Testicular cancer starts when germ cells, the cells that normally develop into sperm, begin growing abnormally inside the testicle. There is no single behavior or exposure that “gives” you testicular cancer the way smoking causes lung cancer. Instead, the disease results from a combination of genetic predisposition, developmental factors that begin before birth, and possibly environmental influences. The median age at diagnosis is 33, and over half of all cases occur in men between 20 and 34.
What Happens Inside the Testicle
In most cases affecting young adults, the cancer traces back to a precursor condition where abnormal germ cells sit quietly inside the tiny tubes of the testicle. These cells carry extra copies of genetic material from chromosome 12, which appears to play a crucial role in driving their growth. For years or even decades, they can remain dormant. But once triggered, typically around or after puberty, they can progress into invasive cancer. About 50% of these precursor lesions become invasive within five years, and roughly 70% do so within seven years.
The two main types, seminomas and nonseminomas, both arise from this same precursor in postpubertal men. A rarer form occurs in men over 40 and involves a completely different genetic pathway, with changes on chromosome 9 instead.
Risk Factors You’re Born With
The strongest known risk factor is an undescended testicle (cryptorchidism), a condition present at birth where one or both testes fail to move into the scrotum. Men born with this condition face a four- to sixfold increased risk of cancer in the undescended testicle. Even the normally descended testicle carries a slightly elevated risk, roughly double the baseline. Surgery to correct the problem before puberty reduces the risk, but doesn’t eliminate it entirely. Men who had the correction still face about two to three times the normal risk.
Family history matters too. Having a father or brother with testicular cancer increases your own risk. Researchers at the National Cancer Institute believe this familial pattern comes from the combined effects of many genes, each contributing a small amount of risk. These genes appear to be involved in how the testes develop in the fetus and how sperm production is regulated later in life. There’s no single “testicular cancer gene” like the BRCA mutations linked to breast cancer.
Who Gets It Most Often
Age is the most striking demographic factor. The breakdown of new cases by age group tells a clear story: 51% of diagnoses occur between ages 20 and 34, another 25% between 35 and 44, and only about 3% in men over 65. It is overwhelmingly a young man’s cancer.
Race and ethnicity also play a role. Historically, non-Hispanic white men in the United States have had the highest rates. But that picture is shifting. Recent data show that incidence among Hispanic men has risen to match white men for the first time. Overall, the age-adjusted incidence rate in the U.S. climbed from 4.71 per 100,000 men in 1992 to 6.22 per 100,000 in 2021, a steady increase that researchers are still working to fully explain.
Environmental and Hormonal Exposures
The rising incidence across populations has pushed researchers to look beyond genetics. A leading theory centers on endocrine-disrupting chemicals, substances in the environment that interfere with hormone signaling during fetal development. Plasticizers called phthalates, found in many consumer products, are among the most studied. In lab and animal studies, these compounds impair the function of cells in the testes responsible for producing testosterone and a hormone called INSL3, which helps guide testicular descent in the fetus. Studies of boys born to mothers with higher phthalate exposure have found increased rates of cryptorchidism and other genital abnormalities.
The connection isn’t fully proven in humans, but the exposure to endocrine-disrupting chemicals is currently considered the leading explanation for why testicular cancer rates keep climbing worldwide. The idea is that these chemicals don’t cause cancer directly in adulthood. Instead, they may disrupt normal testicular development in the womb, setting the stage for abnormal germ cells that become cancerous decades later.
What About HIV?
Men living with HIV have historically faced a higher risk of one specific type, seminoma, with roughly double the expected rate in the general population. The risk was highest in men with advanced, untreated disease. Researchers believe this is tied to the immune system’s weakened ability to detect and destroy abnormal cells. With modern antiretroviral treatment, this elevated risk has largely disappeared. In the era of effective HIV therapy, seminoma rates among men with HIV are no longer significantly elevated compared to the general population.
Things That Don’t Cause It
Physical injury to the testicles does not cause testicular cancer. Specialists at Memorial Sloan Kettering Cancer Center have addressed this directly: there is no evidence linking trauma to testicular cancer development. Getting hit by a ball, carrying a phone in your pocket, using skin creams, horseback riding, and cycling are all unrelated to risk. What sometimes happens is that an injury prompts a man to examine the area or get an ultrasound, which incidentally discovers a tumor that was already growing.
Screening and Early Detection
Unlike many cancers, there is no recommended routine screening for testicular cancer. The U.S. Preventive Services Task Force actually recommends against screening in adolescent and adult men, giving it a grade D rating. The reasoning is straightforward: testicular cancer is rare enough and curable enough, even when caught at later stages, that screening an asymptomatic population would produce more harm from false positives and unnecessary procedures than it would benefit.
That said, being aware of what your testicles normally feel like means you’re more likely to notice a change. A painless lump or swelling, a feeling of heaviness, or a dull ache in the lower abdomen or groin are the most common first signs. Most lumps in the testicle are not cancer, but any new, persistent change is worth getting checked with an ultrasound, which can distinguish a solid tumor from a harmless cyst quickly and painlessly.