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Testicular cancer grows in the testes, the glands within the scrotum that produce sperm and hormones like testosterone. While this is a relatively rare cancer overall, affecting about 1 in 250 men and boys, it is unique because it primarily impacts younger and middle-aged individuals. Understanding how these cellular changes begin and recognizing your specific risk profile are essential steps in maintaining your health and ensuring early clinical detection.

Quick Facts: Testicular Cancer Causes & Risk Factors

  • Germ cell origins: Approximately 90% of all testicular cancers begin in the germ cells, which are the specialized cells responsible for producing sperm.
  • Primary age demographics: This disease possesses a unique age profile; nearly 50% of all diagnosed cases occur in young men between the ages of 20 and 34.
  • Distinct racial variations: For reasons clinical researchers are still investigating, white men have a substantially higher statistical risk, being 4 to 5 times more likely to develop testicular cancer than men of other races.
  • Limited lifestyle ties: Unlike most common malignancies, standard lifestyle variables like tobacco use or obesity have no proven link to the development of testicular tumors.

What causes testicular cancer?

The vast majority of testicular cancers originate in the germ cells—the specialized cells located within the tiny tubes of the testicles that are responsible for producing sperm. The process typically begins as a pre-invasive condition known as germ cell neoplasia in situ (GCNIS). In many cases, these abnormal cells actually form before birth but remain completely dormant for years, failing to mature into healthy sperm cells during early development.

The transition from dormant cells to active cancer is typically triggered during the hormonal shifts of puberty or early adulthood. Sudden mutations disrupt the cells' DNA, damaging the genetic blueprint that controls how they divide. Instead of completing their normal lifecycle, these mutated germ cells begin to multiply uncontrollably, tightly packing together to form a physical mass within the testicular tissue.

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Clinically, these abnormal growths mature into one of two primary types of testicular germ cell tumors:

  • Seminomas: These tumors tend to grow and spread at a slower, more predictable rate and are highly responsive to radiation therapy.
  • Non-seminomas: These are more aggressive tumors made up of various embryonic cell types (like embryonal carcinoma, yolk sac tumor, choriocarcinoma, or teratoma) that tend to develop and spread much earlier.

While oncologists thoroughly map this cellular progression, the exact environmental, chemical, or biological catalyst that triggers the initial DNA mutation in these germ cells remains the focus of intensive ongoing research.

young male with risk factor talks to doctor

Testicular cancer risk factors

While an individual may possess one or more risk factors, their presence does not guarantee a cancer diagnosis. Instead, identifying these variables helps clinical teams establish a precise baseline health profile and guides recommendations for ongoing surveillance. Oncologists classify these influences into two distinct categories: non-modifiable risk factors, which are inherent biological or genetic traits, and modifiable risk factors, which involve behavioral or environmental choices.

Men should perform self-exams and report any unusual masses or concerns to their doctor.

Testicular Cancer Non-Modifiable Risk Factors

The vast majority of documented risks for testicular cancer are entirely unchangeable, rooted in congenital development, genetic inheritance, or demographic baselines. These variables include:

  • Undescended testicle (cryptorchidism): This condition occurs when one or both testicles fail to descend into the scrotum before birth, remaining trapped in the abdomen or groin channel. Men born with cryptorchidism face a significantly higher risk of developing a malignancy. Performing an orchiopexy, a surgical procedure to relocate the testicle into the scrotum, during early childhood can help lower this baseline risk.
  • Congenital structural variations (hypospadias): Being born with hypospadias, a relatively common birth defect where the urethral opening forms on the underside of the penis rather than the tip, is statistically associated with a heightened incidence of testicular tumors.
  • Personal and family medical history: Surviving cancer in one testicle increases the statistical probability of developing a secondary primary tumor in the opposite testicle later in life. Additionally, having an immediate blood relative, such as a father or brother, who has been diagnosed with the disease elevates an individual's risk. Certain inherited genetic conditions, most notably Klinefelter syndrome, are also strongly tied to increased susceptibility.
  • Immune system health: Men living with HIV or active AIDS experience a higher statistical risk of developing testicular tumors, as compromised immune surveillance diminishes the body's natural ability to destroy early abnormal cell growths.
  • Age: While testicular malignancies can develop at any stage of life, the disease exhibits a unique age profile. Approximately half of all clinical diagnoses occur in young adults between the ages of 20 and 34.
  • Race and ethnicity: Marked epidemiological disparities exist within this disease profile. For reasons clinical researchers are still actively investigating, Caucasian men experience a dramatically higher statistical risk, developing testicular cancer at four to five times the rate of Black, Asian, or Hispanic men.

Testicular Cancer Modifiable Risk Factors

Unlike many common cancers, testicular cancer has no proven connection to everyday lifestyle choices. Standard health habits, such as smoking, diet, exercise, or weight management, do not appear to influence your baseline risk for developing these tumors.

For this reason, there are currently no definitive lifestyle changes that can prevent testicular germ cell tumors from forming. While a few isolated studies have explored potential minor links to heavy alcohol consumption (defined as 14 or more drinks per week) or diets unusually high in saturated fats, the overwhelming medical consensus is that behavioral factors do not play a role. Because you cannot prevent these tumors through lifestyle modifications, performing regular testicular self-examinations and promptly reporting any localized swelling, new lumps, or structural changes to a physician remains your most effective proactive habit.

Testicular cancer care at Moffitt Cancer Center

Moffitt’s Urologic Oncology Program offers testicular cancer screening for men who have an elevated risk of developing the malignancy. In fact, our testicular cancer specialists can help patients assess their own unique risk profiles and develop appropriate surveillance or treatment plans, if necessary. Our testicular cancer program offers a complete range of advanced diagnostic tools as well as treatment methods in a single, convenient location. What’s more, each patient with testicular cancer receives a treatment plan that’s tailored to their specific health condition and other factors.

Moffitt is a nationally recognized leader in cancer research, diagnosis and treatment. As the only National Cancer Institute-designated Comprehensive Cancer Center based in Florida, Moffitt participates in an extensive array of clinical trials, which means our patients often have access to groundbreaking treatments that are not widely available at other hospitals. 

For more information about the risk factors for testicular cancer, call 1-888-663-3488 or complete a new patient registration form to meet with one of our highly specialized oncologists. You do not need a referral to visit Moffitt Cancer Center.

References

National Institutes of Health – A case-control study of diet and testicular carcinoma
American Cancer Society – Can Testicular Cancer Be Prevented?