Testicular cancer
The incidence of testicular cancer is rising worldwide at two per cent per year for the last 50 years, for unknown reasons. Younger men, aged between 20 and 40 years, have the highest risk of developing testicular cancer, the second most common cancer in this age group.
What is testicular cancer?
Testicular cancer appears as a painless hard lump or swelling on a testicle, part of a man’s reproductive system. It can be a lump, the size of pea or much larger. The lump is a growth or tumour formed by abnormal cells that have multiplied. Most testicular lumps are not cancer.
What are the types of testicular cancer?
There are different types of testicular cancer, depending on which type of cell the cancer starts in. Testicular cancers from reproductive cells are the most common. These are called testicular germ cell tumours.
Ninety-five per cent of testicular cancers are germ cell tumours, starting in the so called ‘germ cells’ that normally develop into sperm. There are two main sub-types of germ cell tumours:
- Non-seminoma tumours mostly occur in younger men aged from their late teens to early 20s. These tumours grow more quickly.
- Seminoma tumours usually occur in men aged 25-45 years, and are slower growing.
What causes testicular cancer?
The specific causes of testicular cancer are not known, though it most commonly arises when the cells that normally develop into sperm in adult men, the reproductive cells, remain undeveloped. Some factors that increase the likelihood of developing testicular cancer include
- Family history
- Undescended testicle as an infant
- Infertility
- Having cancer in one testicle makes it more likely to develop in the other.
How is testicular cancer diagnosed and treated?
A doctor will perform a physical examination. Other tests include ultrasound, blood, CT or MRI scan and surgery.
Testicular cancer is one of the most treatable cancers. Treatment depends on the how far the cancer has advanced or its stage.
Stage 1 | the cancer is only in the testicle.
Stage 2 | the cancer has spread to pelvic region or stomach lymph nodes.
Stage 3 | the cancer has spread to other areas of the body.
Treatment at stage 1 is removal of the testicle, while stages 2 and 3 may include chemotherapy and/or radiation.
While 95 per cent of men who get testicular germ cell tumours can be cured, the prognosis or outlook is poor for men who relapse.
Testicular cancer and male infertility
While the survival rates from testicular cancer are excellent, with a 90 per cent cure rate, it can still have life-long consequences that include lower fertility and a higher risk of poor health in older age. In 2020, 928 Australian men were diagnosed with testicular cancer and 30 died from the disease.
Importantly, researchers have linked testicular cancer with male infertility.
Our testicular cancer research
Discovering the processes required to make healthy sperm is essential knowledge for reversing the rising incidence of testicular cancer and infertility rates, and for developing treatments to combat these.
Understanding why disrupting testis development can increase testicular risk
Molecular studies. Professor Kate Loveland is identifying the windows of development, from fetal life through to puberty, in which male reproductive function can be affected by environmental exposures that have consequences which reduce adult male fertility or health. The cells in a man’s testis that form one thousand sperm per heartbeat originate in the developing fetus and go through many transitions before they turn into swimming cells which can penetrate an egg and start a new life. The team’s research is uncovering the specific times and ways during transformation from a progenitor into a sperm when things can go wrong. In the case of testicular germ cell tumours, the first incidence occurs in the fetus, when something occurs to probably a few cells to stop them from maturing normally. They remain undetected until puberty when hormonal changes cause the cells to change into tumours.
Team | Professor Kate Loveland, Professor Mark Hedger, Associate Professor Patrick Western
Male fertility and testicular cancer
Molecular studies. Professor Loveland discovered the importance of a key cell signaling molecule, activin A, that is crucial for normal embryonic development and adult health, male fertility and testis cancer. By studying its actions during sperm development, this research revealed that activin A signals are altered in the germ cells that turn into tumour cells, instead of forming sperm, in the human testis. The discovery revealed that activin A is important for normal male fertility and may be suitable target for treatments in men with testicular cancer. Current research is investigating how different cells within the testis respond to disturbances that affect activin A signalling during fetal and infant life. The goal is to find new ways to limit the incidence of these tumours and reduce the risk of relapse.
Team | Professor Kate Loveland, Dr Sarah Moody, Penny Whiley
The yin and yang of testicular immune cells
Molecular studies. Professor Loveland’s team is exploring the roles of immune cells in normal testis development and how they contribute to testis pathologies, including influencing the progression of testicular germ cell tumours. The team has identified changes in the frequency, distribution and identity of immune cells during fetal testis development when these tumours can form, and as the tumours develop in the testes of adult men. Ongoing studies are characterising the molecular signatures of these cells to learn how they ‘talk’ to each other, as the team has shown germ cell tumours can produce factors that stop immune cells from fighting off foreign cancer cells, so that they instead support tumour spread.
Team | Professor Kate Loveland, Professor Mark Hedger
The foundations of testis growth: Steroids in the fetal testis
Soon after the testes form in the male fetus, testosterone is produced to masculinise the embryo, affecting growth of the brain and other organs, as well as penis formation. Professor Loveland’s group discovered that activin A is directly responsible for driving testosterone production in the testes growing in the womb. It promotes synthesis of two enzymes crucial for the final steps of testosterone synthesis. The absence of activin A resulted in an abnormal steroid environment during a window of development when the program of masculinisation is initiated in male offspring.
Team | Penny Whiley, Professor Kate Loveland, Dr Liza O’Donnell, Dr Jennifer Hutchison
Testicular cancer collaborators
Support for people with testicular cancer
Hudson Institute scientists cannot provide medical advice.
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