Note: The Overview section summarizes the published evidence on this topic. The rest of the summary describes the evidence in more detail.
Other PDQ summaries on Prostate Cancer Screening; Prostate Cancer Treatment; and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Benefits From Finasteride and Dutasteride Chemoprevention
Chemoprevention with finasteride and dutasteride reduces the incidence of prostate cancer, but the evidence is inadequate to determine whether chemoprevention with finasteride or dutasteride reduces mortality from prostate cancer.
Magnitude of Effect: In the Prostate Cancer Prevention Trial (PCPT), absolute reduction in incidence for more than 7 years with finasteride as compared with placebo was 6% (18.4% with finasteride and 24.4% with placebo); relative risk reduction (RRR) for incidence was 24.8% (95% confidence interval [CI], 18.6%–30.6%). With long-term follow-up (median, 18.4 years), prostate cancer mortality was not statistically different between men in the placebo and finasteride groups of PCPT (hazard ratio [HR], finasteride vs. placebo, 0.75; 95% CI, 0.50–1.12). Long-term follow-up (median, 16 years) of PCPT participants found that with 7 years of finasteride therapy, there was a 21.1% relative reduction in risk of prostate cancer.[
In the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) randomized trial of dutasteride versus placebo, using the restricted crude rate, the absolute risk reduction was 5.1% at 4 years, and the RRR was 22.8% (95% CI, 15.2%–29.8%; P < .001). There was no difference in prostate cancer or overall mortality, although the number of deaths was small and none were due to prostate cancer. The reduction in prostate cancer incidence occurred primarily in Gleason score 5 to 6 cancers.[
|Study Design: Two randomized controlled trials; one for finasteride and one for dutasteride.|
|Internal Validity: Good for the outcome of incidence, poor for the outcome of mortality.|
|External Validity: The studies focused on different populations. The finasteride trial enrolled men with a prostate-specific antigen (PSA) of less than 3 ng/mL, constituting the majority of U.S. men, but those with a lower risk of cancer. In the dutasteride trial, men were at somewhat higher risk, with a PSA of 2.5 to 10.0 ng/mL and a prior negative biopsy. As such, results are generalizable primarily to these respective populations.|
Harms From Finasteride and Dutasteride Chemoprevention
Men in the finasteride group had statistically significantly more erectile dysfunction, loss of libido, and gynecomastia than men in the placebo group. Men in the finasteride group had a statistically significant higher incidence of high-grade (Gleason score 7–10) cancers during the study than did men in the placebo group (relative risk, 1.27; 95% CI, 1.07–1.50).[
Magnitude of Effect: Statistically significant increases in the following outcomes were observed in the finasteride group (a greater fraction of men in the finasteride group [36.8%] temporarily discontinued treatment at some time during the study for reasons other than death or a diagnosis of prostate cancer than in the placebo group [28.9%]):
|Percentage in finasteride group versus percentage in placebo group:
|Study Design: Two randomized controlled trials; one for finasteride and one for dutasteride.|
|Internal Validity: Good: The finasteride trial used two subject-completed sexual functioning instruments administered at enrollment, randomization, 6 months, and annually over the 7-year study. The dutasteride trial administered a sexual functioning instrument after completion of placebo run-in and annually thereafter.|
|Consistency: Good (evidence other than the randomized controlled trial supports these effects).|
|External Validity: As above, the studies evaluated two different populations: PSA less than or equal to 3 ng/mL in the finasteride trial and PSA of 2.5 to 10.0 ng/mL with a prior negative biopsy in the REDUCE trial. The results are most generalizable to these two populations.|
Overall, 4.3% of men in the dutasteride group compared with 2% of men in the placebo group discontinued the trial because of drug-related adverse events (P < .001). Men in the dutasteride group had a higher incidence of decreased libido, loss of libido, decreased semen volume, erectile dysfunction, and gynecomastia than men in the placebo group.[
Magnitude of Effect: Increases in the following outcomes were observed in the dutasteride group:
| Percentage in dutasteride group versus percentage in placebo group:
U.S. Food and Drug Administration (FDA) Review of Finasteride and Dutasteride
The Oncology Drugs Advisory Committee of the FDA examined both finasteride and dutasteride in 2010. Neither agent was recommended for use for chemoprevention of prostate cancer.
Other Prevention Interventions
The Selenium and Vitamin E Cancer Prevention Trial (SELECT [NCT00006392]) was a large randomized placebo-controlled trial of vitamin E and selenium. It showed no reduction in prostate cancer period prevalence, but an increased risk of prostate cancer with vitamin E alone.[
Magnitude of Effect: Compared with the placebo group in which 529 men developed prostate cancer, there was a statistically significant increase in prostate cancer in the vitamin E group (620 cases) but not in the selenium plus vitamin E group (555 cases) or in the selenium group (575 cases). The magnitude of increase in prostate cancer risk with vitamin E alone was 17%.
|Study Design for Vitamin E and Selenium: Randomized, placebo-controlled trial of selenium (200 µg/d from L-selenomethionine), vitamin E (400 IU/d of all-rac-[alpha]-tocopheryl acetate), or both.|
|Internal Validity: Good.|
|External Validity: Good.|
Carcinoma of the prostate is the most common tumor in men in the United States (other than skin cancer), with an estimated 288,300 new cases and 34,700 deaths expected in 2023.[
The extraordinarily high rate of clinically occult prostate cancer in the general population compared with the 20-fold lower likelihood of death from the disease indicates that many of these cancers have low biological risk. Concordant with this observation are the many series of patients with lower-risk (i.e., Gleason grade 6 and some low-volume Gleason grade 7 tumors) prostate cancer managed by surveillance alone with high survival rates at 5 and 10 years of follow-up.[
Because of marked variability in tumor differentiation from one microscopic field to another, many pathologists will report the range of differentiation among the malignant cells that are present in a biopsy using the Gleason grading system. This grading system includes five histological patterns distinguished by the glandular architecture of the cancer. The architectural patterns are identified and assigned a grade from 1 to 5 with 1 being the most differentiated and 5 being the least differentiated. The sum of the grades of the predominant and next most prevalent will range from 2 (well-differentiated tumors) to 10 (undifferentiated tumors).[
Treatment options available for prostate cancer include radical prostatectomy, external-beam radiation therapy, brachytherapy, cryotherapy, focal ablation, androgen deprivation with luteinizing hormone-releasing hormone analogs and/or antiandrogens, intermittent androgen deprivation, cytotoxic agents, and watchful waiting. Of all the means of management, only radical prostatectomy has been tested in a randomized clinical trial to assess survival benefit. In this study, prostatectomy was found to be superior to surveillance in men with localized prostate cancer, diagnosed in an era before widespread PSA screening. There were reduced rates of prostate cancer mortality (relative risk [RR], 0.56; 95% confidence interval [CI], 0.41–0.77) and overall mortality (RR, 0.71; 95% CI, 0.59–0.86).[
Because of considerable uncertainty regarding the efficacy of treatment and the difficulty with selecting patients for whom there is a known risk of disease progression, opinion in the medical community is divided regarding screening for carcinoma of the prostate. While both digital rectal examination and PSA screening have demonstrated reasonable performance characteristics (sensitivity, specificity, and positive predictive value) for the early detection of prostate cancer, conflicting outcomes of randomized trials examining the impact of screening on mortality has led some organizations to recommend for and others to recommend against screening.[
The tremendous impact of prostate cancer on the U.S. population and the financial burden of the disease for both patients and society have led to an increased interest in primary disease prevention.
The main treatment modalities for prostate cancer are surgery, radiation, hormonal, and active surveillance. For a detailed discussion, see Prostate Cancer Treatment. The goal of prostate cancer prevention interventions is to reduce the occurrence of prostate cancer, thereby obviating the need for treatment. As the effectiveness of prevention interventions improves, it is expected that the need for treatment will diminish.
Prostate cancer incidence escalates with increasing age. Although it is an unusual disease in men younger than 50 years, incidence rates increase substantially thereafter. Data from the Surveillance, Epidemiology and End Results (SEER) program for 2016 to 2020 showed that incidence rates were 111.7 per 100,000 for men aged 50 to 54 years, 253.9 per 100,000 for men aged 55 to 59 years, 438.1 per 100,000 for men aged 60 to 64 years, and 679.7 per 100,000 for men aged 65 to 69 years. After age 70 years, incidence rates stabilized or decreased modestly. Mortality rates showed a greater increasing trend with age than did incidence, increasing from 3.0 per 100,000 for men aged 50 to 54 years to 39.5 per 100,000 for men aged 65 to 69 years to 210.9 per 100,000 for men aged 80 to 84 years.[
Approximately 15% of men with a diagnosis of prostate cancer will be found to have a first-degree relative (e.g., brother, father) with prostate cancer, compared with approximately 8% of the U.S. population.[
The development of the prostate is dependent upon the secretion of dihydrotestosterone (DHT) by the fetal testis. Testosterone causes normal virilization of the Wolffian duct structures and internal genitalia and is acted upon by the enzyme 5-alpha-reductase (5AR) to form DHT. DHT has a 4-fold to 50-fold greater affinity for the androgen receptor than testosterone, and it is DHT that leads to normal prostatic development. Children born with abnormal 5AR (due to a change in a single base pair in exon 5 of the normal type II 5AR gene), are born with ambiguous genitalia (variously described as hypospadias with a blind-ending vagina to a small phallus) but masculinize at puberty because of the surge of testosterone production at that time. Clinical, imaging, and histological studies of kindreds born with 5AR deficiency have demonstrated a small, pancake-appearing prostate with an undetectable prostate-specific antigen (PSA) level and no evidence of prostatic epithelium.[
Other evidence suggesting that the degree of cumulative exposure of the prostate to androgens is related to an increased risk of prostate cancer includes the following:
Ecological studies have found a correlation between serum levels of testosterone, especially DHT, and overall risk of prostate cancer among African American, White, and Japanese males.[
The risk of developing and dying from prostate cancer is higher among Black men, is of intermediate levels among White men, and is lowest among native Japanese.[
An interesting observation is that although the incidence of latent (occult, histologically evident) prostate cancer is similar throughout the world, clinical prostate cancer varies from country to country by as much as 20-fold.[
Two studies were conducted within the PCPT in which prospective nutritional information was collected and all participants were recommended to undergo biopsy. Findings included that, among 9,559 participants there was no association between any supplement or nutrient (including fat) and risk of prostate cancer overall but the risk of high-grade cancer was associated with high intake of polyunsaturated fats. In a subset of 1,658 cases and 1,803 controls, specific fatty acids were examined and docosahexaenoic acid was associated with risk of high-grade disease while trans -fatty acids (TFA) 18:1 and TFA 18:2 were inversely associated with risk of high-grade disease. These large scale studies suggest a complex relationship between nutrients such as fat and risk of prostate cancer.[
The explanation for this possible association between prostate cancer and dietary fat is unknown. Several hypotheses have been advanced, including the following:
Dairy and Calcium Intake
A meta-analysis of ten cohort studies (eight from the United States and two from Europe), concluded that men with the highest intake of dairy products (relative risk [RR], 1.11; 95% confidence interval [CI], 1.00–1.22; P = .04) and calcium (RR, 1.39; 95% CI, 1.09–1.77; P = .18) were more likely to develop prostate cancer than men with the lowest intake. The pooled RRs of advanced prostate cancer were 1.33 (95% CI, 1.00–1.78; P = .055) for the highest versus lowest intake categories of dairy products and 1.46 (95% CI, 0.65–3.25; P > .2) for the highest versus lowest intake categories of calcium. High intake of dairy products and calcium may be associated with an increased risk of prostate cancer although the increase may be small.[
Regular multivitamin use has not been associated with the risk of early or localized prostate cancer. However, in this large (295,344 men) study, there was a statistically significantly increased risk of advanced and fatal prostate cancer among men with excessive use of multivitamins.[
The Aspirin/Folate Polyp Prevention Study, a placebo-controlled randomized trial of aspirin and folic acid supplementation for the chemoprevention of colorectal adenomas, was conducted between July 6, 1994, and December 31, 2006. In a secondary analysis, the authors addressed the effect of folic acid supplementation on the risk of prostate cancer. Participants were followed for up to 10.8 (median, 7.0; interquartile range, 6.0–7.8) years and asked periodically to report all illnesses and hospitalizations.[
Cadmium exposure is occupationally associated with nickel-cadmium batteries and cadmium recovery plant smelters and is associated with cigarette smoke.[
Dioxin (2,3,7,8 tetrachlorodibenzo-p-dioxin or TCDD) is a contaminant of an herbicide used in Vietnam. This agent is similar to many components of herbicides used in farming. A review of the linkage between dioxin and prostate cancer risk by the National Academy of Sciences Institute of Medicine Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides, found only two articles on prostate cancer with sufficient numbers of cases and follow-up to allow analysis.[
Several case-control and cohort studies, as well as two meta-analyses, suggested a significant but modest increase in the risk of prostate cancer in men with prostatitis (RR, 1.6) and in those with a history of syphilis or gonorrhea (RR, 1.4).[
The Prostate Cancer Prevention Trial (PCPT), a large randomized placebo-controlled trial of finasteride (an inhibitor of alpha-reductase), was performed in 18,882 men aged 55 years or older. At 7 years, the incidence of prostate cancer was 18.4% in the finasteride group versus 24.4% in the placebo group, a relative risk reduction (RRR) of 24.8% (95% confidence interval [CI], 18.6%–30.6%; P < .001). The finasteride group had more patients with Gleason grade 7 to 10, but the clinical significance of Gleason scoring is uncertain in conditions of androgen deprivation.[
Finasteride decreases the risk of prostate cancer but may also alter the detection of disease through effects on prostate-specific antigen (PSA), prostate digital rectal examination (DRE), and decreased prostate volume (24%), creating a detection bias.[
Examination of the outcomes of the PCPT found that finasteride significantly reduced the risk of high-grade prostatic intraepithelial neoplasia (HGPIN); HGPIN alone was reduced by 15% (RR, 0.85; 95% CI, 0.73–0.99) and HGPIN with prostate cancer was reduced by 31% (RR, 0.69; 95% CI, 0.56–0.85).[
A follow-up analysis of the PCPT of finasteride mapped study participants with the National Death Index, allowing for an analysis of prostate cancer-specific mortality. With 296,842 person-years of follow-up and a median follow-up of 18.4 years, of the 9,423 men randomly assigned to the finasteride group, there were 3,048 deaths of which 42 were caused by prostate cancer; of the 9,457 men randomly assigned to the placebo group, there were 2,979 deaths of which 56 were caused by prostate cancer. The 25% reduction in risk of prostate cancer death with finasteride was not statistically significant (hazard ratio, finasteride vs. placebo, 0.75; 95% CI, 0.50–1.12). It was concluded that the early concern for an increased risk of high-grade prostate cancer with finasteride was not borne out. In this study, it was notable that, of the 61 prostate cancer deaths for which original Gleason grading was available, 23 (38%) of the prostate cancer deaths were seen in men whose original biopsy Gleason grade was less than or equal to 6.[
A retrospective, population-based, cohort study from the U.S. Department of Veterans Affairs health care system examined the impact of 5-alpha reductase inhibitor (5-ARI) use before prostate cancer diagnosis on prostate cancer-specific mortality.[
When taken together, these biases call into question the conclusions, which appear to be at odds with the prostate cancer–specific mortality outcomes of the randomized PCPT.
The Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial randomly assigned 8,231 men aged 50 to 75 years at higher risk of prostate cancer (i.e., PSA 2.5–10.0 ng/mL) with one recent negative prostate biopsy to dutasteride at 0.5 mg daily or to placebo. The primary end point was prostate cancer diagnosed by prostate biopsy at 2 years and 4 years after randomization. After 4 years, among the 6,729 men (82% of initial population) who had at least one prostate biopsy, 25.1% of the placebo group and 19.9% of the dutasteride group had been diagnosed with prostate cancer, a statistically significant difference (absolute risk reduction, 5.1% and RRR, 22.8% [95% CI, 15.2%–29.8%]). The RRR in years 3 to 4 was similar to the RRR in years 1 to 2. The difference between the groups was entirely due to a reduction in prostate cancers with Gleason score 5 to 7. For years 3 to 4 there was a statistically significant increase in the dutasteride group compared with the placebo group in prostate cancers with Gleason score 8 to 10 (12 cancers in the dutasteride group vs. 1 cancer in the placebo group).[
Overall, there was no statistically significant difference in high-grade tumors for Gleason score 8 to 10 cancers in years 1 to 4 (29 tumors in the dutasteride group vs. 19 tumors in the placebo group, 0.9% vs. 0.6%; P = .15). However, in a retrospective analysis there was a statistically significant difference between years 3 to 4. Because this is a small retrospective subgroup, the finding of an increase in Gleason score 8 to 10 cancers is of uncertain validity. However, the finding of no reduction in these cancers is more significant.[
While long-term data are unavailable for dutasteride as a cancer prevention agent, evidence is now available that finasteride does not have a significant effect on overall survival or prostate cancer–specific survival. Its effect is primarily in preventing the diagnosis of prostate cancer and the subsequent events (staging, treatment, follow-up, and management of treatment-related side effects) after diagnosis.
Agents that are used for hormonal therapy of existing prostate cancers would be unsuitable for prostate cancer chemoprevention because of the cost and wide variety of side effects including sexual dysfunction, osteoporosis, and vasomotor symptoms (hot flushes).[
A Cochrane systematic review of all published studies of clinical outcome investigations of the prostate preventive effects of 5-ARIs through 2010 that were at least 1 year in duration concluded that finasteride and dutasteride reduce the risk of being diagnosed with prostate cancer among men who are screened regularly for prostate cancer. The review also concluded that mortality effects could not be assessed from these studies and that persistent use of these agents increased sexual and erectile dysfunction. The review was based on MEDLINE and Cochrane Collaboration Library computerized searches through June 2010 using the Medical Subject Headings terms and text words finasteride, dutasteride, neoplasms, azasteroids, reductase inhibitors, and enzyme inhibitors to identify randomized trials. Eight studies met the inclusion criteria. Only the PCPT and the REDUCE study were designed to assess the impact of 5-ARIs on prostate cancer period prevalence. Reviews of all eight studies concluded that compared with placebo, 5-ARIs resulted in 25% RR reduction in prostate cancers detected for cause (RR, 0.75; 95% CI, 0.67–0.83 and 1.4% absolute risk reduction [3.5% vs. 4.9%]). Six trials of 5-ARIs versus placebo assessed prostate cancers detected overall. Among these there was a 26% RR reduction favoring 5-ARIs (RR, 0.74; 95% CI, 0.55–1.00 and 2.9% absolute risk reduction [6.3% vs. 9.2%]). There were reductions across age, race, and family history. One placebo-controlled trial of men considered at greater risk for prostate cancer based on age, elevated PSA, and previous suspicion of prostate cancer leading to a prostate biopsy reported that dutasteride did not reduce prostate cancers detected for cause based on needle biopsy but did reduce risk of overall incident prostate cancer detected by biopsy by 23% (RR, 0.77; 95% CI, 0.7–0.85 and absolute risk reduction, 16.1% vs. 20.8%). There were reductions across age, family history of prostate cancer, PSA level, and prostate volume subgroups. The Cochrane review defined for cause cancers as follows:
Dietary Prevention With Fruit, Vegetables, and a Low-fat Diet
Results from studies of the association between dietary intake of fruits and vegetables and risk of prostate cancer are not consistent. A study evaluated 1,619 prostate cancer cases and 1,618 controls in a multicenter, multiethnic population. The study found that intake of legumes and yellow-orange and cruciferous vegetables was associated with a lower risk of prostate cancer.
The European Prospective Investigation into Cancer and Nutrition examined the association between fruit and vegetable intake and subsequent prostate cancer. After an average follow-up of 4.8 years, 1,104 men developed prostate cancer among the 130,544 male participants. No statistically significant associations were observed for fruit intake, vegetable intake, cruciferous vegetable intake, or the intake of fruits and vegetables combined.[
One study of dietary intervention over a 4-year period with reduced fat and increased consumption of fruit, vegetables, and fiber had no impact on serum PSA levels.[
While several agents, including alpha-tocopherol, selenium, lycopene, difluoromethylornithine,[
Chemoprevention with selenium and vitamin E
The SELECT (NCT00006392) was a large randomized placebo-controlled trial of vitamin E and selenium. It showed no reduction in prostate cancer period prevalence, but an increased risk of prostate cancer with vitamin E alone.[
Compared with the placebo group in which 529 men developed prostate cancer, there was a statistically significant increase in prostate cancer in the vitamin E group (620 cases), but not in the selenium plus vitamin E group (555 cases) or in the selenium group (575 cases). The magnitude of increase in prostate cancer risk with vitamin E alone was 17%. Of interest, the statistically increased risk of prostate cancer among men receiving vitamin E was seen after study supplements had been discontinued suggesting a longer-term effect of this agent.[
Chemoprevention with lycopene
Evidence exists that a diet with a high intake of fruits and vegetables is associated with a lower risk of cancer. Which, if any, micronutrients may account for this reduction is unknown. One group of nutrients often postulated as having chemoprevention properties is the carotenoids. Lycopene is the predominant circulating carotenoid in Americans and has a number of potential activities, including an antioxidant effect.[
The earliest studies of the association of lycopene and prostate cancer risk were generally negative before 1995 with only one study of 180 case-control patients showing a reduced risk.[
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Added text to state that the Overview section summarizes the published evidence on the topic of prostate cancer prevention. The rest of the summary describes the evidence in more detail.
Incidence and Mortality of Prostate Cancer
Updated statistics with estimated new cases and deaths for 2023 (cited American Cancer Society as reference 1). Also revised text to state that the lifetime risk of being diagnosed with prostate cancer for U.S. men is 12.9%, while the lifetime risk of dying from prostate cancer is 2.3% (cited Surveillance Research Program, National Cancer Institute as reference 4).
Risk Factors for Prostate Cancer Development
Revised text to state that data from the Surveillance, Epidemiology and End Results (SEER) program for 2016 to 2020 showed that incidence rates were 111.7 per 100,000 for men aged 50 to 54 years, 253.9 per 100,000 for men aged 55 to 59 years, 438.1 per 100,000 for men aged 60 to 64 years, and 679.7 per 100,000 for men aged 65 to 69 years; after age 70 years, incidence rates stabilized or decreased modestly. Mortality rates showed a greater increasing trend with age than did incidence, increasing from 3.0 per 100,000 for men aged 50 to 54 years to 39.5 per 100,000 for men aged 65 to 69 years to 210.9 per 100,000 for men aged 80 to 84 years (cited Surveillance Research Program, National Cancer Institute as reference 1).
This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about prostate cancer prevention. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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PDQ® Screening and Prevention Editorial Board. PDQ Prostate Cancer Prevention. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/types/prostate/hp/prostate-prevention-pdq. Accessed <MM/DD/YYYY>. [PMID: 26389405]
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Last Revised: 2023-05-22
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