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Find out more about the sources which are essential for our statistics. Skip to main content. New cases of prostate cancer each year, average, UK. Deaths from prostate cancer, , UK. Survive prostate cancer for 10 or more years, , England and Wales. Prostate cancer incidence. There are around 52, new prostate cancer cases in the UK every year, that's more than every day Talk with your doctor if you have any questions about this information.
Learn more about understanding statistics. The next section in this guide is Medical Illustrations. It offers drawings of body parts often affected by prostate cancer.
Use the menu to choose a different section to read in this guide. Prostate Cancer: Statistics Approved by the Cancer. Types of Cancer. Prostate Cancer Guide. Net Guide Prostate Cancer. Medical Illustrations. Risk Factors and Prevention. The most common reason for a man to undergo a prostate biopsy is due to an elevated prostate-specific antigen level PSA , determined by a blood test. In the last decade, changes in PSA screening recommendations have affected the rates of prostate cancer diagnosis.
Learn more about screening for prostate cancer. In other words, the chance of a man dying from his prostate cancer is generally low. Despite in the last decades, science has made so much progress to unveil molecular mechanisms and risk factors involved in the prostate cancer, it still is the second leading cause of cancer mortality among males in the USA [ 32 ].
Finally, the general idea for all types of cancers is that the earlier they are caught, the earlier they can be successfully treated remaining the patients disease-free. The etiology of prostate cancer is the subject of numerous studies and remains largely unknown compared to other common cancers.
The well-established prostate cancer risk factors are advanced age, ethnicity, genetic factors and family history [ 33 - 35 ]. Other factors positively associated with prostate cancer include diet increased consumption of saturated animal fat and red meat, lower intake of fruits, vegetables, vitamins, and coffee , obesity and physical inactivity, inflammation, hyperglycemia, infections, and environmental exposure to chemicals or ionizing radiation [ 34 , 36 - 40 ].
Prostate cancer is the most commonly diagnosed malignancy among elderly males [ 1 ]. Indeed, an increasing number of senior men are diagnosed with prostate cancer due to increasing life expectancy and the increased use of PSA screening. It was observed that the risk increases especially after 50 years of age in White men who have no family history of the prostate cancer, and after 40 years of age in Black men or men with a familial history of prostate cancer [ 14 ]. Indeed, due to its indolent course, elderly men who have concurrent severe co-morbid disease during their lifetimes are more likely to die from other related health conditions or other diseases rather than from prostate cancer.
Prevalence of prostate cancer highly varies among different racial groups. The highest incidence rate is seen in African-American men This vast disparity has been associated with both socioeconomic conditions and biologic factors [ 42 ]. For instance, it is believed that African Americans receive lower-quality healthcare and consequently, they are also less likely to undergo PSA screening [ 43 ].
Notably, significantly higher PSA levels were seen in Black men, with or without prostate cancer when compared to White men [ 44 , 45 ]. Several studies proposed that genetic predisposition might play a role.
African-American men have the more common chromosome 8q24 variants, which have been shown to be associated with increased prostate cancer risk [ 46 - 49 ].
Some research studies have also demonstrated that African Americans have a high rate of variations in genes that suppress tumors such as EphB2 [ 50 ] or that regulate cell apoptosis such as BCL2 [ 51 ]. Furthermore, African-American men display a more aggressive form of the disease, which has also been associated with genetic and biologic differences, although lack of adequate screening and delayed presentation was not excluded too [ 42 ].
Gene linkage studies reveal major susceptibility loci for prostate carcinoma on genes in seven different loci. It plays an important role in reducing antiviral activity and the regulation of apoptotic cell death [ 58 ].
Of note, analysis of human prostate cancer samples from patients with RNASEL mutations showed the presence of retrovirus unveiling the importance of antiviral defenses to prostate cancer development [ 59 ]. Moreover, detection of retroviral infections in some cases of prostate cancer also showed the potential connection of chronic retroviral infection and consequent tissue inflammation with cancer initiation [ 60 , 61 ].
However, considering the low penetrance of this allele, several studies failed to confirm its association with HPC [ 65 , 66 ].
Additionally, a subset of HPC was found to occur in men with BRCA1 and 2 mutations that showed a clinically aggressive form of prostate cancer [ 67 ]. The X chromosome is also believed to have a role in prostate cancer inheritance, because it contains the androgen receptor AR and because small deletions in Xq More recent studies in hereditary prostate cancer affected families defined a number of other loci that may contribute to hereditary prostate cancer [ 71 ].
For example, Chu et al [ 18 ] reported that when compared to those in Africa, the incidence rate of prostate cancer among African Americans was as high as 40 times, while Hsing et al in [ 72 ] showed that compared to men living in China, the prostate cancer incidence was fold higher for Chinese men living in the USA, suggesting that environmental factors play an important role.
There are multiple evidences that certain foods are associated at higher risk, while others are even protective. Multiple ecological studies have shown a positive correlation between prostate mortality and per capita intake of meat, fat and dairy products [ 73 , 74 ]. A recent case-control study in patients less than or equal to 60 years found that high intake of total fat was associated with a statistically significant increase in prostate cancer risk [ 75 ].
There are several biological mechanisms that are thought to be involved between saturated animal fat intake and prostate cancer risk: 1 promoting prostate carcinogenesis via androgen; 2 increasing levels of reactive oxygen species ROS and increasing leukotrienes and prostaglandins levels from lipid metabolism; and 3 increasing basal metabolism, insulin growth factor and tumor proliferation.
High-calorie intake of saturated animal fat has shown to increase the growth of prostate cancer cells by increasing the circulating levels of androgens [ 76 , 77 ]. Furthermore, randomized cross-over studies involving low-fat and high-fat diets showed that the level of androgen is lower post-prandial as well as in vegetarians [ 78 ].
Finally, several studies reported that alteration of lipid levels undergoing to a low-fat diet reduces testosterone levels [ 79 - 81 ]. Excessive fat increases oxidative stress and ROS levels that attack the cells causing peroxidation and eventually DNA damage. A role for lipid metabolism and its metabolite have also been observed in mice and found that dietary fat is an important modulator of prostate cancer growth.
For example, while some studies did not find any difference in terms of tumor growth and survival of mice placed on a Western diet, other studies showed a delay in cancer cell growth in mice with low-fat corn-oil diets, suggesting that the amount and type of fat are critical [ 82 ].
Mechanistically, corn-oil may promote cancer growth via the linoleic acid, the most abundant omega-6 fat in the oil. Arachidonic acid which is a metabolite of linoleic acid gives rise to the formation of several pro-inflammatory prostaglandins PG , including PGE2 that promotes cell proliferation, and 5-hydroxyeicosatetraenoic acid that is produced by the action of 5-lipoxygenase, which is found to be increasingly expressed in malignant prostate cancer.
Hence, a decrease in omega-6 fatty acid intake can decrease cancer growth. As opposite to omega-6 fats pro-inflammatory effect, omega-3 fats are found beneficial against cancer growth [ 83 ]. Dietary meat intake has been associated with prostate carcinogenesis by correlating cancer incidence and mortality with per capita meat consumption [ 84 ]. Rohrmann et al [ 85 ] showed that men consuming five or more servings of processed meat per week had a higher risk of prostate cancer when compared with men who consume one or fewer servings per week.
In African-American men, there was no association observed with high consumption of red meats and increased prostate risk. Grilled or barbecued meat can result in the formation of N-nitroso compounds that can result in lipid peroxidation and DNA damage by the production of free radicals [ 89 , 90 ].
Dairy foods have generally been associated with an elevated prostate cancer risk [ 85 , 91 - 94 ]. Both calcium from supplements and dairy put male at high prostate cancer risk.
Greater than 2, mg per day of calcium was associated with a greater risk of prostate cancer. After a year follow-up, prostate cancer was diagnosed in 5, men, which was associated with high calcium intake [ 96 ]. Although conflicting results have been generated regarding dietary fat, a strong relationship was found between intake of Crucifers or Brassica vegetables broccoli, Brussels sprouts, cauliflower, cabbage, and turnips and reduced prostate cancer risk. Crucifers have anticancer properties mediated by phenyethyl isothiocyanate, sulforaphane, phytochemicals and indolecarbinol [ 97 ].
Some studies in the USA on a diet rich with broccoli have shown evidence for the protective effect of Brassica vegetables against prostate cancer [ 98 ].
However, some other studies revealed no anticancer capabilities of Brassica vegetables [ 99 - ]. Prostate cancer incidence is significantly lower in Asia when compared to North America, which has prompted research interest in the potential chemo-preventive action of soy and green tea which are a part of the diet in Asia.
Decreased risk of prostate and several other cancers has been seen with consumption of soy and green tea [ - ]. Catechins found in green tea and isoflavones in soybeans have anticarcinogenic properties, and they inhibit different phases of carcinogenesis [ , ] and metastasis [ - ].
Additionally, green tea polyphenols cause a reduction of IGF-1 levels [ - ]. Tomatoes seem to reduce the risk of prostate cancer. They contain high levels of lycopene which has potent anti-oxidant properties as well as cancer-preventive effects [ - ]. Tomato product consumption and lycopene intake were both associated with a decreased risk of prostate cancer [ ].
The Health Professional Follow-Up Study showed a decreased risk of prostate cancer with 2 - 4 servings of tomato sauce per week [ 95 ]. Venkateswaran and Klotz [ ] demonstrated that in the Lady transgenic mouse model, lycopene is able to reduce prostate cancer incidence only in association with selenium and vitamin E.
On the other hand, an open phase II study of lycopene in advanced prostate cancer could not demonstrate any clinical benefit of this agent [ ]. Similar results were seen in two other small epidemiological studies [ , ]. Thus, the evidence of a connection between tomatoes assumption and prostate cancer risk requires further investigation.
An inverse relationship was observed between sunlight, or UVB exposure, and incidence of prostate cancer [ , ], suggesting that vitamin D deficiency might increase prostate cancer risk development [ ]. The incidence of prostate cancer in African-American men is twice that of Caucasians, suggesting that race might play a role. There might be a role for vitamin D deficiency in this as UV radiation is blocked in darkly pigmented skin due to high melanin levels and this mechanism inhibits the conversion to vitamin D3 [ ].
Biochemical evidence supports a role for vitamin D in prostate growth [ , ]. Cell proliferation and invasion can be inhibited by vitamin D and its analogs, and stimulate cellular differentiation and apoptosis in prostate cancer cells as well as in tumor progression in animal models [ - ].
These findings provide a strong rationale for the use of vitamin D analogs as therapeutic agents for prostate cancer in a case that androgen deprivation therapy has failed [ ]. Further studies are needed to assess the use of vitamin D analogs as a chemopreventive or therapeutic approach in prostate cancer. Vitamin E is a vitamin which is fat soluble. Vegetable oils, egg yolks, and nuts are the important dietary sources of vitamin E. Tocopherols present in vitamin E have both potent cellular anti-oxidant with anticancer properties [ 54 , ].
Studies investigating the relationship between vitamin E and prostate cancer risk have shown contradicting results. The ATBC trial showed that in men who smoked supplementing daily vitamin E was not able to reduce the incidence of prostate cancer [ ]. In another large clinical trial SELECT trial , vitamin E supplementation did not show any benefit in 31, men with incident prostate cancer [ ].
Selenium is an essential micronutrient. It is found in the plants like tubers, cereals and legumes and animal products like meat, eggs, and seafood in the form of selenomethionine and selenocysteine. It has been inversely associated with several cancers, including prostate cancer.
These forms differ significantly in their biological effects, and it was shown they have different mechanisms of action. Selenomethionine acts on prostate cancer cells and induces cell cycle arrest [ , ]. It can also act by inducing apoptosis and inhibiting angiogenesis [ , ]. Methylseleninic acid acts via a caspase-mediated pathway and induces apoptosis [ ]. Interestingly, Chan et al [ ] emphasized the role of genotype with respect to the effectiveness of selenium intervention.
This study revealed that high selenium might be protective against an aggressive form of prostate carcinoma in men with the AA genotype of superoxide dismutase SOD -2 and increase the chances of having a worse tumor in men with a V allele. These data unveil the potential risks and benefits associated with selenium intervention in prostate cancer and may, in part, explain the conflicting results from other studies. Low folate and vitamin B12 can lead to altered methylation and lead to cancer development as these essential vitamins participate in DNA methylation, synthesis and repair [ ].
In vitro [ ], in vivo studies [ ] and genetic studies [ , ] on prostate cancer showed the role of folate in the development of an aggressive form of prostate cancer. Furthermore, elevated serum concentration of folate was associated with an increased proliferation of prostate cancer cells in some prostate samples collected from patients who underwent radical prostatectomy [ ].
In people who have prostate cancer, available data do not show an effect of consumption of folate on disease progression [ ] or survival [ ]. In conclusion, the association of folate and vitamin B 12 with prostate cancer is unclear and requires further investigation.
The relationship between alcohol use and several types of human cancers, including prostate cancer, has been since long observed [ ]. However, several cohort studies have suggested a weak correlation between alcohol intake and prostate cancer mortality [ - ], while others did not find any relation with increased risk [ ]. As opposite, Dennis et al reported a significant relationship between higher alcohol intake and prostate cancer risk with a relative risk RR ranging from 1.
Coffee consumption has been inversely associated with increased prostate cancer risk. Observational studies and some animal studies have revealed an association between long-term coffee drinking and improved glucose metabolism as well as insulin secretion [ ]. Consistently, a reduced risk of type 2 diabetes was observed in those patients who reported higher consumption of coffee.
A large prospective study demonstrated that coffee intake was weakly inversely associated with overall risk of prostate cancer, while it significantly lowered the risk of lethal and advanced prostate cancer when heavy coffee drinkers are compared to the one that drinks less coffee [ ].
Considering the effects of coffee consumption on insulin, antioxidants and androgens [ - ], the findings of this study are in agreement with the strongest associations between insulin, antioxidants and androgens with a lower incidence of prostate cancer in an advanced disease rather than for overall disease. Obesity is linked to advanced and aggressive prostate cancer [ , ], and high body mass index BMI is associated with more aggressive disease too and a worse outcome [ , ].
The possible explanation is that most of the time obese men present with alteration of circulating levels of metabolic and sex steroid hormones, which are known to be involved in prostate development as well as oncogenesis [ ]. Obesity, particularly when combined with physical inactivity, leads to the development of insulin resistance with reduced glucose uptake.
That, in turn, leads to chronically elevated blood levels of insulin. Additionally, adipose cells represent a source of inflammation as well as of macrophages in adipose, which releases inflammatory mediators [ ]. Three meta-analyses reported a modest but consistent association between obesity and prostate cancer incidence independently of BMI increase [ ].
Data from three national surveys in the US population reported that obesity is associated with more aggressive prostate cancer and higher mortality despite its lower incidence [ ].
Consequently, they will less likely undergo a biopsy, and detect the presence of the tumor until a more advanced stage [ , ]. Because obesity is a potential factor leading to lower detection of prostate cancer, clinicians should consider BMI when interpreting PSA concentration. Physicians should be aware of these factors to avoid misdiagnosis among obese men and thus should include BMI along with other well-established risk factors race, digital rectal examination DRE and family history in the existing prostate cancer risk calculator [ ].
Exercise is supposedly one of the easiest modifiable risk factor to manage in a way to obtain many benefits and relatively few side effects when it comes to prostate cancer prevention. Indeed, Keogh and McLeod found that veterans who exercised had a significantly lower risk of prostate cancer [ ]. Prostate cancer patients who are committed to exercise display lower PSA levels and delay in initiating androgen deprivation therapy ADT by 2 years compared with less active peers and have a lower risk of high-grade disease, other than having a greater quality of life and less fatigue [ ].
Active and passive exposures to cigarette smoke are considered carcinogenic for many human cancers [ ]. Association of smoking and prostate cancer risk may have either a hormonal or genetic basis. For instance, male smokers usually have higher levels of circulating sex hormones, which may increase prostate cancer risk or contribute to cancer progression [ , ]. On the other hand, functional polymorphisms in genes involved in polycyclic aromatic hydrocarbons PAHs metabolism, one of the carcinogenic chemical of the cigarette smoke [ ], may affect cancer onset and progression [ ].
Most of the epidemiological studies have not found a relationship between smoking and incidence of prostate cancer, while some cohort studies have documented a 2 - 3 times higher risk in smokers of more than a pack a day compared with nonsmokers [ , ].
However, these studies have not demonstrated a convincing dose-response relationship, neither have they evaluated the influence of possible dietary risk factors that are confusing [ ]. On the other hand, most studies examining the relationship between smoking and prostate cancer mortality demonstrated that smoking patients double the risk of dying from the disease compared to nonsmokers [ - ]. Moreover, there is a dose-response relationship between the numbers of cigarettes per year of the smoker 10 years before diagnosis and the increased mortality risk [ ].
In , Huggins and Hodges proposed that prostate cancer growth was driven by androgens, after observing the benefits of castration in prostate cancer patients [ ]. Several in vitro data obtained with well-differentiated prostate cancer cell lines showed that they respond to androgen stimulation and undergo apoptosis upon androgen withdrawal [ , ]. Likewise, in vivo studies showed that androgens promote tumorigenesis and xenograft growth in animal models, and tumor regression is seen upon androgen deprivation [ , ].
Clinically, ADT remains a mainstay in prostate cancer treatment, especially in advanced disease [ ]. Even though preclinical studies supported a role for androgens in prostate cancer pathogenesis, clinical data are still controversial [ ].
Further studies are needed to understand how those gene variations influence prostate cancer incidence. Although the positive role of androgens on prostate cell growth has been established, some studies found that in prostate cancer patients, the testosterone and DHT levels were low, suggesting that non-androgenic hormones, including estrogens, insulin and vitamin D may be involved in the prostate carcinogenesis.
Several studies have demonstrated that estrogen, including the natural hormone E2, induces multiple forms of genetic lesions such as chromosomal alterations, DNA damage, gene mutations, and microsatellite instability, strongly indicating that estrogen may serve as a carcinogen in the development of prostate cancer [ , ].
Hyperglycemia has been positively associated with cancers such as breast, pancreatic and colorectal [ ]. However, its link with prostate carcinogenesis is conflicting. Several studies found evidence of higher risk of more aggressive or advanced prostate cancer among men with abnormal glucose levels, with the association being not significant in two of the studies [ - ]. Conversely, several other studies reported a protective effect of hyperglycemia or type II diabetes against high-grade or more advanced prostate cancer [ - ].
For several decades, glucose has been documented as an important source of energy for rapid tumor cell proliferation [ ]. Evidence from clinical and genetic studies has also linked the hyperglycemic environment to carcinogenic processes such as apoptosis, oxidative stress, DNA damage and chronic inflammation, which may drive the aggressiveness and progression of cancer [ - ].
Lehrer et al showed that patients with high-risk prostate cancer had higher insulin levels [ ]. In addition, diet-induced hyperinsulinemia was associated with increased tumor growth in a xenograft model [ ].
Finally, the high level of circulating insulin decreases the production of insulin-like growth factor IGF-1 -binding proteins, increases the level of IGF-1 and increases the production of advanced glycation end products, which promote carcinogenesis [ ]. In the past years, several studies have recognized a crucial role for the components of IGF system in prostate cancer biology and its implication in both mitogenic and anti-apoptotic events in prostate cancer cell lines [ ].
The IGF system regulates many important cellular processes critical for normal prostate growth and development, such as proliferation, differentiation and cellular metabolism. The relevance of the IGF system has been evaluated in several studies. Increased serum concentration of IGF-1 was correlated to higher risk of prostate cancer [ - ]. However, preclinical studies [ - ] as well as clinical studies [ , ] showed conflicting results. Therefore, whether IGF-1 serum levels can be used as a prognostic tool requires further investigation.
There is a strong link between prostate cancer and inflammation, and in , Rudolf Virchow was the first to identify the high density of leukocytes in neoplastic samples, suggesting a positive association between inflammation and cancer [ ]. After that, both epidemiological and biological studies provided evidence that inflammation is behind the high-grade or aggressive prostate tumors and ultimately metastatic spread [ , ].
The evidence-based knowledge so far supports the role of inflammatory responses in the regulation of tumor microenvironment through the remodeling of the extracellular matrix ECM and initiation of epithelial-mesenchymal transition EMT. Indeed, inflammatory cells release growth factors and cytokines within the tumor microenvironment to promote angiogenesis and remodeling of the ECM, while further inflammatory cytokines released within the reactive stroma induce EMT-mediated responses [ ].
Patients with elevated PSA often present with intraprostatic inflammation detected with biopsies [ ]. Recently, an inflammatory effector, pentraxin 3, has been identified as a biomarker for predicting tumor progression due to prostatic inflammation in prostate cancer patients [ ]. Chronic inflammation causes proliferative inflammatory atrophy PIA [ ], which may develop prostatic intraepithelial neoplasia PIN a well-known precursor of prostate cancer [ ].
Prostatitis is the inflammation of the prostate gland that is hard to diagnose because it is often asymptomatic [ ]. Notably, men with symptoms of prostatitis are more likely to be diagnosed with prostate cancer as a result of the increased prevalence of biopsy [ ].
A first meta-analysis involving 11 studies between and provided statistical evidence that prostatitis is a significant risk factor in prostate cancer [ ]. This observation was confirmed later with another meta-analysis that included studies between and [ ].
Development of prostatitis is induced by one or a combination of factors including infections, chemical and physical trauma, and diet. Chemical irritation because of urine reflux, or abnormal flow of urine from the bladder back through the ureters, may cause chronic inflammation in the prostate [ ]. Non-sexually transmitted pathogens such as E. Also, many sexually transmitted organisms, including Neisseria gonorrhea [ ] and Chlamydia trachomatis [ ], can induce chronic infection and inflammation, that potentially increase the risk of developing prostate cancer [ ].
It appears clear that inflammation is the ubiquitous factor associated with increased risk of prostate cancer, independently of its source either pathogens or environmental factors.
Finally, the several signaling pathways involved in the inflammatory process that modifies prostate microenvironment and the complexity of biological events linking inflammation to prostate cancer progression and metastatic spread provide a broad range of promising targets for pharmaceutical treatments. Several epidemiologic studies evidenced that factors related to sexual behavior and STDs may be associated with prostate cancer [ ].
STDs represent a major public health problem worldwide. Human papilloma virus HPV and herpes simplex virus HSV are common STDs worldwide [ , ], the former being also involved in the etiology of cancer of cervix uteri and other anatomical sites [ , ]. The first claims of an etiological role of STDs in the development of prostate cancer date back to the s [ ] and several mechanisms were subsequently proposed to explain this association.
For gonorrhea and other bacterial infections, prostate inflammation and prostate atrophy are the processes that lead to prostate cancer, whereas for viral infections, the emphasis was placed on the transforming properties of viruses, in particular, HSV [ ]. A large population-based case-control study among African-American and white men, revealed an elevated risk of prostate cancer among men with a history of gonorrhea or syphilis [ ]. HPV, which occurs in human prostate cancer and benign prostatic tissue [ ], has been shown to transform human prostate cells in vitro.
Furthermore, seropositivity for HPV and HPV has been associated with subsequent prostate cancer in a Finnish cohort study [ , ], but a small case-control study of HPV and HPV [ ], and a large population-based case-control study [ ] showed little evidence of risk.
Finally, a recently published meta-analysis showed a weak association between HPV and prostate cancer and no association for HPV [ ]. To our knowledge, only three studies have been published so far investigating the association between Trichomonas vaginalis infection, a common cause of vaginitis in women, and prostate cancer risk.
Trichomonas vaginalis can also infect men, where it may cause asymptomatic urethritis and prostatitis. In particular, its frequent asymptomatic presentation may make it possible to persist untreated and ascend to the prostate, where it can establish foci of chronic inflammation that may eventually lead to prostate cancer [ ].
Mechanistically, Trichomonas vaginalis infection causes adherence of the protozoan to epithelial cells by decreasing the expression of anti-apoptotic genes; it also alters the production of IL-6 and monocyte chemotaxis proteins. Whereas an association between Trichomonas vaginalis serostatus and increased risk of prostate cancer was found, the same connection between seropositivity for this pathogen and progression to death from prostate cancer was not demonstrated [ ].
Despite the knowledge gained over the years about the etiopathogenesis of prostate cancer and the known high risk for men to be diagnosed with the disease during their lifetime, effective chemo-preventive agent that can safely be administered to impact the lives of men is still missing positively. The role of testosterone and pro-inflammatory pathways in the pathogenesis of prostate cancer provided some clues about the possibility to use inhibitors of testosterone endogenous production and inflammation.
By far the most promising and well-studied chemo-preventive agents are finasteride and dutasteride, which are inhibitors of 5-AR enzyme that converts testosterone into dihydrotestosterone, the most prevalent and potent androgen in prostate tissue, which is responsible for embryologic development [ ] and growth of the prostate as well as promotion of prostate cancer [ ].
Finasteride and dutasteride are effectively used for the treatment of benign prostatic hyperplasia [ - ] and were studied in clinical trials as potential chemopreventive agents. However, the results of these two trials were largely criticized for many aspects, including results from biopsies performed towards the end of the study as opposed to biopsies that are done when patients have elevated PSA or DRE abnormalities, the capability to prevent only low-grade cancers that will unlikely lead to death.
Therefore, identification of these subgroup of patients who may then undergo clinical trials with 5-AR inhibitors would address this intriguing question. A recent meta-analysis that included 20 observation studies with a total of 25, individuals evaluated the efficacy of NSAIDs in reducing prostate cancer risk [ ]. Several experimental studies have documented that COX-2 overexpression in prostate cancer can be effectively targeted by COX-2 selective inhibitors such as celecoxib [ ].
Several epidemiological and experimental evidence has demonstrated an inverse relationship between ASA use and prostate cancer, particularly after 5 or more years of use in men with metastatic disease [ ]. Surprisingly, low dose of ASA was associated with the highest risk [ ].
Finally, a multicenter study of over 90, documented a direct protective effect in patients ingesting six ASAs daily [ ]. Statin medications are inhibitors of the synthesis of lipids, particularly cholesterol and recently they showed to reduce PSA levels [ , ], and the risk of advanced or aggressive prostate cancer [ ]. They are also associated with improved outcomes after radiation therapy [ ] and radical prostatectomy [ ], although data for the latter are conflicting [ ]. The use of statins as a preventive agent may offer the advantage to reduce cholesterol levels and the risk of cardiac disease other than being safe.
Statins effect as a secondary preventive agent was recently tested in two studies. One trial enrolled patients and randomly assigned them to simvastatin or placebo treatment before radical prostatectomy and examined changes in benign and malignant tissue in the prostate specimen [ ].
The second trial is a phase II study evaluating the effect of atorvastatin and celecoxib on the levels of prostate cancer biomarkers, including PSA, in those patients with rising PSA levels after definitive local therapy [ ].
In conclusion, more clinical evidence is called to prove the effective advantage of using statins for prostate cancer prevention. The slow process of prostate carcinogenesis is also influenced by exposure to certain environmental factors that increase the risk of developing cancer. These include insecticides, herbicides and other organic compounds. Herbicides are active chemical compounds that are used to fight plant pests.
Agent orange AO is a mixture of two herbicides that were used as a defoliant between and in the Vietnam War and was contaminated with the toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin TCDD , a putative carcinogen.
Dioxins remain an area of important interest as these environmental toxins continue to be produced through chemical processing and municipal waste incineration. These chemicals can then enter the food chain through soil contamination [ ]. In , the National Academy of Science of the US recognized a positive association between herbicide exposure and many human cancers.
In a review published in , the authors found twice as many cases of prostate cancer among the exposed veterans of the Vietnam War compared with no-exposed veterans [ ]. They presented with earlier diagnostic ages, high-grade tumor, independently of other modifiable risk factors. It suggests that AO is the most predictive factor not only of developing prostate cancer but also of a higher histological grade and a greater probability of metastatic disease at diagnosis.
These data were later confirmed by the study of Ansbaugh et al that demonstrated a high correlation between AO exposure and risk of high-grade prostate cancer among Vietnam War veterans [ ]. Chlordecone also known as Kepone is an organochlorine insecticide with well-defined estrogenic properties [ , ] extensively used for decades in the French West Indies, to control the banana root borer. It is a carcinogenic agent with a long biologic half-life, and among its long-term effects, cancer is not excluded.
Indeed, it was shown that chlordecone causes hepatic tumors in laboratory mice and rats [ ] and it has been associated with increased risk of prostate cancer too. The prostate cancer risk associated with chlordecone exposure was higher in those men with a family history of prostate cancer, and similar findings were reported for pesticide exposure in the Agricultural Health Study [ - ].
There are two possible explanation: 1 Study subjects and their first-degree relatives may have similar patterns of exposure, which consequently lead to a statistical interaction between chlordecone exposure and family history of prostate cancer; 2 Genetic variations, such as inheritance of polymorphism in a metabolic enzyme that alters the balance between chlordecone bioactivation and detoxification in the body.
In line with the latter hypothesis, previous studies have shown differences in the inter-individual liver activity of chlordecone reductase between White and Japanese men [ , ]. Another harmful compound associated with a high risk of prostate cancer is BPA. BPA has been used to harden plastic since the s in the manufacture of polycarbonate plastic and epoxy resins that appear in thousands of consumer products since then [ ].
BPA is also used as a cross-linking compound in many food product containers [ ]. BPA leaching from these containers may contaminate food and beverage, which constitutes the main source of exposure of humans via a route of ingestion [ ].
In addition to ingestion, intake of BPA from the routes of inhalation or absorption via direct contact cannot be ignored [ , ]. The first evidence on the direct link between BPA exposure and human prostate cancer was reported in by two US research teams based on in vitro and in vivo experimental studies [ , ]. Abnormalities of centrosome a hallmark of malignant transformation induced by a low level of BPA and its analogs were underlined as the potential mechanism in promoting the formation of prostate cancer [ , ].
Tse et al published epidemiological evidence that cumulative exposure to BPA was associated with an excess risk of prostate cancer in the Chinese population [ ]. The authors found a positive association of prostate cancer with intake of deep-fried food and pickled vegetable that were independent of other risk factors [ - ]. Deep fried foods e. Vasectomy is the most frequent male contraception in the USA, with approximately , procedures performed annually. Its association with prostate cancer risk was explored in case-control and cohort studies with conflicting results.
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