Testicular Cancer

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This blog is for informational purposes only and should not be taken as medical advice. Content is sourced from third parties, and we do not guarantee accuracy or accept any liability for its use. Always consult a qualified healthcare professional for medical guidance.

What is Testicular Cancer?

Testicular cancer originates in the testicles, the male reproductive organs responsible for producing sperm and testosterone, located within the scrotum. It primarily affects germ cells (sperm-producing cells) and is classified into seminomas (40-50%, slow-growing, radiosensitive) and non-seminomatous germ cell tumors (NSGCTs, 50-60%, including embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma). Mixed tumors and stromal tumors (Leydig/Sertoli cell, <5%) are less common. Testicular cancer is rare, representing 1% of male cancers, with approximately 9,700 new US cases annually in 2025. It predominantly affects younger men (ages 15-44, median age 34), with a 95% cure rate when detected early due to its high treatment responsiveness, though late-stage disease remains challenging.

Symptoms

Early symptoms include a painless lump or swelling in one testicle (most common, often pea-sized or larger), scrotal heaviness or aching, discomfort or dull pain in the scrotum or lower abdomen, and testicular size/shape changes. Less commonly, gynecomastia (breast enlargement from hormone secretion, seen in 5-10% of NSGCTs), back pain (from retroperitoneal lymph node spread), or lower extremity swelling (from venous compression) may occur. Advanced disease may cause weight loss, fatigue, shortness of breath (lung metastases), or abdominal masses. Symptoms can be subtle, often mistaken for epididymitis, hydrocele, or injury, leading to delayed diagnosis in 10-20% of cases. Regular self-exams are critical for early detection.

Causes

The exact cause is unknown, but genetic and environmental factors contribute. Key risk factors include cryptorchidism (undescended testicle, increasing risk 4-8 fold), family history (6-10 times higher risk with affected first-degree relative), prior testicular cancer (12-18% risk in contralateral testicle), and Klinefelter syndrome. White men have a 4-5 times higher incidence than Black or Asian men. Genetic alterations, such as KIT or KRAS mutations, drive tumor growth, with isochromosome 12p common in germ cell tumors. Environmental exposures (e.g., pesticides, endocrine disruptors) are under study, but no strong link exists. In 2025, research emphasizes testicular dysgenesis syndrome (linked to fetal development) as a unifying risk factor, with epigenetic changes like DNA methylation playing a role in oncogenesis.

Diagnosis

Diagnosis begins with a physical exam to assess testicular abnormalities, followed by scrotal ultrasound to differentiate solid masses (95% malignant) from cysts or benign conditions. Blood tests measure tumor markers: alpha-fetoprotein (AFP, elevated in 50-70% of NSGCTs), beta-human chorionic gonadotropin (β-hCG, elevated in 40-60%), and lactate dehydrogenase (LDH, indicating tumor burden). Imaging (CT/MRI of abdomen/pelvis, chest X-ray/CT) evaluates metastasis to lymph nodes (retroperitoneal, 70% of spread), lungs, or liver. Orchiectomy (surgical removal of the affected testicle) confirms histology and stage (I-III). Molecular testing for KIT or PD-L1 expression guides therapy. In 2025, AI-enhanced ultrasound improves detection sensitivity by 15%, and liquid biopsies (circulating tumor DNA) aid in detecting minimal residual disease (MRD) post-treatment, reducing false negatives.

Treatment

Treatment is highly effective, tailored to stage, histology, and risk. Stage I seminomas often require orchiectomy alone (95% cure rate) or adjuvant radiation/chemotherapy (carboplatin) to reduce recurrence to <5%. NSGCTs may need adjuvant chemotherapy (BEP: bleomycin, etoposide, cisplatin) for high-risk stage I. Stages II-III involve chemotherapy (3-4 cycles BEP, 80-90% remission), with retroperitoneal lymph node dissection (RPLND) for residual masses or NSGCTs. Radiation is less common for NSGCTs due to lower sensitivity. Metastatic disease uses high-dose chemotherapy and stem cell transplant (SCT) for relapsed cases. In 2025, immunotherapy (checkpoint inhibitors like nivolumab) achieves 20-30% response in platinum-refractory cases, and fertility-preserving techniques (sperm banking, testicular-sparing surgery) are standard. Supportive care manages chemotherapy side effects like neuropathy or infertility.

Future Outlook

In 2025, testicular cancer has a 95% 5-year survival rate overall, 99% for localized (70% of cases), 96% for regional, and 73% for metastatic disease. Advances in MRD monitoring reduce relapse rates by 10-15%, and targeted therapies (e.g., KIT inhibitors) improve outcomes in resistant seminomas. Research focuses on reducing long-term toxicities (e.g., cardiovascular risk, secondary cancers from chemotherapy), with trials exploring immunotherapy combinations and tumor vaccines. By 2030, precision medicine, including ctDNA-guided therapy and less toxic regimens, could achieve near-100% cure for early-stage and 85% for metastatic cases, with emphasis on quality-of-life improvements like fertility preservation and psychological support.

Sources

Cleveland Clinic’s “Testicular Cancer: Symptoms, Causes, Diagnosis & Treatment”; Mayo Clinic’s “Testicular cancer – Symptoms and causes”; NCI’s “Testicular Cancer Treatment (PDQ®)”; American Cancer Society’s “Testicular Cancer”; PMC’s “Testicular Cancer: Advances in Diagnosis and Treatment 2025”.