Testicular cancer (TC) is the most frequently diagnosed solid tumor in young men, typically between the ages of 15 and 35. The disease originates in the germ cells, which are responsible for producing sperm. While the precise cause remains unknown, researchers have identified several risk factors rooted in developmental history and cellular changes that increase susceptibility.
Primary Developmental Risk Factors
The most significant risk factor for testicular cancer is cryptorchidism, a condition where one or both testicles fail to descend into the scrotum before birth. This developmental abnormality is associated with a three to sevenfold increase in cancer risk compared to the general population. The risk stems from an underlying problem in germ cell development, known as testicular dysgenesis, rather than just the misplaced position.
The elevated temperature of the body cavity, compared to the cooler scrotum, inhibits normal germ cell maturation, contributing to the risk. If only one testicle is undescended, the risk is highest there, but the normally descended testicle still carries a slightly increased risk. Early surgical correction, known as orchiopexy, before puberty can reduce the risk, but it does not eliminate it because the underlying cellular abnormality persists.
Other conditions related to Testicular Dysgenesis Syndrome (TDS), which involves disruptions in fetal development, are weakly associated with a higher risk. These include hypospadias and specific forms of male infertility. These associations suggest a common developmental pathway may be flawed in men who later develop the cancer.
Biological Precursors and Inherited Susceptibility
The immediate precursor lesion for most testicular germ cell tumors is Germ Cell Neoplasia In Situ (GCNIS), a non-invasive condition. GCNIS consists of abnormal germ cells confined within the seminiferous tubules, the structures where sperm production occurs. This condition is present in the tissue surrounding 90 to 95 percent of invasive testicular cancers.
GCNIS is not cancer, but it carries a high probability of progression; roughly 50 percent of men with untreated GCNIS will develop invasive cancer within five years. The risk of developing a second tumor in the healthy testicle is approximately 5 percent, which is often linked to the presence of GCNIS in that testicle.
Inherited susceptibility plays a distinct role in the disease’s etiology. Men who have a first-degree relative, such as a father or brother, with a history of testicular cancer face a significantly increased risk, sometimes up to 8 to 12 times higher. While researchers have identified genetic markers that correlate with this family history, the full spectrum of inherited risk factors is not yet completely understood.
Addressing Common Misunderstandings
Contrary to frequent concern, physical trauma, such as a sports injury or a direct blow to the testicles, does not cause the disease. An injury may draw attention to an existing, painless tumor, leading to the false conclusion that the trauma caused the mass.
Similarly, there is no established link between having a vasectomy and an increased risk of developing testicular cancer. Extensive studies have concluded that the rate of cancer in men who have had a vasectomy is no higher than in the general male population. Other non-causal factors include infection, heavy physical activity, or wearing tight clothing.
Demographic data reveals certain risk patterns that influence incidence, though they are not direct causes. Testicular cancer is overwhelmingly a disease of younger men, with the highest rates occurring between the ages of 15 and 35. Furthermore, the incidence is highest among Caucasian males in the United States and Europe compared to men of African American or Asian descent.