The risk factors that heighten your chances of developing testicular cancer
If you were to pose this simple question to your doctor, you would get the response that science does not know for sure what triggers cancer in the testes. But if you were to dig a little deeper, you may be drawn into a discussion on chromosomes and genes, the basic building blocks of life, and how mutational changes (wholly beyond human control) can affect genetic behavior.
Unraveling the genetic puzzle of testicular cell behavior might reveal the core reasons why our testes turn cancerous. However, till that breakthrough happens, all that medical specialists can do is evaluate studies and identify certain risk factors that are seen to increase the chances of men developing testicular cancer.
What Happens Within Cancerous Testes
The testicles are a pair of spheroid glands enclosed within the loose folds of the skin of the scrotum beneath the male penis and are held in place by a thick spermatic cord that brings nerves and blood vessels to the testes. The testes control the development of predominantly male sexual features and oversee libido and sexual drive. They are also responsible for producing the male sex cells or sperm.
Germ cells are specialized cells that line an intricate spiraling maze of tubular structures within the testes. Over time, these germ cells transform into sperm that are moved along the epididymis (a larger tubular structure) before being emptied into the vas deferens, large paired ducts that transport matured sperm to the seminal vesicle. Here, the sperm combine with viscous seminal fluid and prostate gland secretions to form a thicker semen that is ejaculated through the urethral opening shortly after the male reaches his sexual climax.
In cancerous testes, the germ cells that are supposed to mature into sperm cells suddenly abandon their primary role and switch to replicating themselves unceasingly – something they were not originally programmed to do. They eventually form clusters of cancerous cells or tumors that disrupt testicular functioning. These tumors harden the testes and make the surface appear rough and swollen.
The Genetic Basis of Testicular Cancer
When the female egg is fertilized by a male sperm, the resulting embryo contains two sets of 23 chromosomes, one set contributed by each parent. What we observe outwardly in a baby as parental traits reflects the baby’s shared inheritance. But the genetic influence exerted by these chromosomes goes much deeper than physical features.
Scientists have observed that there are specific genes (chemicals) within the chromosomes that control cell growth and cell division (oncogenes), and genes that trigger cell destruction (tumor suppressors) upon aging. For unknown reasons, mutations cause changes that make these genes forget when to switch off cell division or when to trigger cell death, and this could explain why testicular tumors proliferate wildly and uncontrollably. Only cells containing mutated chromosomes and genes show this replicating characteristic.
Moreover, it has been observed that tumorous testicular cells possess extra copies of the same genes and some additional genes. Their existence is a mystery, and their function is still being researched.
The Factors That Enhance the Risk of Developing Testicular Cancer
Though the fundamental reasons provoking testicular cancer remain in the realm of theory and speculation, doctors are unanimous that there are risk factors that multiply the chances of men developing testicular cancer.
The presence of a high-risk factor doesn’t mean that you are certain to develop some form of cancer. Many men in high-risk categories do not develop any sign of cancer and continue to lead normal lives, while those unexposed to any risk factor may suddenly develop cancer. But doctors do tend to agree that falling under a high-risk category automatically predisposes you to testicular cancer.
The following are the major risk factors that are believed to trigger cancer in the testes. If you show any one or more of these features, you need to screen yourself medically to rule out testicular cancer.
Cryptorchidism (Undescended Testes)
During fetal development and just prior to birth, the testes located in the abdomen gradually descend and take up their permanent position within the scrotal sac. In some cases, for unknown reasons, the testes remain in the groin area the entire time. It may take a year or so after the baby is born for the testes to descend, although sometimes, they do not do so at all. Undescended testes have the potential to create male fertility problems because these testes are unable to grow sperm at normal body temperatures. Healthy sperm can only be produced by testes that have properly descended into the scrotal folds.
Orchiopexy is the procedure that corrects this anomaly and places undescended testes in their rightful positions. Men with this uncorrected problem, and who thereby experience difficulty in impregnating women, are at a higher risk of developing cancer in the undescended testicle(s).
A Known History of Cancer in Past Generations
Having a father or brother or some other male relative with testicular cancer spikes your chances of developing the cancer. But this is not a necessary condition, as people without any incidence of cancer in their families have developed cancer of the testes.
The HIV Infection
An HIV infection severely compromises the immune system and impairs the ability of the body to ward off threats. The reduced immune protection may trigger oncogenes that precipitate cancer of the testes.
This is also called carcinoma in situ (CIS). In this condition, germ cells appear abnormal but are locked within the tubular structures of the testes, and do not invade other tissues. As there is no outward swelling or discomfort, the only way to diagnose CIS is through tissue biopsies or imaging tests that may be conducted when infertility is being probed or when a structural abnormality is being assessed. If an individual exhibits problems in impregnating women, he needs to be medically evaluated for CIS.
Cancer That Recurs
The risk of getting testicular cancer is higher if you have already been treated for cancer (and cured) in one of the testicles. This happens in around 4 percent of cases where cancer rebounds in the remaining testicle.
Racial Profile and Age
For unknown reasons, the prevalence of testicular cancer is highest in Europe and the United States, and it affects white males many times more than it does Asians or African Americans. An American white male aged between 20 and 35 labors under a far higher risk of testicular cancer than his counterparts in Africa and Asia.
In this rare disorder, the male is born with additional X chromosomes that in the long term regress male sexual characteristics and libido, and cause infertility. Those afflicted with this condition are at a higher risk of developing breast and testicular cancer before they reach 30 years of age.
Body Size and Stature
In clinical studies, body mass was not shown to have a significant correlation with the incidence of testicular cancer, but increased height (tallness) appears to raise the risks. Consumption of a high protein diet in early childhood seemed to up the risk in tall men.
Strenuous Activity and Physical Injury
It is a myth that physical trauma such as a sports injury to the testicles triggers cancer. Studies have not revealed any correlation between physical trauma and cancer of the testes. On the contrary, it is on record that an active lifestyle strengthens the immune system, warding off many ailments, and thus significantly reduces the risk of testicular and many other forms of cancer.
- Unraveling the genetic puzzle of testicular cell behavior might reveal the core reasons why our testes turn cancerous. Till that happens, all that medical specialists can do is identify certain risk factors that are seen to increase the chances of men developing testicular cancer.
- The germ cells that are supposed to mature into sperm cells suddenly abandon their primary role and switch to replicating themselves unceasingly – something they were not originally programmed to do.