Genetic and Other Influences That Increase Your Risk of Testicular Cancer
Testicular cancer happens when germ cells within the male testicles start reproducing in an uncontrolled manner, resulting in a mass of tissue called a tumor. Germ cells are cells that eventually grow into sperm cells, and germ cell tumors account for more than 98 percent of all cancers affecting the male reproductive glands or testes. For unexplained reasons, testicular cancer occurs prominently in white males of American and North European origin, and figures are statistically lowest in males of African and Asian origin. While we are not sure on the exact causes of testicular cancer, we do know that certain genetic and physiological factors increase the risk of developing testicular cancer.
The Two Most Striking Risk Factors That Trigger Testicular Cancer
Being a white male between the ages of 15 and 34 makes you prone to developing testicular cancer. This is the period marked by heightened sexual maturity and sexual activity, yet the incidence of testicular cancer has been steadily climbing in this age group over the past few decades. The positive dynamic is that the survival rate is 98 to 100 percent, regardless of the stage of testicular cancer.
Being a white male of North European or American ancestry automatically places you in the high-risk category, and the risk remains high regardless of your geographical distribution. Men of Danish and Norwegian origins, for example, are ten times more likely to develop testicular cancer than their corresponding age groups in African and Asian societies. In North America, white males are more likely to develop testicular cancer than Native American tribes and Americans of African or Asian ancestry. The reasons still remain unexplained.
Risk Factors That Enhance Your Chances of Developing Testicular Cancer
In the normal course, the testicles descend into the scrotum just before birth, but in some males, this doesn’t happen. Around 14 percent of testicular cancers can be traced to a history of cryptorchidism, a condition in which one or both testicles fails to descend into the scrotum outside the abdominal cavity. It is also observed that surgically correcting the anomaly (through an Orchiopexy) within a year after birth reduces chances of developing cancer in the testes.
Family Propensity to Reproductive Cell Cancer
Having a grandfather, father, or brother that suffered reproductive cell cancer significantly increases your risk of developing testicular cancer. Having a white male ancestry increases your risk tenfold compared to generations having African or Asian origins, although the reasons for this are unclear.
Own History of Testicular Cancer
Being operated on for the removal of a cancer-affected testicle places you at risk of developing cancer in the healthy testicle. The silver lining is that testicular cancer is curable, regardless of the stage of its detection, something that may not be true of many other cancers.
The Silent Undetected Carcinoma in Testes
Carcinoma in situ or CIS is a kind of germ cell tumor that grows within the seminiferous tubules without creating pain, swelling, or hardness in the testes. What provokes CIS to affect some individuals more than others is still a mystery. For the better part of its existence, CIS remains noninvasive. The only way CIS can be detected is through a testicular biopsy, a procedure that becomes imperative when infertility prompts a person to visit the doctor. Because CIS is not as life-threatening as most other cancers, doctors usually wait it out and prefer to examine the results of periodic blood tests and scans to follow the tumor’s progress.
Stone Formation in the Testes
Microlithiasis, the accumulation of clusters of calcium deposits within the testes, has been touted as a risk factor based on studies that found excess calcium concentration in patients treated for testicular cancer. However, this is by no means the universal norm, because apparently healthy males with normal testicular function have been reported to be carrying high deposits without elevating their cancer risk. Hence, Microlithiasis as an independent risk factor triggering testicular cancer may have no basis.
Studies indicate that AIDS patients have a proclivity for testicular cancer, particularly with the seminoma variety, which spreads slowly and is 100 percent curable. Testicular cancer may be triggered due to the impaired immune function of the body and because AIDS triggers gradual testicular degradation.
It is generally accepted that testicular cancer affects the quality and output of semen, and it is also responsible for diminishing the production of testosterone, which adversely affects male physiology in multiple ways. It must also be acknowledged that a history of testicular dysfunction can also become a risk factor for developing testicular cancer.
Many testicular cancer patients suffer from abnormal growth cycles (impaired spermatogenesis), where sperm production and maturation gets delayed, and this, in turn, creates a host of side effects, such as diminishing libido, erectile dysfunction, and male infertility. The abnormality itself becomes a risk factor capable of triggering cancer at later stages.
Owing to a weakness in the abdominal wall muscles, a part of the abdominal organs like the colon may protrude downward into the scrotal sac. This creates pain and swelling, and it strangulates the blood supply to the testes, leading to their wastage or atrophy. The incidence of an inguinal hernia has been observed in larger numbers of patients, and it is classified as a risk factor triggering testicular cancer.
Testicular Cancer Linked to Congenital Abnormalities
- Klinefelter Syndrome
This is an abnormality where the male cell, which normally possesses one X chromosome and one Y chromosome, is endowed with an extra X chromosome, which triggers physiological changes unusual for males. Such men will display a softer voice, less body hair, a smaller sex organ, wider hips, and larger breasts. Their sexual drive will be diminished, and they will be incapable of fathering children. Klinefelter syndrome becomes a risk factor that can trigger testicular cancer in adulthood.
Down syndrome is a chromosomal abnormality that produces distinctive facial features, a shorter stouter neck, and impaired mental abilities. Clinical studies have proved that the abnormality affects testicular growth in the fetus, leading to impaired germ cell growth, which can later develop into testicular cancer.
Hypospadias is a congenital abnormality where the penis may develop an angular deviation, and the urethra doesn’t open from the head of the glans. The foreskin also fails to cover the glans completely. Males having this abnormality are at much higher risk of developing testicular cancer than normal males.
Testicular Cancer Risk Is Higher in the Following Categories
- Males that are the first born and which do not have siblings, the risk diminishing in proportion to the rise in number of siblings
- Males that have identical twins
- Males that are born extremely prematurely
- Where mothers suffered excessive bleeding during pregnancy and delivery
- Where the fetus was exposed to higher than recommended levels of diethylstilbestrol (DES), a synthetic form of the female sex hormone estrogen administered to women to prevent premature delivery
The Last Word
Unlike many other cancers, it is quite difficult to predict what may trigger testicular cancer. However, clinical research has clearly established that there are high-risk factors that increase your chances of developing this form of cancer. Understanding these risk factors is the best way of identifying your weak spots so that you can take evasive action to ensure you survive this curable disease.
- Being a white male of Northern European or North American origin and falling in the age bracket of 15 to 34 years makes you a high-risk candidate for testicular cancer.
- A family history of reproductive cell cancer makes you prone to testicular cancer.
- Congenital abnormalities like Klinefelter syndrome, Down syndrome, and Hypospadias can predispose men to testicular cancer.