UK Testicular Cancer incidence statistics
UK Testicular Cancer incidence statistics
This page presents testicular cancer incidence statistics by age and sex, histology, socio-economic deprivation, geographical variation and trends.The ICD code for testicular cancer is ICD9 186, and ICD 10 C62.
Testicular cancer incidence in the UK
Testicular cancer is a relatively rare cancer with 2,065 new cases registered in 2006 in the UK. 1-4 It is responsible for 1-2% of all male cancers. It has been estimated that the lifetime risk of developing testicular cancer is 1 in 210 for men in the UK. These were calculated on February 2009 using incidence and mortality data for 2001-2005 28.
Testicular cancer has several distinct features when compared with other cancers. Firstly, it has an unusual age-distribution, occurring most commonly in young and middle-aged men. Secondly, its incidence is rising, particularly in white Caucasian populations throughout the world, for reasons as yet unknown. And thirdly, testicular cancer is curable in the majority of cases.
In 2006 there were around 2,065 new cases of testicular cancer diagnosed in the UK. 4-7Table 1.1 shows the numbers and rates for the UK and its constituent countries. 1-4
Testicular cancer incidence by age
Around half (46%) of all cases occur in men under 35 years and over 90% occur in men under 55 years. Testicular cancer rarely occurs before puberty but it is the most common cancer in men aged 15-44 years. Incidence rates peak at around 17 to 18 per 100,000 in the 25-34 age group ( Figure 1.1). 1-4
This pattern of higher rates in younger men gradually developed during the twentieth century (see Figure 2.2 in the Mortality section).
Testicular cancer histology
95% of testicular tumours are germ-cell tumours (GCTs), 4% are lymphomas and the remaining 1% is composed of various rare histologies. Lymphomas are nearly always found in men aged over 50 and are generally treated as a different disease entity from GCTs.
GCTs can be divided into two main groups: about 40-45% are seminomas and a similar percentage are nonseminomas.
The nonseminoma group contains a variety of histological subtypes including malignant teratoma differentiated (MTD), malignant teratoma intermediate (MTI) and malignant teratoma undifferentiated (MTU).
Nonseminomas tend to occur on average ten years earlier than seminomas. Incidence of nonseminomas peaks in the 20-35 age group while incidence of seminomas peaks in the 30-45 age group. Some GCTs (10-15%) are a mixture of seminoma and nonseminoma and have a peak age incidence halfway between the nonseminomas and seminomas. They are usually classified and treated as nonseminomas.
GCTs are thought to develop from a non-invasive lesion called carcinoma in situ (CIS) of the testis (also called intratubular germ-cell neoplasia unclassified (IGCNU) and testicular intraepithelial neoplasia (TIN)), whose malignant transformation is likely to be influenced by hormones at or after puberty. 5, 6
Socio-economic deprivation and testicular cancer incidence
Data from men diagnosed in England between 2000 and 2004 show a deprivation gradient, with the highest incidence rates in the least deprived groups (7.2 cases per 100,000 in the least deprived compared with 5.5 in the most deprived). 7 However, there was no clear trend for Scottish data between 1986 and 1995. 8
Geographic variation in testicular cancer incidence
Although the incidence of testicular cancer is low throughout the world, it is estimated to have doubled in the last 40 years and there is appreciable variation between countries. 9
The highest rates of testicular cancer are reported for white Caucasian populations in industrialised countries, particularly in western and northern Europe ( Figure 1.2), while the disease is generally rare in non-Caucasian populations - the New Zealand Maoris being the exception. 10, 11
Overall, rates of testicular cancer in the developed regions of the world are five times higher than those in the less developed regions. Within North America, the consistently lower rates reported for black Americans compared with white Americans suggest a genetic component to the disease, while the rates for Asian and Hispanic men are intermediate between those of white and black Americans. 12
Within the European Union (EU), there is an approximately five-fold variation in incidence between countries with the highest and lowest incidence rates. For example, Denmark, Germany and Austria report age-standardised rates (ASRs) of around 10 per 100,000, while Lithuania, Estonia, Spain and Latvia have ASRs of around 2 per 100,000 ( Figure 1.3) 10, 13.
The UK ASR (6.9 per 100,000) is towards the upper end of those reported in the EU. A surprising finding is that there are appreciable differences between neighbouring countries and within countries. For example, the testicular cancer incidence rate in Sweden is more than double that of Finland 14, and regional rates in France vary from 2.8 to 7.9 per 100,000. 9
Across the UK and Ireland, higher rates of testicular cancer are reported in Scotland and the south of England, with lower rates in Ireland, London and the north of England. 15 Lower rates recorded in urban areas may reflect the fact that urban populations generally have a higher percentage of minority ethnic groups with a lower testicular cancer risk than the general UK population.
Trends in testicular cancer incidence
Large increases in incidence of testicular cancer have been reported in many countries around the world over the last 40 years including the USA, 16 Canada 17,Europe 18 Nordic countries, 19 Australia 20 and the UK. 21-23
On average, the increases are 1-6% per annum and are reported for both seminomas and nonseminomas. 18 Rises are mainly in young, white Caucasian populations, but since 1988, incidence for young, black Americans has also increased. 24
These trends appear to be influenced more by birth-cohort than period effects, with increasing risk for each generation of men born from the 1920s until the 1960s. 25
A dip in this continuous rise was recorded for men born during World War II in Denmark and Norway, who had a lower risk of testicular cancer than either previous or subsequent birth cohorts, suggesting that environmental and lifestyle factors affect risk.
For high risk countries there is evidence that the rate of increase has slowed over time 16,26 and in several countries ,including the UK, the most recent testicular cancer incidence rates have fallen slightly. 19
One exception to these trends is Switzerland, where the testicular cancer incidence rate is one of the highest in Europe. The rate has risen only slightly, from around 8.5 per 100,000 in the 1970s and 1980s to 10 per 100,000 in the 1990s, with no evidence of further increase. 26
Analysis of testicular cancer incidence trends by histology in eight European countries, including the UK, concluded that the trends were similar for both seminomas and nonseminomas and were based on birth cohort effects. However the declining rates seen in the 1990s in Switzerland, Denmark, Norway, Italy and Sweden were for nonseminomas only, a situation also reported for the USA. 16,27 As these tumours are diagnosed on average ten years before seminomas, it is possible that a decline in seminoma incidence will lag by ten years.
In Great Britain, the rise in the numbers of new cases of testicular cancer and the age-standardised rates (ASRs) between 1975 and 2006 is shown in Figure 1.4. 13
The annual number of new cases of testicular cancer in Great Britain more than doubled, from 850 to 2,014, between 1975 and 2006 although with a slight reduction between 2001-2003.
The ASRs show a similar trend rising steadily from 3.3 per 100,000 in 1975 to 6.9 per 100,000 in 2006.
When the rates are analysed by age, it is evident that the increase has occurred mainly in younger men ( Figure 1.5). 13
The greatest increase was for men aged 45-59: rates in this age group more than doubled from 2.6 per 100,000 males in 1975 to 6.3 per 100,000 in 2006.
UK Testicular Cancer mortality statistics
This page contains testicular cancer mortality statistics by age and trends.
Testicular cancer mortality by age
In 2007 there were 58 deaths from testicular cancer in the UK; 46 in England, 4 in Wales, 8 in Scotland, and none in Northern Ireland.( Table 2.1) 1-3 The overall UK death rate age-standardised was 0.2 per 100,000.
Most of the deaths occurred between the ages of 30-49 years, although 12 deaths occurred in males under 30 years old. ( Figure 2.1). 1-3
Testicular cancer mortality trends
Figure 2.2 shows the testicular cancer mortality trends from 1971 to 2007.
The introduction of platinum-based chemotherapy in the 1970s resulted in a dramatic fall in the death rate in the UK and other westernised countries.
Such falls in mortality following the introduction of effective treatment are seen in most developed countries, but not all at the same time, due to the inequitable distribution of resources and expertise between countries. 4
Mortality began to decline earlier in the USA than in the EU, and rates in Eastern Europe did not begin to decline until the late 1980s, resulting in the ‘avoidable’ deaths of several hundred young men each year. 5 The Japanese incidence and mortality rates are relatively low compared with the USA and Europe 6, but they also benefited from improved treatment: the mortality rate fell by 43% in Japanese testicular cancer patients aged 20-44 between 1975-79 and 1995-97. 7
Testicular Cancer survival statistics
This page presents testicular cancer survival statistics including one, five and ten year survival, survival by histology, and international comparisons.
One, five and ten-year testicular cancer survival rates
Since the introduction of combination chemotherapy in the 1970s, survival rates for testicular cancer have risen every year to cure rates of over 95%.
The latest population-based five- and ten-year survival rates for all patients registered in England and Wales are both 98% ( Figure 3.1) 1, 2.
Testicular cancer survival rates by histology
Much of the increase has been due to improvements in the treatment (see Treatment section) of ( metastatic testicular cancer ( Figure 3.2).
Before 1970, only around 5% of patients with metastatic testicular cancer survived, but around 80% survive today - a highly unusual result for a metastatic solid tumour. 3, 4
International comparison of testicular cancer survival rates
International comparisons reveal that testicular cancer is one of the few cancers for which survival rates in the UK equal or even exceed those recorded in Europe ( Figure 3.3). 1
Testicular Cancer risk factors
This page presents information on the risk factors for testicular cancer.
The dramatic increase in the incidence of testicular cancer has led to an intense search for its causes, but, as yet, no preventable risk factors have been found. Both environmental and genetic factors are likely to be involved.
Some groups of men are at increased risk of developing testicular cancer ( Table 4.1).
The risks for testicular cancer associated with age and race have already been described in the Incidence section. A previous diagnosis of testicular cancer increases the risk of developing a subsequent (metachronous) testicular tumour by around 12-fold. 1
Men with a previous extragonadal germ cell tumour (GCT) also have a higher risk. 2 Untreated carcinoma in situ (CIS)of the testis will almost certainly progress to malignancy: around half of all men diagnosed with CIS of the testis where it is not treated will develop testicular cancer within five years. 3, 4,47
Cryptorchism, a common congenital abnormality in males - at birth 6% of all male babies have undescended testes but most of these descend spontaneously by 3 months by which time only 1.6% of babies still have one or more undescended testes, or maldescent testicle (MDT), is one of a range of testicular abnormalities known to increase the risk of testicular cancer.
About 10% of GCT patients have a history of this condition. Cryptorchism is associated with a two- to 11-fold increased risk of testicular cancer in most studies, with higher risk for bilateral undescended testes, or if the condition is not resolved before the age of 11. 5,41,46
Correction of cryptorchism at a young age by orchidopexy, particularly before the age of four and at latest by the age of 10 (ie before puberty), reduces risk of testicular cancer, but it still remains higher than that for the general population. Cryptorchism is also associated with CIS of the testis, with around 2-3% of men with a history of cryptorchism at risk of developing CIS. 6 Cryptorchism is more common in low birth weight babies, a characteristic associated with an increased risk of testicular cancer. 7, 8
Other urological maldevelopments associated with an increased risk of testicular cancer include inguinal hernia and hydrocoele (a collection of fluid around the testicles). 9
More recently the diagnosis of microlithasis (micro-calcifications in the testis detected by ultrasound) has been associated with an increase in risk of testicular cancer, though the precise relationship remains to be determined. 10-12
It has been suggested that population trends for problems with male reproductive health (including an increase in MDT, 13 decreasing sperm quality, 14 and increasing rates of testicular cancer) may have a common, but as yet unproven, aetiology15, 16 Low fertility in general is linked to a higher risk of testicular cancer and CIS. 17, 19 There is some evidence that brothers of men with testicular cancer have reduced fertility. 20
Inherited genetic factors play a role in a small percentage of testicular cancer patients. More information is in the Molecular biology and genetics section. 21
It is thought that GCTs are initiated during foetal development, most likely in the first trimester, and that they progress to invasive cancer under the influence of adult hormones. 22, 23 Research has focused on maternal factors which could influence foetal development.
Of particular interest is the relationship between high levels of circulating oestrogen and a number of male reproductive disorders that are increasing in frequency, including cryptorchism, urethral abnormalities, poor semen quality and testicular cancer. 24 Indirect evidence supports this oestrogen over-exposure hypothesis. Conditions that increase foetal exposure to oestrogen, including first pregnancy, 25 dizygotic twins and severe maternal nausea, 26 are also associated with increased risk of testicular cancer. However, epidemiological studies do not consistently confirm this association and more research is needed to clarify the role of in utero hormonal exposure.
Low birth weight babies and babies who are small for gestational age are at increased risk of testicular cancer, supporting the theory that prenatal influences are important. 7,27 However, there appears to be an "s-shaped" relationship between birth weight and testicular cancer risk, with men that weigh more than 4 kilos at birth also at an increased risk. 44 This may be related to adult height (see below).
Evidence on maternal smoking is conflicting. A strong correlation has been identified between female smoking trends and rates of testicular cancer in Nordic countries 28 and a positive association with maternal lung cancer has been observed in Sweden. 29
However, one case-control study showed a significant reduction in risk of testicular cancer in offspring of women who smoke heavily 30 while others report no association. 7,31,32
Increased adult height is associated with risk of testicular cancer, with a three-fold risk increase for the tallest men, and a reduction in risk for men who are shorter than average. 33-35 This factor may be connected to hormonal and dietary factors. Population trends towards increasing adult height are consistent with the rising trends of testicular cancer incidence.
Many occupations have been linked to increased testicular cancer risk, but the specific risks are not clear. 5
There is evidence that men with HIV or AIDS have a 35% increased risk of testicular cancer. 45
Testicular Cancer molecular biology and genetics
This page contains information on the molecular biology and genetics of testicular cancer such as inherited genetic factors.
Inherited genetic factors play a role in the development of testicular cancer in some patients.
Men with an affected first degree relative have a higher risk of developing testicular cancer than the general population. About 2% of testicular cancer patients report having an affected relative. A number of studies have been carried out to assess the risk of testicular cancers in first-degree relatives. 1 The increased risk seen in siblings of patients is particularly high, with a relative risk of 8-10. For father-son pairs, the relative risk is 4-6. 1
Rather than being the result of mutation of a major susceptibility gene, it is thought that a number of genes, each with a relatively weak effect, are responsible for the development of testicular cancer. 2, 3 Work is ongoing to try to identify susceptibility genes, using technologies such as single nucleotide polymorphism (SNP) genotyping. 2
Sporadic cases of testicular cancer often display amplification of the short arm of chromosome 12. This suggests that genes in this region are important in the development of GCT. 4
Testicular cancer symptoms and treatment
This page presents information on the symptoms and treatment of testicular cancer.
Testicular cancer symptoms
The most common symptom of germ-cell tumours(GCT) is a painless lump or swelling on one of the testicles, usually noticed by the patient. Other warning signals include enlargement of a testicle, an increase in testicular firmness, pain in a testicle, an unusual difference between one testicle and the other, an ache in the lower stomach or groin and heaviness in the scrotum. Rarely patients may present with the symptoms of advanced disease, which include breast tenderness, back pain, shortness of breath and haemoptysis (coughing up blood).
Testicular cancer treatment
Two important advances have changed the treatment of testicular cancer. Firstly, the discovery of two serum markers, human chorionic gonadotrophin (HCG) and alpha fetoprotein (AFP) during the late 1960s. Both have proved to be reliable indicators of tumour burden within the body and of response to treatment. Secondly, combination chemotherapy, used since 1970 - at first without cisplatin and since the mid-1970s with cisplatin - has proved highly successful as a treatment tool even in patients with metastatic disease.
Testicular cancers are curable in the great majority of cases. Curative treatment varies by type of tumour and the stage of disease at diagnosis.
Treatment guidelines 1-6 and reviews of the management of testicular cancer have been published. 7-9 As most patients can be successfully treated, the emphasis of clinical research has shifted to finding ways to minimise treatment-related toxicity (which may increase risk of second cancers, 10 cardiovascular morbidity and reduced fertility 7,11) for low-risk patients.
For the small number of patients who are not cured, novel treatments are being investigated. 9, 12 Research has shown that better outcomes are achieved in larger rather than smaller treatment centres. 13, 14
Treatment of Seminoma testicular cancer
Seminomas are more radiosensitive and more chemosensitive than nonseminomas and survival rates have always been high. Seminoma patients also tend to present with earlier stage disease than those with nonseminoma ( Figure 6.1).
Approximately 80% of seminoma patients present with early disease. For many years the standard treatment for seminoma in the UK has been surgery (inguinal orchidectomy) followed by adjuvant radiotherapy. 7 Following clinical trials, both the radiation field and the amount of radiation needed were reduced to minimise long-term effects. 15, 16 Excellent survival rates of 95-100% are achieved with minimal morbidity.
A randomised trial has shown that surgery followed by a single cycle of carboplatin is equivalent to surgery followed by radiotherapy in reducing the risk of recurrence of testicular caancer, and has lower toxicity. Concerns about the long term toxicity of radiotherapy (see above) have led recently to adoption of surgery plus carboplatin as the standard treatment for seminomas in the UK. 17, 18 Patients with stage I disease have an approximately 20% chance of relapse with surgery and no further treatment, which has led to an increase in popularity of managing testicular cancer in these patients with surveillance.
Risk of relapse is higher (around 32%) if tumour size is >4cm and there is evidence of rete testis (the rete testis is a network of tubules in the centre of the testis) invasion (risk is reduced if only one of these factors is present). 19 More advanced disease and disease recurrence can be treated effectively with combination chemotherapy.
Between a third and a half of nonseminoma patients have early disease when first treated and again inguinal orchidectomy is the main treatment. Larger UK centres divide clinical stage I cases into low- and high-risk according to the presence or absence of vascular invasion. Following surgery, low-risk patients are managed with surveillance, while high-risk patients receive either adjuvant chemotherapy or undergo surveillance. This results in cure rates of 99%. 20
A trial of functional imaging showed that positron emission tomography (PET) scanning had only marginal effect on diagnostic accuracy. 21
More advanced nonseminoma patients are treated with chemotherapy. Usually this is with a schedule called BEP (consisting of three drugs, bleomycin, etoposide and cisplatin). Surgery is used to remove any post-treatment masses. Outcome of treatment can be predicted by a prognostic index ( Figure 6.2) based on the level of tumour markers, site of primary tumour and the presence or absence of nonpulmonary metastases. 22, 23
Between 1987 and 1996, around 50% of all nonseminoma patients were categorised in the good prognosis group. For this group, ten-year survival rates are over 90%.
A further third of patients fall into the intermediate prognosis group, which has ten-year survival rates of 87%. The largest increase in survival has been for the poor prognosis group. For those diagnosed between 1977 and 1986, ten-year survival rates were 37%. This rate has risen to 66% for patients diagnosed between 1987 and 1996.
24 High-dose chemotherapy with autologous bone marrow or peripheral blood stem-cell transplantation has been tested in an attempt to improve survival of patients relapsing after initial treatment. However this treatment did not improve survival compared to standard treatment 25 so it is generally now reserved for carefully selected patients in second relapse. 7, 26Contralateral testicular cancer
In a very small percentage (5%) of patients, the contralateral testis shows signs of CIS which would be expected to progress to carcinoma in the majority of cases. Because of this low risk and the attendant morbidity associated with testicular biopsy, there is not yet a consensus on whether to screen the contralateral testis in all cases. 2,8 Options need to be discussed with the patient.
The future of testicular cancer treatment
During the last 40 years, testicular cancer has become a curable malignancy in over 95% of patients ( Figure 6.3). This success has led to a new emphasis on decreasing the side effects of treatment and improving patients’ quality of life, both during and after treatment. 16,27-31
For patients with metastatic disease that cannot be cured using current treatments, more effective therapies are being developed and tested. 12,32, 33 As there is a clear association between delay in diagnosis and more advanced disease, 34 it is important to improve and extend health education so that fewer patients present with metastatic disease. 35 Recent data from London has shown that this is already occurring, but further improvements could be made. 36
At present, three groups of risk factors stand out. Firstly, those acting in utero during foetal gonadal development; secondly, post-pubertal factors and thirdly, genetic factors. Understanding the interplay between these risk factors will be essential for a full understanding of the aetiology of germ cell testicular tumours.
References
UK Testicular Cancer incidence statistics
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- Statistical Information Team, Cancer Research UK, 2009
UK Testicular Cancer mortality statistics
- Office for National Statistics Mortality Statistics: Cause. England and Wales 2007 London TSO 2009
- Northern Ireland Cancer Registry, 2009, Cancer Mortality in Northern Ireland, 2007
- ISD Online, 2009, Cancer Mortality in Scotland, 2007
- Boyle, P., Testicular cancer: the challenge for cancer control. Lancet Oncol, 2004. 5(1): p. 56-61.
- Levi, F., et al., Testicular cancer mortality in Eastern Europe. Int J Cancer, 2003. 105(4): p. 574.
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Testicular Cancer survival statistics
- Coleman, M., P. Babb, and P. Damiecki, Cancer Survival Trends in England and Wales, 1971-1995: Deprivation and NHS Region. 1999> TSO>
- Coleman, M.P. et al Trends in socioeconomic inequalities in cancer survival in England and Wales up to 2001. BrJC 2004. 90 (7): p1367-73
- Jones, R.H. and P.A. Vasey, . Part II: testicular cancer--management of advanced disease. Lancet Oncol, 2003. 4(12): p. 738-47
- Masters, J.R. and B. Koberle, . Curing metastatic cancer: lessons from testicular germ-cell tumours. Nat Rev Cancer, 2003. 3(7): p. 517-25
Testicular Cancer risk factors
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- Oosterhuis, J.W. and L.H. Looijenga, Current views on the pathogenesis of testicular germ cell tumours and perspectives for future research: highlights of the 5th Copenhagen Workshop on Carcinoma in situ and Cancer of the Testis. Apmis, 2003. 111(1): p. 280-9.
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