Bladder cancer - UK incidence statistics

Bladder cancer - UK incidence statistics

This page presents bladder cancer incidence statistics including incidence by age and sex, socio-economic deprivation, geographical variation and trends over time and histology. The ICD code for bladder cancer is ICD9 188, ICD10 C67.

Bladder cancer is a common cancer in the UK, with 10,264 new cases in 2006. 1-4 It is the most frequently occurring tumour of the urinary system and accounts for around 1 in every 29 new cases of cancer each year in the UK.

This page presents bladder cancer incidence statistics including incidence by age and sex, socio-economic deprivation, geographical variation and trends over time and histology. The ICD code for bladder cancer is ICD9 188, ICD10 C67.

Bladder cancer is a common cancer in the UK, with 10,264 new cases in 2006. 1-4 It is the most frequently occurring tumour of the urinary system and accounts for around 1 in every 29 new cases of cancer each year in the UK.

Bladder cancer incidence by age and sex

In the UK bladder cancer is the fourth most common cancer in males, with 7,307 new cases diagnosed in 2006. 1-4 This compares to 2,957 female cases, giving a male:female ratio of 5:2. In females it is the eleventh most common cancer.

The numbers and rates for the UK and its constituent countries are shown in Table 1.1. 1-4

Table showing the number of new cases and rates of bladder cancer in the UK

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Few cases occur under the age of 50, but thereafter the rates rise with age to reach a peak in the oldest age-groups when rates in elderly men are more than three times higher than in elderly women ( Figure 1.1). 1-4

Chart showing the number of new cases of bladder cancer in the UK

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Bladder cancer incidence by socio-economic deprivation

British data show only a small deprivation gradient, with the lowest bladder cancer rates recorded for the most affluent and the highest for the most deprived groups. 7,8 The latest analysis for data from England showed similar results with age-standardised bladder cancer incidence rates of 11.2 per 100,000 population for the most affluent compared with 13.7 for the most deprived. 14

Geographic variation in bladder cancer incidence

An analysis of cancer incidence in the UK and Ireland highlighted considerable differences between cancer registries in the classification of bladder tumours which make the interpretation of any geographical patterns difficult. 6 These differences in registration practice will also limit international comparisons.

The 2002 estimated age-standardised bladder cancer incidence rates reported for UK men are well below the EU average (25.3 v 34.4 per 100,000 population respectively) and the rate for women in the UK is slightly higher than (7.9 v 7.0 per 100,000 population respectively) as Figure 1.2 shows. More recent age-standardised rates for the UK show a further drop - 19.8 for men and 5.9 for women (see Figure 1.5 below).

Chart showing the age-standardised incidence rates for bladder cancer, by sex, for the European Union, 2002 estimates

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Worldwide an estimated 356,600 new cases of bladder cancer occur each year and, in terms of overall cancer frequency, it is ranked as ninth. 5 World incidence rates for bladder cancer show comparatively low variation ( Figure 1.3) compared to other cancers. 9

Chart showing the age-standardised incidence rates for bladder cancer, by sex, for the world regions, 2002

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The highest bladder cancer incidence rates are generally found in industrially developed countries, particularly in North America and Western Europe, and in areas associated with endemic schistosomiasis in Africa and the Middle East. Egypt has the highest reported rates (37 per 100,000 population) in the world due to endemic schistosomiasis. Very low rates (< 5 per 100,000 population) are reported for India and China.

Marked racial differences have been reported for bladder cancer incidence with higher rates in white than non-white populations. For example, in the USA, rates for white men are double those for black men: in 2000-2003 the age-adjusted incidence rate per 100,000 population was 40.2 for white males compared to 19.8 in black Americans. Bladder risk for US black women is about two-thirds that of US white women. 10

These differences may be partly due to genes, as studies have shown that certain genetic polymorphisms linked to an increased risk of bladder cancer (for example, the NAT2 slow acetylator polymorphism) are much more prevalent in white than non-white populations 11 - see Molecular Biology and Genetics section for more details.

Bladder cancer incidence trends

Time trends in bladder cancer incidence rates are difficult to interpret because of different and changing classification/coding practices affecting the definition of invasive carcinoma of the bladder.

In Great Britain, the age-standardised incidence rates per 100,000 population rose throughout the 1970s and 1980s to reach a peak of 32 in men and 9 in women in the early 1990s and since then have fallen by around a third. ( Figure 1.4). 12

Chart showing the age-standardised incidence rates for bladder cancer in Great Britain since 1975

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UK bladder cancer incidence trends are shown in Figure 1.5

Figure showing age-standardised (European) incidence rates of bladder cancer, by sex, in the UK since 1993

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The age-specific bladder cancer incidence rates in Great Britain Figure 1.6 and Figure 1.7 show a consistent decrease since the early 1990s for all age-groups under age 85. 12 Some of this decrease is likely to be due coding changes but reductions in smoking and exposure to occupational carcinogens may also have played a role, especially as the mortality rates have also decreased. 13

Figure showing age-specific incidence rates of bladder cancer for males in Great Britain

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Figure showing age-specific incidence rates of bladder cancer for females in Great Britain

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Bladder cancer histology

In developed countries around 90% of bladder cancers are transitional cell carcinomas while the remaining 10% are squamous cell carcinomas and adenocarcinomas. Benign transitional cell papillomas have sometimes and in some places been registered as invasive carcinomas. This variation in registration practice has to be taken into account when comparing incidence and survival rates over time and place. 6

Where the bladder cancer is associated with chronic bladder infection, most commonly with waterborne parasitic flatworms called schistosomes, the usual histology is squamous cell carcinoma. Schistosomiasis-associated bladder cancer has an earlier mean age at onset, typically in the fifth decade of life, and tends to present at a later stage than transitional cell carcinomas.

In countries where schistosomiasis (also called bilharzia ) is endemic, such as Egypt, bladder cancer is the most common cancer in men. 5 Prevention of infection in these countries is paramount. 7 Subsequent information in this section concerns bladder cancer in the UK and other developed countries unless otherwise specified.

Updated: 25/06/2009 0:00

Bladder cancer - molecular biology and genetics

This page contains information on the molecular biology and genetics of bladder cancer that has so far been discovered and the likely future developments in this field.

Bladder cancer molecular biology and genetics

In addition to marked racial differences, it has been observed that there is wide variation in bladder cancer risks amongst populations with similar exposure to tobacco andoccupational bladder carcinogens. 1

Genetically determined differences in metabolic activation and detoxification of bladder carcinogens may play an important role in individual variations in susceptibility to the disease. Associations of bladder cancer with genetic variants ( Polymorphisms) of, for example, the enzymes glutathione S-transferase (GST) and N-acetyl transferase (NAT) have been proposed.

GST is the product of the GSTM1 gene and is involved in the detoxification of polycyclic aromatic hydrocarbons found in tobacco smoke. Around 50 per cent of Caucasians and Asians have a deleted GSTM1 gene and there is evidence that this genetic status is associated with a modest increase in the overall risk of bladder cancer. 2 Furthermore, there appears to be a GSTM1 gene dosage effect, with individuals with either no copies, as well as those with a single copy of GSTM1, having increased bladder cancer risk compared to those with two copies of the gene. 3

 

The N-acetyl transferase 2 (NAT2) enzyme is important in the inactivation of aromatic amines and is present in ‘fast’ and ‘slow’ forms, indicating the speed at which it is able to inactivate environmental carcinogens. Studies have suggested that people who carry the ‘slow’ variant are at increased risk of bladder cancer and that this may be especially true for smokers. 3

Recent studies identify polymorphisms in DNA repair genes as possible risk factors. Two relatively large recent series support the view that genetic variation in the nucleotide excision repair pathway influences bladder cancer risk. 4,5 Further research into the genetic understanding of individual susceptibility to bladder cancer, the interaction of environment and genes in disease pathogenesis and the opportunities for prevention is needed.

There have been few reported cases of inherited bladder cancer and familial cases are usually part of the HNPCC syndrome. 6,7 One study has shown a particularly high risk for brothers of bladder cancer probands diagnosed before the age of 45 years which may reflect an X linked susceptibility gene. 8 However, a recent study which used a relatively powerful technique failed to identify any genetic abnormalities in hereditary bladder cancer patients. 9

 

A number of genetic changes have been identified in bladder tumours. 10-12 Numerous alterations have been reported in invasive cancers but fewer in non-invasive forms. Both tumour types commonly exhibit deletions affecting chromosome 9 (50-60% of cases) and a number of candidate genes have been identified including CDKN2A (INK4a). The fibroblast growth factor 3 gene (FGFR3) is mutated in more than 70% of non-invasive cancers. Other reported alterations include mutations affecting the cyclin D1 gene (CCDN1), oncogenes including ERBB2 and  tumour suppressor genes including TP53. 10-12

The Future

Research into the gene alterations that drive the development of bladder cancer, and more detailed understanding of the molecular pathways involved in disease progression continues. The increasing use of microarray technology to study gene expression will offer improved prospects for identifying prognostic and predictive factors and continue to the development of new targeted therapies.

The search continues for a better and less invasive diagnostic test for bladder cancer. Raised levels of the DNA replication initiation factor Mcm5 in urine have been shown to provide a highly sensitive and specific marker for primary and recurrent bladder cancers. Clinical trials are currently ongoing. . 13 A recent study showed that testing for nuclear matrix proteins (NMP22) in urine samples alongside cystoscopy could detect 99% of recurrent bladder cancers. . 14

Studies of genetic variation in individual susceptibility to bladder carcinogens will lead to a better understanding of the disease and provide new leads for prevention. But prevention, through minimising exposure to known carcinogens, particularly those in tobacco smoke, will remain a priority.

Updated: 18/09/2007 0:00

Bladder cancer - UK mortality statistics

This page presents bladder cancer mortality statistics including by age and sex, trends over time.

Bladder cancer is the sixth most common cause of cancer death in UK men and the eleventh in women.

Bladder cancer mortality by age and sex

In 2007 there were 3,283 male deaths from bladder cancer and 1,635 female bladder cancer deaths in the UK. 1-3 The number of bladder cancer deaths and mortality rates for the constituent countries in the UK are shown in Table 2.1.

Table showing the number of deaths from bladder cancer for males, females and persons in the UK

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The distribution of deaths by age ( Figure 2.1) shows a steep climb with age with around 90% of both male and female deaths occurring after the age of 65. 4

Chart showing the number of deaths and age-specific mortality rates for bladder cancer in the UK

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Bladder cancer mortality trends

The bladder cancer age-standardised mortality rates between 1971 and 2007 for the UK are shown in Figure 2.2. 4

Chart showing the bladder cancer mortality rates for males, females and persons in the UK since 1971

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Generally there has been little change in the female bladder cancer mortality rates although overall rates have fallen slightly from around 3.5 in the late 1970s/early 1980s to 2.8 in 2007. In contrast, the male rates have shown a consistent fall since 1992, from 12.2 to 8.1 per 100,000 in the year 2007, a fall of over 30%.

Bladder cancer mortality rates by age are shown for males in Figure 2.3 and females in Figure 2.4.

Chart showing bladder cancer mortality rates for men by age at diagnosis since 1971

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Chart showing bladder cancer mortality rates for females by age at diagnosis since 1971

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Between 1971 and 2007 the mortality rates for men aged 45-64 fell by around 60% from 12.8 to 5.0 per 100,000. Decreases in mortality rates have also been seen in the other age -groups.

It is clear that for females the largest falls in bladder cancer mortality have been in the 45-64 age-group. Rates have fallen from 3.8 per 100,000 in the early 1970s to 2.0 in 2007, a fall of around 50%. The all-ages rate masks this trend.

Updated: 13/05/2009 0:00

Bladder cancer - risk factors

This page presents information on the risk factors for bladder cancer including by tobacco, occupation exposure, hair dyes, medicines and medical conditions, hormonal factors, family history and food and drink.

Tobacco and bladder cancer risk

Smoking cigarettes is the principal preventable risk factor for bladder cancer in both men and women. In Europe it is estimated that two-thirds of bladder cancer cases in men and a third in women are caused by cigarette smoking. 1,2

Current smokers have two-six times the risk of never-smokers of developing bladder cancer, with the highest risks for people smoking for the longest, or smoking a greater amount of cigarettes each day. 1-2

Smoking cessation reduces risk, but risk in ex-smokers remains higher than never-smokers for more than 20 years. 1,2

Passive smoking may also increase risk. In a recent European study, exposure to environmental tobacco smoke (ETS) during childhood (but not adulthood) increased the risk of bladder cancer by 40%. 4 Another study showed a three-fold increased risk of bladder cancer in women heavily exposed to ETS in childhood, although no association for men. This study showed an even higher five-fold risk increase for women most heavily exposed to ETS throughout their lifetime. 49 A record linkage study of bladder cancer incidence in the offspring of men and women diagnosed with lung cancer found a significant increase in risk of bladder cancer in those whose mothers had lung cancer, but no increased risk for paternal lung cancer. The authors interpret this as evidence that exposure to tobacco carcinogens in utero or while breastfeeding may lead to bladder cancer in later life. 5

Smoking cessation after diagnosis may favourably alter the course of the disease but the evidence is incomplete. 6 It has also been suggested that high fruit consumption may reduce the effect of smoking on developing bladder cancer. 7

The precise mechanism by which cigarette smoking induces bladder cancer is unclear. Studies show that risk varies by type of tobacco, with a higher risk for black ‘air-cured’ than blond ‘flue-cured’ tobacco . 8 Smokers of black tobacco have higher reported levels of aromatic amines in their urine than smokers of blond tobacco. 9 These aromatic amines are known urothelial carcinogens and the ability to detoxify them is compromised in people who are ‘slow acetylators’ and it is suggested that these people are at higher risk than ‘fast acetylators’( see Molecular biology and genetics section). 10

Tobacco tars have been shown to induce bladder papillomas and carcinomas in mice. 11 It is thought that prolonged exposure of the bladder to such urinary carcinogens during the excretory process ( Figure 4.1) may lead to the development of bladder cancer.

Figure 4.1: Diagram of the male urinary tract

Occupational exposure and bladder cancer risk

Bladder cancer was one of the first cancers shown to be industrially associated and has an important place in the history of occupational disease.

In 1895 Rehn reported cases of bladder cancer in a German aniline dye factory. 12 This led to occupational studies in other countries but it was not until the 1950s that the risk from aromatic amines, particularly benzidine and a-and ß-naphthylamine, was established by Case. 13

Aromatic amines were widely used in the manufacture of dyes and pigments for textiles, paints, plastics, paper and hair dyes, in drugs, pesticides and as antioxidants in the rubber industry. 14 Production of ß-naphthylamine ceased in the UK in 1952 (its use was withdrawn from the rubber and cable industry prior to this in 1949) 15 and in 1953 bladder cancer became, and still is, a prescribed industrial disease. 16

Exposure to polycyclic aromatic hydrocarbons (PAH), which are by-products of combustion processes and therefore present in a range of industries, has also been investigated. It is calculated that about 4% of bladder cancer cases in European men are due to exposure to PAH. 17

Altogether it is estimated that between 5 and 10% of male bladder cancer cases in Europe are caused by occupational exposure. 64 This proportion may be higher in countries with less-regulated industrial processes.

Hair dyes and bladder cancer risk

Within the EU, the Scientific Committee on Cosmetic Products and Non-food Products (SCCNFP) is establishing a system for the regulation of hair dye substances. 44

Occupational studies of hairdressers and barbers have reported elevated risks for bladder cancer but a recent study in Sweden showed no increase among hairdressers in recent decades and suggested that modern hair dyes are not carcinogenic. 18

Personal use of hair dyes has also been studied with conflicting results The SCCNFP’s strategy is to require the industry to provide safety dossiers for all dye precursors and dyes for permanent and semi-permanent hair dye formulations and then to evaluate these with the aim of setting up a ‘positive list’ of hair dyes. 45-48

Medicines and medical conditions and bladder cancer risk

In addition to aromatic amines, there are other established bladder carcinogens including phenacetin and certain cancer chemotherapeutic agents including cyclophosphamide. 19,20

A very small proportion of bladder cancer cases are associated with therapeutic irradiation in the pelvic region, for example for testicular cancer 21 or cervical cancer. 22 Men with a history of prostate cancer, both those treated with and without radiotherapy, have an increased risk of bladder cancer. 23-25 The risk of bladder cancer has been shown to be increased two-fold in women treated for cervical cancer without radiotherapy, which may be due to shared risk factors such as smoking. Among women treated with radiotherapy the risk increased with years since treatment, to almost six-fold for women treated for cervical cancer 40 or more years previously. 50

Paraplegics have a greatly increased risk of squamous cell carcinomas of the bladder, due to their disposition to chronic urinary tract infection. Kidney and urinary stones may also slightly increase risk. 26

There is some evidence that diabetics have an increased risk of bladder cancer, with risk ratios of 2-3 reported 27-29 and limited evidence that a history of gastric ulcer increases risk. 30,31 One study showed a doubling in risk of bladder cancer in patients with condylomata acuminata (genital warts). 60 Genital warts are caused by infection with the human papillomavirus (HPV), and a meta-analysis showed a three-fold increased risk associated with HPV infection. 61

Hormonal factors and bladder cancer risk

Two cohort studies show a 50-75% increase in risk of bladder cancer in women undergoing menopause before the age of 47 compared to at 48 or later. 51,52 Women who have had a bilateral oophorectomy have a 60% increased risk. 51

Family history and bladder cancer risk

Most studies show a two-six-fold increased risk of bladder cancer in first-degree relatives of bladder cancer patients, with a higher risk if the relative was diagnosed before the age of 45. 53-55

Food and drink and bladder cancer risk

Higher intake of fruit has been associated with a small but significant reduction in the risk of bladder cancer. An increase in fruit consumption of 100 grams a day is estimated to reduce risk by approximately 20%. 32-34 However, some studies have shown no association with fruit intake and it is not possible to say there is a definite protective association. 56-58

Two Chinese cohort studies have reported a significant increase in risk with higher consumption of soya foods. 35,36 This association is not clearly understood: one theory is that the chemical reaction of chlorine in water with humic substances in beans during fermentation may act as a bladder carcinogen.

Results of a pooled analysis of 10 European studies show that heavy coffee consumption (more than 10 cups per day) is associated with a significantly increased risk of bladder cancer in men and women 37 but there is no evidence of risk increase with moderate consumption. 38,39

The body of evidence indicates that overall fluid consumption does not affect bladder cancer risk. 34 Some studies have shown that high tap water consumption increases risk of bladder cancer, which may be linked to chlorination . 41 However, three studies have shown a lower risk of bladder cancer with higher water consumption, particularly among people who urinate frequently. 59,62, 63A meta-analysis has reported a significant risk ratio of 1.4 for having a chlorinated water supply. 42 In another pooled analysis, having a water supply containing high levels of trihalomethanes (by-products of chlorination) was associated with a significant risk increase in men but not women. 43

Updated: 16/04/2009 0:00

Bladder cancer - survival statistics for England and Wales

The most important prognostic factor is the depth of tumour penetration into the bladder wall: T staging of bladder cancer is shown in Figure 3.1. 1,2

Figure 3.1: T Staging of bladder cancer

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Tumours not invading beyond the lamina propria (T1) are classified as superficial. Other prognostic factors include multiple tumour foci, grade and tumour type. Patients with superficial tumours have an excellent prognosis with five-year survival rates between 80-90%. Patients with muscle-invasive bladder cancer have five-year survival rates of less than 50%. Radical treatment deals effectively with locally invasive disease but many patients die from metastatic disease. Early detection while the tumour is still superficial is therefore very important.

One and five-year relative survival rates have risen consistently as Figure 3.2 shows for men and women diagnosed from the early 1970s to 2000/01. 3-5

Figure 3.2: Age-standardised five-year survival for male and female bladder cancer patients diagnosed in England and Wales, 1971-2001

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Over this time period, one-year relative survival rates rose from 66-81% for men and 59-71% for women while five-year relative rates rose from 44-66% for men and 42-57% for women. An unusual feature of these survival rates is that men have consistently higher survival rates than women (among common cancers in England and Wales only two cancers, larynx and bladder, have significantly higher male than female survival rates) . This male survival advantage for bladder cancer is seen in many countries. 6 Men seem to be diagnosed at a slightly earlier stage than women but this does not explain all their survival advantage, as stage-specific survival is also higher in men than women 7,8

It has been suggested that the different anatomy of male and female bladders may account for some of the variation in survival between the sexes. 8 However, survival for both men and women decreases strongly with age ( Figure 3.3). 3

Figure 3.3: Five-year relative survival for male and female patients diagnosed with bladder cancer in England and Wales, 1996-1999, by age at diagnosis

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It is possible that differences in survival over time, between sexes and ages, have been influenced by changes in defining malignant bladder tumours. 4

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Updated: 21/12/2006 0:00

Bladder cancer - symptoms and treatment

This page contains information on bladder cancer symptoms and both current and future treatments.

Bladder cancer symptoms and current treatment

The most common symptom in over 80% of patients is painless and usually intermittent haematuria (blood in the urine), which is also often a sign of less serious problems. 1 However, haematuria should always be investigated if early diagnosis is to be achieved. Other symptoms include urinary frequency and pain on passing urine, but again these often indicate the presence of non-malignant conditions such as urinary tract infections.

Around three-quarters of patients present with superficial tumours (i.e. confined to the bladder mucosa or submucosal layer without muscle invasion) which are treated by transurethral resection and have a very good prognosis2. Unfortunately, superficial recurrence is a problem and regular cystoscopies are required to manage this condition.

Progression occurs in approximately 15-25% of patients. To prevent or postpone superficial recurrence, intravesical therapy is used (treatment inside the bladder), either with drugs ( chemotherapy) or with the bacillus Calmette-Guèrin (BCG) (immunotherapy). BCG is particularly useful for transitional cell carcinoma in situ where it has a significant effect on reducing its high rate of progression to invasive carcinoma. 3

 

More advanced tumours which have invaded the muscle require treatment with surgery and/or radiotherapy. Radical cystectomy, which involves removing the bladder, is standard treatment in most countries.

In women, radical cystectomy involves removing the bladder, urethra, lower end of ureters, front wall of vagina, uterus, fallopian tubes and ovaries. In younger women the ovaries may be preserved.

In men, cystectomy involves removal of the bladder, prostate, lower end of ureters and sometimes the urethra. The operation has to be extensive due to the likelihood of local invasion from the original site. For most patients the ureters are then attached to a piece of bowel (ileum) the other end of which comes out of the abdominal wall and the urine is collected in a bag on the abdominal wall.

Recent advances in surgical techniques now mean that the bladder can be removed and an internal bladder replacement (called a neo-bladder) can be fashioned in some patients. Full dose external beam radiotherapy may permit bladder preservation and seems to offer similar long-term survival to surgery.

It is possible that the results of radiotherapy could be further improved by combining this with mild chemotherapy, an approach currently being tested in a clinical trial. 4 However, it suffers from the disadvantage that some patients have recurrent disease requiring subsequent surgery.

Neoadjuvant chemotherapy (chemotherapy before local treatment) has been shown to improve survival in recent overviews of randomised trials. Best estimates suggest that using multi-agent platinum-based chemotherapy reduces the risk of dying of bladder cancer by about 15%. 5,6.

Using chemotherapy after local treatment is more controversial though a recent overview suggests that this approach may have similar value to neoadjuvant treatment. 7 Confirmation for this is being sought from a large international trial. Response to neoadjuvant chemotherapy has been used to select patients who may benefit most from radiotherapy. 8 This approach is being tested against a policy of cystectomy in a UK trial. 9

 

Patients with metastatic disease can benefit from palliative radiotherapy which improves symptoms.

Intensive cisplatin-based chemotherapy has been shown to provide a survival advantage compared to less intensive chemotherapy. 10 Recent advances in chemotherapy schedules using either growth factor support 11 or schedules including gemcitabine 12 mean that this treatment can be administered with lower toxicity than previously used schedules.

Guidelines on improving the outcome for bladder and other urological cancers have been published and stress the importance of multidisciplinary urological teams with specialised skills at each level of the service and the need to provide timely and relevant information to patients. 13,2

It is recommended that radical surgery should only be undertaken by specialist teams who carry out a minimum of 50 radical operations (cystectomies or radical prostatectomies) per annum. The NICE guidance identifies the need for more active treatment of bladder cancer patients and predicts the need for additional intravesical chemotherapy for superficial cancers and an additional 850 cystectomies per annum. 13

 

The future of bladder cancer treatment

Improved surgery has increased the quality of life for patients with invasive bladder cancer. But although the disease can be controlled locally by surgery or radiotherapy, the problem of occult metastases, which may ultimately kill half the patients with invasive disease remains and some form of systemic therapy is needed. 14

New treatments using radiotherapy or chemotherapy alone, or in combination, as well as a number of immunotherapies are being tested in clinical trials. The best use of intravesical chemotherapy and BC for early bladder cancer is also being investigated. Further improvements in neoadjuvant chemotherapy may lead to improved survival.

Updated: 21/12/2006 0:00

References

Bladder cancer - UK incidence statistics

  1.  Office for National Statistics, 2009 Cancer Statistics registrations: registrations of cancer diagnosed in 2006, England.
  2.  Welsh Cancer Intelligence and Surveillance Unit, Cancer Incidence in Wales
  3.  ISD Online, 2009 Cancer Incidence, Mortality and Survival data.Accessed 2009
  4.  Northern Ireland Cancer Registry, 2009 Cancer Incidence and Mortality.
  5.  IARC. GLOBOCAN 2002. Cancer Incidence, Mortality and Prevalence Worldwide (2002 estimates). Accessed 2005
  6.  Cooper N, C.R., Chapter 3, Bladder, in Cancer Atlas of the United Kingdom and Ireland 1991-2000, W.H. Quinn M, Cooper N, Rowan S, Editors. 2005, Palgrave Macmillan: Basingstoke, UK.
  7.  WHO, Schistosomiasis, 2006.
  8.  Quinn, M., et al., Cancer Trends in England & Wales 1950-1999. ed. Vol. SMPS No. 66. 2001: TSO.
  9.  Parkin, D.M., et al., Global cancer statistics, 2002. CA Cancer J Clin, 2005. 55(2): p. 74-108.
  10.  Ries LAG, H., Krapch M et al (eds). SEER Cancer Statistics Review, 1975-2003. Accessed 2006
  11.  Garcia-Closas, M., et al., NAT2 slow acetylation, GSTM1 null genotype, and risk of bladder cancer: results from the Spanish Bladder Cancer Study and meta-analyses. Lancet, 2005. 366(9486): p. 649-59.
  12.  Cancer Research UK, Statistical Information Team. Email: stats.team@cancer.org.uk.
  13.  Pelucchi, C., et al., Mechanisms of disease: The epidemiology of bladder cancer. Nat Clin Pract Urol, 2006. 3(6): p. 327-40.
  14.  National Cancer Intelligence Network, 2008 Cancer Incidence by Deprivation, England 1995-2004.

Bladder cancer - molecular biology and genetics

  1.  Ross, R.K., P.A. Jones, and M.C. Yu, Bladder cancer epidemiology and pathogenesis. Semin Oncol, 1996. 23(5): p. 536-45.
  2.  Engel, L.S., et al., Pooled analysis and meta-analysis of glutathione S-transferase M1 and bladder cancer: a HuGE review. Am J Epidemiol, 2002. 156(2): p. 95-109.
  3.  Garcia-Closas, M., et al., NAT2 slow acetylation, GSTM1 null genotype, and risk of bladder cancer: results from the Spanish Bladder Cancer Study and meta-analyses. Lancet, 2005. 366(9486): p. 649-59.
  4.  Garcia-Closas, M., et al., Genetic variation in the nucleotide excision repair pathway and bladder cancer risk. Cancer Epidemiol Biomarkers Prev, 2006. 15(3): p. 536-42.
  5.  Wu, X., et al., Bladder cancer predisposition: a multigenic approach to DNA-repair and cell-cycle-control genes. Am J Hum Genet, 2006. 78(3): p. 464-79.
  6.  Lynch, H.T., et al., Genetics, natural history, tumor spectrum, and pathology of hereditary nonpolyposis colorectal cancer: an updated review. Gastroenterology, 1993. 104(5): p. 1535-49.
  7.  Sijmons, R.H., et al., Urinary tract cancer and hereditary nonpolyposis colorectal cancer: risks and screening options. J Urol, 1998. 160(2): p. 466-70.
  8.  Plna, K. and K. Hemminki, Familial bladder cancer in the National Swedish Family Cancer Database. J Urol, 2001. 166(6): p. 2129-33.
  9.  Kiemeney, L.A., et al., No evidence for large-scale germline genomic aberrations in hereditary bladder cancer patients with high-resolution array-based comparative genomic hybridization. Cancer Epidemiol Biomarkers Prev, 2006. 15(1): p. 180-3.
  10.  Kim, W.J. and C. Quan, Genetic and epigenetic aspects of bladder cancer. J Cell Biochem, 2005. 95(1): p. 24-33.
  11.  Knowles, M.A., . Molecular subtypes of bladder cancer: Jekyll and Hyde or chalk and cheese? Carcinogenesis, 2006. 27(3): p. 361-73P
  12.  Wu, X.R., Urothelial tumorigenesis: a tale of divergent pathways. Nat Rev Cancer, 2005. 5(9): p. 713-25.
  13.  Stoeber K, Swinn R, Prevost AT, et al. Diagnosis of genito-urinary tract cancer by detection of minichromosome maintenance 5 protein in urine sediments. J Natl Cancer Inst 2002;94(14):1071-9.
  14.  Grossman HB, Soloway M, Messing E, et al. Surveillance for recurrent bladder cancer using a point-of-care proteomic assay. Jama 2006;295(3):299-305.

Bladder cancer - UK mortality statistics

  1.  Office for National Statistics. Mortality Statistics, England and Wales, 2007. Accessed 2009
  2.  Scottish Health Statistics 2007 ISD Scotland Accessed 2009
  3.  Northern Ireland Cancer Registry. Cancer Mortality in Northern Ireland, 2007. Accessed 2009
  4.  Cancer Research UK, Statistical Information Team. Email: stats.team@cancer.org.uk.

Bladder cancer - risk factors

  1.  Brennan, P., et al., Cigarette smoking and bladder cancer in men: a pooled analysis of 11 case-control studies. Int J Cancer, 2000. 86(2): p. 289-94.
  2.  Brennan, P., et al., The contribution of cigarette smoking to bladder cancer in women (pooled European data). Cancer Causes Control, 2001. 12(5): p. 411-7.
  3.  NICE, Guidance on Cancer Services. Improving Outcome in Urological Cancers, 2002, National Institute for Clinical Excellence.
  4.  Bjerregaard, B.K., et al., Tobacco smoke and bladder cancer-in the European prospective investigation into cancer and nutrition. Int J Cancer, 2006. p.
  5.  Hemminki, K. and B. Chen, Parental lung cancer as predictor of cancer risks in offspring: clues about multiple routes of harmful influence?. Int J Cancer, 2006. 118(3): p. 744-8.
  6.  Aveyard, P., et al., Does smoking status influence the prognosis of bladder cancer? A systematic review. BJU Int, 2002. 90(3): p. 228-39.
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Bladder cancer - survival statistics for England and Wales

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Bladder cancer - symptoms and treatment

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