Testicular cancer

• Testicular cancer is a highly curable cancer of young men, usually arising from germ cells in a testis.
• It most often appears as a painless testicular lump; tumour markers (AFP, beta-hCG, LDH) support the diagnosis.
• The diagnosis is confirmed by scrotal ultrasound and then by removing the testis through the groin, never by a scrotal biopsy.
• Treatment depends on type and stage: surveillance, one dose of carboplatin for stage I seminoma, single-cycle or multi-cycle BEP chemotherapy, radiotherapy for selected seminoma, and retroperitoneal lymph node surgery when needed.
• Cure rates are very high, even with metastatic disease, but late effects and fertility need lifelong attention.

By the end of this page you should be able to:

1. Explain why testicular cancer is a cancer of young men and name its main risk factors.
2. Classify germ-cell and non-germ-cell testicular tumours and interpret AFP, beta-hCG and LDH.
3. Describe the safe diagnostic pathway, including why the scrotum is not biopsied.
4. Stage a testicular cancer using the TNM system and the IGCCCG risk groups.
5. Outline the stage-adapted management of seminoma and non-seminoma, including surveillance, carboplatin, BEP, radiotherapy and RPLND.
6. Discuss fertility preservation, prognosis, late effects and care in low-resource settings.

Staging in testicular cancer is unusual because the serum tumour markers measured after orchidectomy are built into the stage (the "S" component).

Testicular cancer is rare - about 1% of cancers in men overall - but it is the most common solid cancer in men aged roughly 15 to 44 years ^[1]. It represents about 5% of urological tumours ^[1]. In the West, incidence is roughly 3 to 10 new cases per 100,000 men per year and has been rising ^[1]. Despite this, long-term survival exceeds 95% across most stages ^[1][4] - one of the great success stories of modern oncology, built on cisplatin chemotherapy and careful stage-adapted treatment.

The reason testicular cancer matters far more than its rarity suggests is that it strikes men in their twenties and thirties, and decisions made in the first weeks - sperm banking, orchidectomy approach, accurate staging - shape outcomes for decades.

Germ-cell tumours make up 90 to 95% of testicular cancers ^[1]; 1 to 2% are bilateral at diagnosis ^[1]. The peak age differs by type: non-seminomatous germ cell tumours (including mixed tumours) peak in the third decade, and seminoma peaks in the fourth decade ^[1]. Up to 5% arise at an extragonadal site such as the mediastinum or retroperitoneum ^[1].

The risk factors cluster into the testicular dysgenesis syndrome - conditions thought to share disturbed development of the fetal testis:

• Cryptorchidism (undescended testis). This is the best-established risk factor.
• Previous germ-cell tumour or GCNIS in one testis raises the risk of a new tumour in the other.
• Family history of testicular cancer in a first-degree relative.
• Hypospadias, impaired spermatogenesis and infertility.
• Disorders of sex development, including Klinefelter syndrome (47,XXY). Klinefelter syndrome is classically listed, but newer evidence shows its clearest cancer link is with mediastinal (extragonadal) germ-cell tumours in adolescence and young adulthood rather than with testicular cancer itself; a Danish cohort of 696 men with Klinefelter syndrome found no cases of testicular cancer while mediastinal germ-cell tumours were grossly over-represented ^[5].

GCNIS confers about a 50% risk of invasive testicular cancer at five years if it is left in place ^[1].

Testicular cancers fall into two groups, which matters enormously because they choose different treatments.

These arise from germ cells and are almost all derived from GCNIS. They split into:

• Seminoma. The commoner type in the older age group within germ cell cancer; radiosensitive and chemosensitive.
• Non-seminoma, which contains one or more of:
  • Embryonal carcinoma (the least differentiated, most aggressive element)
  • Yolk sac tumour (post-pubertal type; the commonest testicular cancer of infancy is a separate pre-pubertal type)
  • Choriocarcinoma (trophoblastic; drives very high beta-hCG, metastasises early to lungs and brain)
  • Teratoma (post-pubertal type), containing tissues from more than one germ layer; "somatic" malignant transformation can occur
• Mixed germ-cell tumour, very common in practice.

• Leydig cell tumours - an uncommon sex-cord stromal tumour; may produce androgens or oestrogens causing gynaecomastia or Cushing syndrome; only a small minority metastasise ^[1].
• Sertoli cell tumours - rare, a small fraction of testicular neoplasms ^[1].
• Other rare sex-cord stromal tumours (granulosa cell, thecoma/fibroma), spermatocytic tumour (an older-man GCNIS-unrelated tumour with no marker rise) and mesothelioma of the tunica vaginalis.
• Primary testicular lymphoma, usually diffuse large B-cell lymphoma. Rare (about 5% of testicular neoplasms and 1 to 2% of non-Hodgkin lymphoma) but the commonest testicular malignancy in men aged 60 to 80 ^[2]. It presents like other testicular masses, is often bilateral and spreads to the CNS; AFP and beta-hCG are rarely elevated ^[2].

AFP, beta-hCG and LDH support diagnosis, indicate GCT histology, stage the disease and monitor treatment ^[1].

Normal adult reference ranges give context: AFP under 15 ng/mL, beta-hCG undetectable (0), total LDH 48 to 115 IU/L ^[3]. In practice the laboratories' own ranges and the size of the elevation matter more than a single normal/abnormal.

Important marker points ^[1]:

• Up to 90% of non-seminomas have a raised AFP or beta-hCG; 39% have both raised.
• Pure seminomas can raise beta-hCG in up to 30% of cases.
• A markedly raised AFP in a tumour called "seminoma" means a non-seminoma component is present - do not miss it.
• All three markers have low sensitivity: normal markers never exclude testicular cancer.
• LDH is the least specific marker; it reflects tumour bulk and contributes prognostic information.
• Pre- and post-orchidectomy values are both needed because staging uses markers measured after orchidectomy.
• Half-lives are 5 to 7 days for AFP and 1 to 3 days for beta-hCG. If markers fail to fall with their half-life, metastatic disease is likely ^[1]; conversely, normalisation does not exclude metastasis.

Testicular germ-cell tumours are diagnosed on the orchidectomy specimen; review by a specialist genitourinary pathologist is recommended ^[1]. Nomenclature follows the WHO classification of tumours of the urinary system and male genital organs ^[1].

Germ-cell tumours usually replace most of a testis as a firm, pale or variegated mass. Seminomas tend to be large, lobulated and homogeneous; non-seminomas are often more heterogeneous, with haemorrhage and necrosis - choriocarcinoma especially may be small in the testis yet already widely metastatic. Teratoma shows cystic spaces along with cartilage or other mature tissues. Leydig-cell tumours are small, well-circumscribed yellow nodules because of their lipid content. GCNIS, the precursor, is invisible to the naked eye.

GCNIS cells lie along the basement membrane with large clear cytoplasm and prominent nucleoli. Seminoma shows large cells in nests separated by fibrous septa with lymphocytes. The non-seminoma components are diagnosed by morphology: embryonal carcinoma (primitive epithelium), yolk sac (mesenchymal and epithelial patterns, Schiller-Duval bodies), choriocarcinoma (cytotrophoblast and syncytiotrophoblast), and teratoma (mature or immature tissues from multiple germ layers). Stage and risk are assigned from the specimen - vascular or lymphatic invasion, cord or scrotal invasion, and tumour size.

See Epidemiology above. The cause of most tumours is unknown and there is no proven modifiable risk factor.

Testicular cancer is understood to arise from GCNIS, which is a neoplastic transformation of gonocytes that persist in the adult testis. Most germ-cell tumours develop through GCNIS, so the risk factors above feed one common precursor. GCNIS confers about a 50% risk of invasive testicular cancer at five years if left in place ^[1].

From GCNIS the tumour either:

• remains as a seminoma, the more differentiated default state, or
• differentiates along embryonic or extra-embryonic lines into embryonal carcinoma, yolk sac tumour, choriocarcinoma and teratoma.

Local spread is by direct invasion through the tunica into the spermatic cord or scrotum. Lymphatic spread follows predictable routes: testicular lymphatics drain to the para-aortic (retroperitoneal) nodes, not to the groin nodes. This is why a testis lump spreads to the back and not to the groin, and why scrotal surgery violates the drainage pattern. Haematogenous spread (lung, liver, bone, brain) appears with non-seminoma - especially choriocarcinoma - and with advanced disease.

• A painless, firm lump or swelling in one testis - the classic presentation; it may be noticed on self-examination or by a partner.
• A sense of heaviness or dragging in the scrotum.
• A dull ache in the groin, lower abdomen or back. Pain is reported in a minority and often delays diagnosis because it is mistaken for infection.
• Gynaecomastia (breast development or tenderness) occurs in a small number, driven by beta-hCG stimulating Leydig-cell oestrogen production ^[1].
• Sudden enlargement after minor trauma - trauma does not cause cancer but may draw attention to a mass that was already present.
• Breathlessness, cough, haemoptysis or a neck mass when disease has spread to lungs or supraclavicular nodes.
• Back pain from para-aortic nodal disease ^[1].
• Systemic symptoms (weight loss, fatigue) in advanced disease.

• Inspect and palpate both testes with the patient standing. Gently roll each testis between the fingers - the normal testis is smooth and firm. A tumour feels firm and nodular and usually does not transilluminate.
• Identify the separate epididymis behind the testis (a mass may be mistaken for it).
• Examine the cord, both groins (no inguinal node is expected from a testis tumour; an inguinal node suggests scrotal-skin or systemic disease), the abdomen (para-aortic mass) and the chest and supraclavicular fossae.
• Check for gynaecomastia and testicular atrophy (past cryptorchidism).
• Transillumination - a torch behind the scrotum. Cystic swellings light up; solid tumours do not.
• A hydrocele may coexist and hide a tumour; ultrasound is mandatory for any new scrotal mass.

Germ-cell tumours spread first to the retroperitoneum, so a young man with a para-aortic mass and a normal-feeling testis still needs testicular ultrasound and markers before "unknown primary" is assumed ^[1].

• Bilateral scrotal ultrasound (high-frequency probe, above 10 MHz) is the first investigation for any suspicious testicular mass. It confirms a solid intratesticular mass, assesses the contralateral testis, and picks up very small or incidental lesions, which are often benign ^[1]. Ultrasound is also recommended for all men with a retroperitoneal or visceral mass, with or without raised hCG/AFP and no palpable testicular mass ^[1].
• Serum AFP, beta-hCG and LDH before orchidectomy ^[1].
• Full blood count, renal and liver function, LDH, plus testosterone/LH if atrophy is suspected.

• Contrast-enhanced CT of chest, abdomen and pelvis before or promptly after orchidectomy, in every confirmed case (abdominal and pelvic MRI if iodine contrast is contraindicated) ^[1]. The expected nodal drainage is para-aortic, so inspect those nodes carefully.
• Brain imaging (CT or MRI) in men with multiple lung metastases, very high hCG (above 5,000), poor-prognosis IGCCCG group or neurological symptoms ^[1].
• PET-CT is not used for initial staging or surveillance.
• Do not biopsy the testis (see callout).

• Ultrasound distinguishes intratesticular solid (usually malignant) from extratesticular (usually benign) and from cystic disease. It records side, size, multifocality and blood flow.
• Markers give histological clues (see the table above). A persistently raised or rising marker after orchidectomy means metastatic disease until proved otherwise.
• Post-orchidectomy markers are taken until normalisation on two consecutive measurements, judging the fall by the half-lives.
• Pathology of the orchidectomy specimen is the gold standard for type and local extent; central review by a specialist genitourinary pathologist is recommended ^[1].
• Fertility assessment: semen analysis and banking before any treatment, since sperm quality is often already impaired ^[1].

Orchidectomy remains the standard because adjacent GCNIS is found in 20 to 30% of specimens ^[1]. Testis-sparing surgery with frozen section may be appropriate for synchronous bilateral tumours, a tumour in a solitary testis (selected cases) and small indeterminate masses with negative markers and a normal contralateral testis, provided more than half the parenchyma remains and the case is discussed ^[1].

The UICC TNM classification (2025, 9th edition) is recommended ^[1]. Key points:

• pT describes the primary tumour after orchidectomy (pT1 limited to testis/epididymis without vascular invasion; pT2 vascular or lymphatic invasion, hilar soft tissue involvement or extension through the tunica albuginea into the tunica vaginalis; pT3 spermatic cord; pT4 scrotum).
• N1/N2/N3 are clinical node sizes: 2 cm or less; more than 2 to 5 cm or more than five positive nodes; more than 5 cm.
• M1a non-regional node or lung; M1b other distant sites.
• S (markers, measured pre-chemotherapy) is what makes this cancer unique:
  • S0 normal, S1 low (LDH under 1.5 x ULN, beta-hCG under 5,000, AFP under 1,000), S2 mid (LDH 1.5 to 10 x ULN, beta-hCG 5,000 to 50,000, AFP 1,000 to 10,000), S3 high (LDH over 10 x ULN, beta-hCG over 50,000, AFP over 10,000).
  • Only one elevated marker is enough for S2 or S3.

Stage 0 is GCNIS (pTis). Stage I is disease confined to the testis with no nodes or metastases (IA T1, IB T2 to T4, IS with raised markers). Stage II is para-aortic or pelvic nodal disease only (IIA small, IIB medium, IIC large nodes). Stage III is distant disease, subdivided by M1a versus M1b and marker level into IIIA, IIIB and IIIC ^[1].

In developed countries, 75 to 80% of seminoma and 55 to 64% of non-seminoma present as stage I, and about 5% of non-seminoma are stage IS ^[1].

The IGCCCG system stratifies metastatic germ-cell cancer into good, intermediate and poor prognosis groups using primary site, metastatic site and post-orchidectomy markers, with re-validated five-year outcomes ^[1]:

• Good-prognosis seminoma: 5-year progression-free survival 89%, overall survival 95%. Good-prognosis non-seminoma: PFS 90%, survival 96% (testis or retroperitoneal primary, no non-pulmonary visceral metastases, AFP under 1,000, beta-hCG under 5,000, LDH under 1.5 x ULN).
• Intermediate-prognosis seminoma: PFS 79%, survival 88% (non-pulmonary visceral metastases present but markers normal). Intermediate-prognosis non-seminoma: PFS 78%, survival 89%.
• Poor-prognosis non-seminoma only: PFS 54%, survival 67% (mediastinal primary, non-pulmonary visceral metastases, AFP over 10,000, beta-hCG over 50,000, or LDH over 10 x ULN).
• There is no poor-prognosis seminoma category.

Relapse after five years is very rare (about 0.5%); after this point the focus shifts to late effects and survivorship ^[1].

• Radical inguinal orchidectomy with high ligation of the spermatic cord at the internal inguinal ring is the standard; it is both treatment and a pathological diagnosis ^[1]. In a life-threatening situation with extensive metastasis, chemotherapy may be started before orchidectomy ^[1].
• Sperm bank before treatment - discuss with every man; semen preservation is the most cost-effective fertility strategy ^[1].
• Offer a testicular prosthesis to all who undergo uni- or bilateral orchidectomy ^[1].
• Surveillance after apparently curative treatment is the norm; most men need no adjuvant treatment beyond orchidectomy.

About one in five men with stage I seminoma have subclinical retroperitoneal disease and will relapse after orchidectomy alone, yet 80% are cured by orchidectomy alone and survival in stage I is almost 100% whatever is done ^[1]. Surveillance is the preferred option where resources and patient compliance allow ^[1].

• Relapse risk under surveillance is about 12 to 20% at five years (17% in the largest series of more than 1,500 patients), mostly retroperitoneal and within two years ^[1]. Cancer-specific survival on surveillance is over 99% ^[1].
• Carboplatin: one cycle at AUC 7 (area under the curve 7 mg/mL/min) is an alternative to radiotherapy or surveillance, with relapse rates around 5% and no clear increase in long-term toxicity ^[1].
• Adjuvant radiotherapy should generally be avoided, especially in young men with a long life expectancy, because it carries a long-term risk of second cancers. It is reserved for selected men who cannot undergo surveillance or chemotherapy ^[1].
• In risk-factor-driven management (tumour size larger than 4 cm and stromal rete testis invasion), five-year relapse under surveillance ranges from about 6 to 8% without conventional risk factors to 15 to 20% with one or two ^[1].

About 70% are cured by orchidectomy alone. With lymphovascular invasion (LVI), relapse risk is about 50%; without it about 15% ^[1]. LVI is the single strongest risk factor.

• Surveillance: relapse around 30% overall (42% high-risk, 17% low-risk), with 92% of relapses within two years ^[1].
• Adjuvant chemotherapy: one cycle of BEP (cisplatin, etoposide, bleomycin) is preferred when adjuvant treatment is given. It reduces five-year relapse to around 2 to 3% in both risk groups ^[1].
• RPLND has a limited role in stage I: about 10% relapse if nodes are negative, up to 30% if tumour is in the nodes. It is reserved for men unsuitable for or unwilling to accept surveillance or chemotherapy, teratoma with somatic malignant transformation, or selected patients; where nodes are positive, adjuvant chemotherapy of at most two cycles may be added ^[1].
• Contralateral biopsy is not routine. It is discussed with high-risk men (small testis under 12 mL, cryptorchidism history); it is unnecessary over 40 without risk factors ^[1].
• GCNIS in the contralateral testis: if the other testis is normal, observe or remove; in a solitary testis, radiotherapy 18 to 20 Gy in 2 Gy fractions treats GCNIS but leaves the man infertile and at risk of Leydig-cell insufficiency ^[1].

• With enlarged nodes under 2 cm and normal markers, observe for 6 to 8 weeks and only treat if metastasis is unequivocal (increasing nodes, marker rise) - many small nodes are reactive ^[1].
• Radiotherapy remains an option: 30 Gy for stage IIA and 36 Gy for stage IIB, with 5-year relapse-free rates of 92% and 90% respectively; a reduced dose of 27 Gy has higher relapse ^[1].
• Chemotherapy - BEP x 3 or EP x 4 - has relapse rates of 0 to 8% for IIA and 8 to 14% for IIB, with 99% survival, and is at least as effective with potentially less long-term toxicity ^[1].
• Primary RPLND for stage II seminoma remains experimental and belongs in expert centres and trials.
• De-escalation strategies (PET-based, involved-node radiotherapy) are still under evaluation.

• Equivocal small nodes (under 2 cm) with normal markers may be watched for 6 weeks.
• Marker-negative disease: bilateral nerve-sparing RPLND by an experienced surgeon is the recommended initial treatment - up to 20% are down-staged to pN0, teratoma patients avoid chemotherapy entirely, and adding adjuvant chemotherapy (at most two cycles) reduces relapse from 12 to 40% to 0 to 4% ^[1].
• Marker-positive or IIB disease is treated up front as metastatic (usually BEP x 3).

Standard treatment is cisplatin-based chemotherapy, chosen by IGCCCG group ^[1]:

• Good-risk seminoma and non-seminoma: BEP x 3 (three 21-day cycles) or EP x 4 where bleomycin is contraindicated.
• Intermediate-risk: BEP x 4, or VIP x 4 if bleomycin is contraindicated.
• Poor-risk non-seminoma: BEP x 4, or VIP x 4 if bleomycin is contraindicated.
• With unfavourable marker decline after the first cycle, dose-intensification may be used. Very high-risk presentations (mediastinal primary, brain metastases) belong in specialist centres on protocols.
• Thrombosis prevention on chemotherapy: high-VTE-risk cancer patients may benefit from an anticoagulant (apixaban, rivaroxaban or low-molecular-weight heparin), but metastatic germ-cell patients were under-represented in the trials, so the decision is individual; avoid long-term central venous catheters where possible ^[1].

• Non-seminoma: any residual mass over 1 cm on cross-sectional imaging must be resected (about 7% contain active cancer, 33% teratoma, 40% necrosis or fibrosis). Surgery should be performed within 6 to 8 weeks of the last cycle ^[1].
• Seminoma: monitor with imaging and markers. Use FDG-PET for residual masses over 3 cm at least 2 months after chemotherapy (very good negative predictive value, poor positive predictive value - do not act on PET alone). Progressing or marker-rising disease needs salvage therapy ^[1].

Surveillance is lifelong in spirit: most relapses occur within two years, and very late relapse is 0.5%. Minimal schedules are, for example ^[1]:

• Stage I seminoma on surveillance or after adjuvant treatment: markers with a clinician visit twice in years 1 to 3 and once in years 4 and 5; abdominopelvic MRI or CT twice in year 1, twice in year 2, once at 36 months and once at 60 months.
• Stage I non-seminoma on surveillance: markers four times in years 1 and 2, twice in year 3 and one to two times in years 4 and 5; chest imaging for high-risk men; abdominopelvic imaging twice in year 1, at 24 months, at 36 months and at 60 months.
• After adjuvant or curative treatment for advanced disease: markers four times in years 1 and 2 and twice in years 3 to 5, with imaging planned around known metastatic sites.

• Discuss sperm banking with every man before starting treatment ^[1]. Baseline semen quality is often already impaired. Storage should still be offered to men receiving only orchidectomy if future fertility matters to them.
• Orchidectomy alone usually leaves fertility intact in the remaining testis; chemotherapy, radiotherapy and retroperitoneal surgery can damage spermatogenesis or ejaculation.
• Testosterone levels should be checked during follow-up, and hypogonadism treated.
• Testis-sparing and deferred radiotherapy for GCNIS are deliberately traded against cancer risk in selected men in a solitary testis, after informed consent.

More than 95% of men in Western Europe are cured, outliving a diagnosis made between 18 and 40 years of age ^[1]. Survivors treated with chemotherapy have more adverse health outcomes than men cured by surgery alone: hypertension, hyperlipidaemia and testosterone deficiency, while Raynaud phenomenon and hearing loss are contributed to by modifiable factors such as smoking and noise exposure ^[1]. A written survivorship plan should cover late effects, lifestyle, recurrence risk and cancer-specific follow-up ^[1]. When bleomycin or cisplatin have been used, respiratory and renal function deserve attention as part of local follow-up.

• Local and regional spread: para-aortic and retroperitoneal nodes, with compression or displacement of ureters (hydronephrosis), duodenum or great vessels.
• Distant metastases: lung, liver, bone and brain, especially in non-seminoma and with high beta-hCG.
• Transformation risk: post-pubertal teratoma can show somatic malignant differentiation, and growing teratoma syndrome can appear after chemotherapy.
• Treatment complications: cisplatin nephrotoxicity, neurotoxicity and ototoxicity, bleomycin pulmonary toxicity, hypogonadism, infertility and second malignancy after radiotherapy; restricted use of adjuvant radiotherapy and careful staging reduce these.
• GCNIS in the contralateral testis can produce a metachronous contralateral tumour, which is why high-risk men are monitored.

Five-year relative survival in Western Europe is about 95% ^[1]. Survival in stage I disease approaches 100% regardless of which management option is chosen ^[1]. Even metastatic, poor-prognosis non-seminoma is cured in about two thirds of men with modern cisplatin-based chemotherapy ^[1]. Once cured, the main issues over the following decades are late effects, fertility and quality of life rather than cancer recurrence.

• There is no high-quality evidence for population screening; instead, encourage testicular self-examination, especially in high-risk groups (cryptorchidism, personal or family history of testicular cancer) ^[1].
• Orchidopexy in childhood moves the undescended testis into the scrotum; whether it reduces cancer risk is debated, but it makes examination possible and corrects the anatomic anomaly.
• Counsel first-degree relatives of affected men, particularly in familial cases, about self-examination.
• Avoid unnecessary scrotal surgery or biopsy for testicular lesions; these distort staging rather than prevent disease.

• Children. Malignant testicular tumours in boys are uncommon (roughly 1 to 2% of childhood cancers). Yolk sac tumours and teratomas predominate, and the adult GCNIS-derived pathway does not apply; management is specialist and organ-sparing where feasible.
• Solitary testis or bilateral disease. Testis-sparing surgery and deferred radiotherapy for GCNIS are used so fertility and endocrine function can be protected; cancer risk is deliberately traded and only after informed consent.
• Older men. Consider primary testicular lymphoma, the commonest testicular malignancy in men over 60, and stromal tumours. AFP and beta-hCG are typically normal, so histology and a lymphoma work-up matter ^[2].
• HIV infection increases the risk of primary testicular lymphoma and affects response to treatment.
• Women partners. A partner's pregnancy does not change the treatment; sperm banking before chemotherapy remains essential.

In many low- and middle-income settings, testicular cancer remains a lethal disease despite being curable. A Sudanese cohort reported a median delay of 6 months from symptom onset to diagnosis, 64% stage III disease and an outcome of 44% remission with more than a third of patients dying, against 85 to 95% five-year survival in the West ^[4]. Barriers include lack of awareness, cultural stigma around male reproductive health, distance to specialist care, poverty, and shortages of imaging and drugs ^[4].

Practical adaptations that respect international guidance:

• Treat any solid testicular mass as malignant until proved otherwise and perform inguinal orchidectomy; it serves as both diagnosis and therapy and is feasible in most settings.
• Check scrotal ultrasound first and markers (AFP, beta-hCG, LDH) before any intervention, including orchidectomy ^[4].
• Staging without CT: when CT is unavailable, chest X-ray and abdominal ultrasound can triage. Normal markers make skip metastasis unlikely, so a chest film may suffice for stage I seminoma, although CT remains preferred ^[4].
• In low-resource settings, a scrotal approach is sometimes used because a solid mass was mistaken for a hydrocele. If this happens, re-evaluate at a specialist centre; re-excision of scrotal skin with adjuvant treatment can still achieve cure ^[4].
• Cisplatin-based chemotherapy is available in many low-income countries and is highly effective; the greater problem is usually transporting and accommodating patients for prolonged treatment ^[4].
• Radiotherapy facilities may be distant: arrange referral, or plan combination treatments that can be delivered locally.
• Centralise complex cases - poor-prognosis, metastatic, or RPLND candidates - in high-volume centres where possible.
• Promote testicular self-examination and awareness among young men, since late presentation is the single biggest driver of mortality ^[4].

• Testicular cancer is the commonest solid cancer in men aged 15 to 44 and is highly curable.
• Risk factors group in the testicular dysgenesis syndrome: cryptorchidism, previous GCT/GCNIS, family history, hypospadias, impaired fertility.
• Germ-cell tumours dominate (90 to 95%); non-germ-cell tumours (Leydig, Sertoli, lymphoma in older men) are the exceptions.
• Seminoma and non-seminoma behave and are treated differently.
• Tumour markers AFP, beta-hCG and LDH support diagnosis, staging and monitoring; pure seminoma never raises AFP; half-lives allow post-orchidectomy interpretation.
• Diagnosis: scrotal ultrasound, markers, staging CT; radical inguinal orchidectomy. Never a scrotal biopsy.
• Stage, including the post-orchidectomy marker level (S), and the IGCCCG risk group guide treatment.
• Stage I seminoma: surveillance preferred; carboplatin AUC 7 is an alternative; avoid radiotherapy in young men.
• Stage I non-seminoma: LVI predicts relapse; single-cycle BEP cuts relapse to 2 to 3%; RPLND reserved for selected cases.
• Metastatic disease: cisplatin-based BEP or EP by risk group; residual non-seminoma masses over 1 cm need surgery.
• Fertility must be addressed before treatment with sperm banking.
• Cure exceeds 95% in Western Europe, but late effects and survivorship matter.
• Low-resource care hinges on early presentation, inguinal orchidectomy and adapted staging.

Renal cell carcinoma; bladder cancer; prostate cancer; benign prostatic hyperplasia; erectile dysfunction; urinary tract infection; nephrolithiasis; hydronephrosis; palliative care and survivorship.