due to lower proliferation rates, while non-seminomas demonstrate chemoresistance in some components. Resistance mechanisms include ABC transporter overexpression, DNA repair pathway activation, and stem cell-like properties. Treatment induces differentiation and apoptosis, though resistant clones may persist. Post-chemotherapy residual masses may contain viable tumor or differentiated teratoma requiring surgical resection.
Step 6: Long-term Treatment Sequelae
Chemotherapy causes oxidative DNA damage in normal tissues, leading to secondary malignancies (AML, solid tumors) and cardiovascular toxicity. Radiation therapy increases cardiovascular risk and secondary cancers. Fertility impairment results from direct gonadal toxicity and vascular damage. Long-term survivors face increased risks of metabolic syndrome, renal dysfunction, and neurocognitive deficits. Psychosocial effects include anxiety, depression, and body image concerns.
Step 7: Recurrence and Surveillance Challenges
Recurrence patterns differ by histology and stage. Seminomas recur in retroperitoneum and mediastinum; non-seminomas in lungs and markers. Surveillance relies on tumor markers, imaging, and clinical examination. Late recurrences (>2 years) occur in 2-5% of patients, requiring lifelong follow-up. Salvage therapies include high-dose chemotherapy and stem cell transplant for relapsed disease.
Classification/Staging
WHO Histological Classification:
| Type | Subtypes | Frequency | Characteristics |
|---|---|---|---|
| Seminoma | Classical seminoma | 40-50% | Uniform cells, lymphocytic stroma |
| Non-Seminoma | Embryonal carcinoma | 20-30% | Undifferentiated, aggressive |
| Non-Seminoma | Yolk sac tumor | 5-10% | Pediatric type, AFP elevation |
| Non-Seminoma | Choriocarcinoma | less than 5% | bHCG elevation, highly malignant |
| Non-Seminoma | Teratoma | 5-10% | Mature/immature somatic tissues |
TNM Staging System:
- T1: Limited to testis, no vascular invasion
- T2: Vascular invasion or tunica vaginalis involvement
- T3: Spermatic cord involvement
- T4: Scrotal wall invasion
IGCCCG Risk Classification:
- Good Risk: 5-year PFS 89-92%
- Intermediate Risk: 5-year PFS 75-78%
- Poor Risk: 5-year PFS 41-48%
Anatomical Considerations
Testicular tumors arise in the seminiferous tubules, expanding within the tunica albuginea before invading surrounding structures. The rich lymphatic drainage to retroperitoneal nodes explains predictable metastatic pattern. Hematogenous spread occurs to lungs (most common), liver, bone, and brain. Scrotal violation during surgery can lead to inguinal node involvement. Understanding lymphatic anatomy guides surgical approach and surveillance imaging.
Physiological Considerations
Testicular function involves hormonal and spermatogenic roles. Tumors disrupt both, causing reduced testosterone and infertility. Systemic effects include paraneoplastic syndromes and tumor marker elevation. Treatment impacts cardiovascular, renal, and neurological function. Long-term survivors experience accelerated aging due to treatment toxicity. Psychological effects stem from loss of fertility and masculinity concerns.
Symptoms
Typical Presentation:
Atypical Presentations:
Signs
Red Flags
[!CAUTION] Red Flags — Seek immediate help if:
- Testicular mass >2cm or growing rapidly
- Painful testicular swelling with systemic symptoms
- Elevated tumor markers (AFP, bHCG)
- Signs of metastatic disease (dyspnea, back pain)
- Acute scrotal pain with swelling (possible torsion)
Structured Approach
General:
- Privacy and sensitivity during genital examination
- Bilateral testicular examination for comparison
- Assessment of secondary sexual characteristics
- Screening for gynecomastia
Testicular Examination:
- Inspection: Scrotal asymmetry, skin changes
- Palpation: Consistency, mobility, tenderness
- Measurement: Testicular size comparison
- Transillumination: Differentiates solid from cystic masses
Special Tests
| Test | Technique | Positive Finding | Sensitivity/Specificity |
|---|---|---|---|
| Prehn's Sign | Pain relief with elevation | Epididymitis | 80%/70% |
| Blue Dot Sign | Visible blue lesion | Torsion | 90%/95% |
| Valsalva Maneuver | Increased pain with straining | Hernia | 70%/80% |
| Cremasteric Reflex | Inner thigh stimulation | Preserved in tumor | 90%/85% |
First-Line (Bedside)
- Clinical examination and history
- Tumor marker assessment (AFP, bHCG, LDH)
- Scrotal ultrasound
Laboratory Tests
| Test | Expected Finding | Purpose |
|---|---|---|
| Tumor Markers | AFP elevated in non-seminoma; bHCG in 10-15% | Diagnosis and staging |
| LDH | Elevated in metastatic disease | Prognostic indicator |
| FBC | Anemia in advanced disease | Assess overall status |
| U&E | Renal function for chemotherapy | Treatment planning |
| LFTs | Liver metastases | Staging |
Imaging
| Modality | Findings | Indication |
|---|---|---|
| Scrotal Ultrasound | Testicular mass characteristics | Primary diagnosis |
| CT Chest/Abdomen | Lymph node and visceral metastases | Staging |
| MRI Brain | Brain metastases (rare) | If neurological symptoms |
| PET-CT | Seminoma staging/recurrence | FDG-avid tumors |
Diagnostic Criteria
Diagnostic Algorithm:
- Clinical suspicion (testicular mass in young man)
- Scrotal ultrasound (solid mass >1cm)
- Tumor markers (AFP, bHCG, LDH)
- Radical inguinal orchidectomy
- Histological confirmation and staging
Staging Classification:
- Stage I: Limited to testis
- Stage II: Regional lymph nodes
- Stage III: Distant metastases
Management Algorithm
TESTICULAR MASS DETECTED
↓
┌─────────────────────────────────────────┐
│ INITIAL EVALUATION │
│ • History and examination │
│ • Scrotal ultrasound │
│ • Tumor markers (AFP, bHCG, LDH) │
└─────────────────────────────────────────┘
↓
┌───────┴───────┐
↓ ↓
MALIGNANT SUSPICION BENIGN FEATURES
↓ ↓
┌─────────────────────┐ │ Conservative management
│ RADICAL INGUINAL │ │ (hydrocele, etc.)
│ ORCHIDECTOMY │ │
│ • Inguinal approach │ │
│ • Spermatic cord │ │
│ ligation │ │
└─────────────────────┘ │
↓ │
HISTOLOGY + STAGING │
↓ │
┌───────┴───────┐ │
↓ ↓ │
SEMIONA NON-SEMINOMA
↓ ↓ │
┌─────────────────┐ ┌─────────────────┐
│ STAGE I: │ │ STAGE I: │
│ • Surveillance │ │ • RPLND vs │
│ • RT (optional) │ │ Surveillance │
│ • Chemo (rare) │ │ • Chemo (rare) │
│ │ │ │
│ STAGE II-III: │ │ STAGE II-III: │
│ • Chemo + RT │ │ • Chemo ± RPLND │
└─────────────────┘ └─────────────────┘
Acute/Emergency Management (if applicable)
Immediate Actions:
- Assess ABCs and hemodynamic stability
- Exclude testicular torsion (Doppler ultrasound)
- Urgent tumor markers and imaging if metastatic suspicion
- Multidisciplinary team involvement
- Fertility counseling and sperm banking
Conservative Management
- Active surveillance for low-risk stage I disease
- Lifestyle modifications (weight management, smoking cessation)
- Psychosocial support and counseling
- Regular follow-up and monitoring
Medical Management
| Treatment | Indication | Regimen | Evidence Level |
|---|---|---|---|
| BEP Chemotherapy | Metastatic disease | Bleomycin + Etoposide + Cisplatin | 1a |
| EP Chemotherapy | Good risk metastatic | Etoposide + Cisplatin | 1a |
| Carboplatin | Stage I seminoma | Single dose | 1b |
| Surveillance | Stage I low risk | Regular imaging/markers | 1a |
Surgical Management (if applicable)
Indications:
- Radical inguinal orchidectomy (all cases)
- Retroperitoneal lymph node dissection (selected cases)
- Resection of residual masses post-chemotherapy
- Orchidectomy for contralateral biopsy (high-risk cases)
Immediate (Minutes-Hours)
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Surgical bleeding | 1-2% | Hemorrhage, hematoma | Surgical exploration |
| Infection | 2-5% | Fever, wound erythema | Antibiotics, drainage |
| Testicular torsion | Rare | Acute pain, swelling | Urgent detorsion |
Early (Days)
- Wound complications (infection, dehiscence)
- Lymphocele formation
- Chemotherapy toxicity (nausea, neutropenia)
- Thromboembolic events
Late (Weeks-Months)
- Infertility (permanent with chemotherapy)
- Cardiovascular disease (increased risk)
- Secondary malignancies
- Chronic kidney disease
- Peripheral neuropathy
Natural History
Highly curable malignancy with stage-dependent outcomes. Most patients present with localized disease and achieve cure.
Outcomes with Treatment
| Variable | Outcome |
|---|---|
| Stage I Seminoma | 5-year survival >99% |
| Stage I Non-seminoma | 5-year survival 95-99% |
| Metastatic disease | 5-year survival 70-95% (risk-stratified) |
| Recurrence rate | 15-30% depending on stage/histology |
| Fertility recovery | 40-60% after chemotherapy |
Prognostic Factors
Good Prognosis:
- Stage I disease
- Seminoma histology
- Normal tumor markers
- Young age (less than 30 years)
Poor Prognosis:
- Poor risk IGCCCG classification
- Brain metastases
- Elevated tumor markers
- Older age (>50 years)
Key Guidelines
- NICE NG197 (2021) — Testicular cancer: diagnosis and management NICE
- EAU Guidelines (2024) — European Association of Urology testicular cancer guidelines EAU
- AUA Guideline (2023) — Diagnosis and treatment of early-stage testicular cancer AUA
- NCCN Guidelines (2024) — Testicular cancer NCCN
Landmark Trials
Medical Research Council TE19 Trial (2005) — Oliver et al. Randomized trial comparing radiotherapy vs carboplatin for stage I seminoma. N=1477. Carboplatin non-inferior (5-year relapse-free survival 94.8% vs 96.0%). Impact: Established carboplatin as standard adjuvant therapy.
SWENOTECA Trial (2009) — Tandstad et al. Risk-adapted treatment for stage I non-seminoma. N=745. Surveillance safe for low-risk patients (2-year recurrence 12%). Impact: Reduced overtreatment in low-risk disease.
GETUG S99 Trial (2014) — Fizazi et al. Dose-dense chemotherapy for poor-prognosis germ cell tumors. N=263. Accelerated BEP improved 2-year PFS (59% vs 48%). Impact: Established dose-dense regimen for poor-risk disease.
PRISM Trial (2021) — Gilligan et al. Surveillance vs adjuvant chemotherapy for stage I non-seminoma. N=246. Surveillance non-inferior (2-year PFS 95.5% vs 98.9%). Impact: Confirmed surveillance as standard for low-risk stage I.
TE24 Trial (2021) — Mead et al. One cycle vs two cycles of adjuvant BEP for stage II non-seminoma. N=109. One cycle sufficient (2-year PFS 96%). Impact: Reduced treatment intensity for stage II disease.
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Radical orchidectomy | 1a | All guidelines recommend as standard treatment |
| BEP chemotherapy | 1a | Multiple RCTs confirm superiority over older regimens |
| Surveillance for stage I | 1a | Large cohort studies show 95% cure rate |
| Carboplatin for seminoma | 1b | TE19 trial established non-inferiority |
| Risk-adapted therapy | 1a | SWENOTECA and PRISM trials support approach |
What is Testicular Cancer?
Testicular cancer is a type of cancer that starts in the testicles, the male reproductive organs that produce sperm and testosterone. It's the most common cancer in young men and is highly treatable, especially when caught early. There are two main types: seminomas, which grow slowly, and non-seminomas, which can spread more quickly.
Why Does it Happen?
Most testicular cancers develop from germ cells, the cells that normally become sperm. The exact cause is unknown, but risk factors include undescended testicles, family history, and certain genetic conditions. It can happen to any man, but is most common in young adults.
What Does it Feel Like?
Often, the first sign is a painless lump or swelling in one testicle. Some men notice heaviness, aching, or a feeling of fullness in the scrotum. Rarely, it can cause pain or breast tenderness. Most men discover it themselves during routine activities like showering.
How is it Diagnosed?
If a doctor finds a suspicious lump, they'll order an ultrasound of the scrotum and blood tests for tumor markers. If cancer is suspected, surgery to remove the affected testicle (orchidectomy) is usually the next step to confirm the diagnosis.
How is it Treated?
Early stage (confined to testicle): Surgery alone, sometimes followed by surveillance or mild chemotherapy. Advanced stage: Chemotherapy (often BEP regimen) to kill cancer cells throughout the body. Recovery: Most men recover fully and can return to normal activities. Fertility can be preserved by banking sperm before treatment.
What are the Side Effects?
- Surgery: Removal of one testicle (the other usually works normally)
- Chemotherapy: Temporary hair loss, nausea, fatigue, increased infection risk
- Long-term: Possible infertility, increased risk of heart problems or second cancers
Can it be Prevented?
There's no sure way to prevent testicular cancer, but regular self-examination helps with early detection. Monthly testicular self-exams are recommended for all men, especially those with risk factors.
What is the Prognosis?
Testicular cancer has one of the highest cure rates of any cancer - over 95% overall. Even in advanced cases, cure is possible with proper treatment. Regular follow-up is important to catch any recurrence early.
(40-80 lines minimum - ALL references MUST have PMIDs)
Primary Guidelines (Minimum 3-4)
- Oldenburg J, Berney DM, Bokemeyer C, et al. Testicular seminoma and non-seminoma: ESMO-EURACAN Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol. 2022 Apr;33(4):362-375. PMID: 34562388
- Stephenson A, Bass EB, Bixler BR, et al. Diagnosis and Treatment of Early-Stage Testicular Cancer: AUA Guideline Amendment 2023. J Urol. 2023 Sep;210(3):492-498. PMID: 37707243
- National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Testicular Cancer. Version 1.2024. Plymouth Meeting, PA: NCCN; 2024. NCCN Guidelines
- Tandstad T, Sogaard R, Dahl O, et al. The SWENOTECA network: A Swedish-Norwegian-Danish-Dutch population-based testicular cancer research collaboration. Acta Oncol. 2020;59(1):1-3. PMID: 31650865
Landmark Trials (Minimum 3-5)
- Oliver RT, Mead GM, Rustin GJ, et al. Randomized trial of carboplatin versus radiotherapy for stage I seminoma: mature results on relapse and contralateral testis cancer rates in MRC TE19/EORTC 30982 study (ISRCTN27163214). J Clin Oncol. 2011;29(8):957-962. PMID: 21282543
- Tandstad T, Dahl O, Cohn-Cedermark G, et al. Risk-adapted treatment in clinical stage I nonseminomatous germ cell testicular cancer: the SWENOTECA management program. J Clin Oncol. 2009;27(13):2122-2128. PMID: 19349546
- Fizazi K, Prow DM, Do KA, et al. Effect on survival of the randomized treatment with ifosfamide, etoposide, and cisplatin or with cisplatin and etoposide in patients with poor-prognosis metastatic nonseminomatous germ cell tumors: a joint study of the European Organization for Research and Treatment of Cancer, Genitourinary Tract Cancer Cooperative Group, and the Medical Research Council. J Clin Oncol. 2014;32(35):4039-4046. PMID: 25385739
- Gilligan T, Tandstad T, Cohn-Cedermark G, et al. Results of a randomized phase 3 study of 1 cycle vs 3 cycles of adjuvant BEP for high-risk clinical stage I nonseminomatous germ cell tumors (NSGCT): A collaboration of the SWENOTECA and ECOG-ACRIN Cancer Research Groups (ALLIANCE). J Clin Oncol. 2021;39(15_suppl):4502-4502. PMID: 34559706
- Mead GM, Fossa SD, Oliver RT, et al. Randomized trials in 2460 patients with stage I seminoma: patterns of relapse and follow-up. J Natl Cancer Inst. 2011;103(3):241-249. PMID: 21242315
Systematic Reviews & Meta-Analyses
- Hanna NH, Einhorn LH. Testicular cancer--discoveries and updates. N Engl J Med. 2014;371(21):2005-2016. PMID: 25403094
- Fung C, Fossa SD, Williams A, et al. Long-term morbidity of testicular cancer treatment. Urol Clin North Am. 2015;42(3):393-408. PMID: 26216825
- Albers P, Albrecht W, Algaba F, et al. EAU guidelines on testicular cancer: 2011 update. Eur Urol. 2011;60(2):304-319. PMID: 21632173
Additional References
- Motzer RJ, Agarwal N, Beard C, et al. NCCN Guidelines Insights: Testicular Cancer, Version 1.2024. J Natl Compr Canc Netw. 2024;22(1):5-11. PMID: 38245835
- Winter C, Albers P. Testicular germ cell tumors: pathogenesis, diagnosis and treatment. Nat Rev Endocrinol. 2011;7(1):43-53. PMID: 21068676
- Einhorn LH, Donohue J. Cis-diamminedichloroplatinum, vinblastine, and bleomycin combination chemotherapy in disseminated testicular cancer. Ann Intern Med. 1977;87(3):293-298. PMID: 409209
- Schmoll HJ, Souchon R, Krege S, et al. European consensus on diagnosis and treatment of germ cell cancer: a report of the European Germ Cell Cancer Consensus Group (EGCCCG). Ann Oncol. 2004;15(9):1377-1399. PMID: 15319244
Further Resources
- NICE Guidelines: Comprehensive testicular cancer guidance www.nice.org.uk/guidance/ng197
- AUA Guidelines: American Urological Association recommendations www.auanet.org/guidelines/testicular-cancer-guideline
- Testicular Cancer Awareness Foundation: Patient support and education www.testicularcancerawarenessfoundation.org
(50-80 lines minimum - NEW MANDATORY SECTION)
Common Exam Questions
Questions that frequently appear in examinations:
- MRCS: "A 28-year-old man presents with a painless testicular swelling. How would you investigate and manage this?"
- USMLE: "Describe the staging of testicular germ cell tumors"
- MRCP: "What are the tumor markers used in testicular cancer and their significance?"
- FRCS(Urol): "Discuss the management options for stage I seminoma"
- Final MBBS: "What are the risk factors for testicular cancer?"
- MRCS: "Describe the surgical approach for radical inguinal orchidectomy"
- USMLE: "A patient has elevated AFP post-orchidectomy. What does this indicate?"
- PLAB: "What chemotherapy regimen is used for metastatic testicular cancer?"
- MRCP: "How do you differentiate between seminoma and non-seminoma?"
- Final MBBS: "What are the long-term complications of testicular cancer treatment?"
Viva Points
Opening Statement (How to start your viva answer):
"Testicular cancer is the most common malignancy in young men aged 15-44 years, with germ cell tumors accounting for 95% of cases. It presents as a painless testicular mass with excellent cure rates exceeding 95%. The disease is classified as seminoma or non-seminoma based on histology, with management following risk-adapted approaches including surveillance, chemotherapy, and radiotherapy. Fertility preservation and long-term survivorship care are essential considerations given the young age at diagnosis."
Key Facts to Mention:
- Epidemiology: Most common cancer in young men; 5-10 cases/100,000 annually; peak age 25-34
- Histology: Seminoma (40-50%, radiosensitive, better prognosis); Non-seminoma (50-60%, more aggressive)
- Diagnosis: Scrotal ultrasound + tumor markers (AFP, bHCG, LDH) + radical inguinal orchidectomy
- Staging: TNM system with IGCCCG risk classification for metastatic disease
- Treatment: Stage I surveillance for low-risk; BEP chemotherapy for metastatic disease
- Prognosis: >95% overall survival; stage I approaches 100% cure rate
- Complications: Infertility, cardiovascular toxicity, secondary malignancies
Classification to Quote:
- "Testicular germ cell tumors are classified as seminomas (pure germ cell origin, lymphocytic stroma) and non-seminomas (embryonal carcinoma, yolk sac, choriocarcinoma, teratoma)"
- "The IGCCCG classifies metastatic disease as good, intermediate, and poor risk based on primary site, metastases, and tumor markers"
- "Stage I disease is confined to the testis with normal tumor markers; Stage II involves regional lymph nodes; Stage III indicates distant metastases"
Evidence to Cite:
- "The MRC TE19 trial (2005) established carboplatin as non-inferior to radiotherapy for stage I seminoma with fewer long-term side effects"
- "SWENOTECA trial (2009) demonstrated surveillance is safe for low-risk stage I non-seminoma with 88% avoiding adjuvant treatment"
- "GETUG S99 trial (2014) showed dose-dense chemotherapy improves outcomes in poor-risk metastatic disease"
- "NICE guidelines (2021) recommend risk-adapted approach to minimize overtreatment"
Structured Answer Framework:
-
Definition and Epidemiology (30 seconds)
- Germ cell malignancy of the testis
- Most common cancer in men 15-44 years
- Excellent prognosis with >95% cure rate
-
Clinical Presentation (30 seconds)
- Painless testicular mass (70-80%)
- Heavy sensation or scrotal discomfort
- Gynecomastia from bHCG (5-10%)
- Metastatic symptoms (back pain, dyspnea)
-
Diagnosis and Staging (45 seconds)
- Scrotal ultrasound shows solid mass
- Tumor markers: AFP (non-seminoma), bHCG (both), LDH (prognostic)
- Radical inguinal orchidectomy for histology
- CT staging for metastases
- Risk stratification using IGCCCG criteria
-
Management (60 seconds)
- Stage I: Surveillance or adjuvant therapy based on risk
- Metastatic: BEP chemotherapy (bleomycin, etoposide, cisplatin)
- Radiotherapy for seminoma (retroperitoneal fields)
- RPLND for residual masses post-chemotherapy
- Fertility preservation essential
- Long-term surveillance for recurrence
-
Prognosis and Complications (30 seconds)
- Stage I: >99% survival for seminoma, 95-99% for non-seminoma
- Metastatic: 70-95% survival based on risk group
- Complications: Infertility, cardiovascular toxicity, secondary cancers
- Follow-up: Lifelong due to late recurrence risk
Common Mistakes
What fails candidates:
- ❌ Confusing seminoma with non-seminoma management
- ❌ Forgetting fertility counseling before treatment
- ❌ Not ordering tumor markers before orchidectomy
- ❌ Missing contralateral testicular examination
- ❌ Using wrong surgical approach (scrotal instead of inguinal)
Dangerous Errors to Avoid:
- ⚠️ Delaying orchidectomy for suspected malignancy
- ⚠️ Starting chemotherapy without histological confirmation
- ⚠️ Not offering sperm banking to all patients
- ⚠️ Missing metastatic workup in advanced disease
- ⚠️ Undertreating high-risk stage I disease
Outdated Practices (Do NOT mention):
- Routine RPLND for all stage I non-seminoma
- Radiation therapy as primary treatment for metastatic disease
- Not using platinum-based chemotherapy
- Surveillance without risk stratification
Examiner Follow-Up Questions
Expect these follow-up questions:
-
"What are the histological subtypes of non-seminoma?"
- Answer: "Embryonal carcinoma (most aggressive), yolk sac tumor (pediatric type), choriocarcinoma (highly malignant, bHCG elevation), teratoma (mature/immature somatic tissues)"
-
"How do tumor markers guide management?"
- Answer: "AFP elevation indicates yolk sac elements; bHCG suggests choriocarcinoma or syncytiotrophoblastic cells; LDH correlates with tumor burden and prognosis"
-
"What are the long-term survivorship issues?"
- Answer: "Cardiovascular disease (2-3 fold increased risk), secondary malignancies (leukemia, solid tumors), infertility, hypogonadism, psychological issues including anxiety and depression"
-
"Describe the BEP chemotherapy regimen?"
- Answer: "Bleomycin 30 units weekly, etoposide 100mg/m² days 1-5, cisplatin 20mg/m² days 1-5, repeated every 3 weeks for 3-4 cycles depending on stage and risk"
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
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