Learn  /  Prostate Cancer, Explained
Chapter 2

Prostate Cancer

This chapter is general patient education from the book Prostate Cancer, Explained. It is not medical advice for your specific situation. Always discuss your care with your own doctor.

Opening Story

David, a 58-year-old firefighter, went to his doctor for a routine physical. His PSA came back at 5.2 ng/mL. "When my doctor said the word 'cancer,' my mind went blank," he recalls. "I didn't hear anything else for the next ten minutes. All I could think about was: Am I going to die?" David's biopsy showed Gleason 3+4 prostate cancer. Today, three years after treatment, he is cancer-free and back at work. "The fear was worse than the disease," he says. "Once I understood what prostate cancer actually is — how common it is, how treatable it is — I could breathe again."

This chapter will explain what prostate cancer is, how common it is, what causes it, how it spreads, and what can be done to reduce the risk of getting it.

What Is Prostate Cancer?

In Chapter 1, we learned that the prostate is a gland — meaning it is made mostly of glandular cells that produce fluid. Prostate cancer occurs when these glandular cells begin to grow in an abnormal, uncontrolled way. Because the cancer arises from glandular cells, the medical term for it is adenocarcinoma. More than 95% of all prostate cancers are adenocarcinomas.¹

However, the prostate also contains other types of cells, and rarely, cancer can arise from these non-glandular cells. These rare types include:

These rare types together account for fewer than 5% of prostate cancers and are discussed in a later chapter on special cases.

How is prostate cancer different from BPH?

Both BPH and prostate cancer involve abnormal cell growth, but they are fundamentally different:

An important point: BPH does not turn into cancer. They are separate conditions that happen to occur in the same organ.

Prostate cancer is multifocal

Unlike many other cancers that form a single tumor, prostate cancer is often multifocal — meaning there are multiple separate areas of cancer within the prostate at the same time. This is why a biopsy may miss some areas of cancer, and why the full extent of the disease is sometimes only discovered when the entire prostate is removed during surgery and examined by a pathologist.

Prostate cancer is not contagious. It cannot be passed from one person to another through any form of contact.

Symptoms of Prostate Cancer

One of the most important things to understand about prostate cancer is that early prostate cancer usually has no symptoms at all. Most men are diagnosed because of an abnormal PSA blood test or an abnormal finding on a digital rectal exam (DRE), not because they felt something was wrong.¹ ²

When symptoms do occur, they can be similar to those caused by BPH:

Urinary symptoms:

Sexual symptoms:

Symptoms of advanced (metastatic) prostate cancer:

Important: Having these symptoms does not mean you have cancer. Many of these symptoms are far more commonly caused by BPH, prostatitis, or other non-cancerous conditions. But they should always be evaluated by a doctor.

How Prostate Cancer Spreads

Prostate cancer growth is usually driven by testosterone (produced mostly in the testes, and to a lesser extent in the adrenal glands) and its more potent form, dihydrotestosterone (DHT). This is why prostate cancer is classified as a hormone-driven cancer, and why treatments that lower testosterone levels are effective.¹ ³

Prostate cancer can spread in several ways:

1. Local spread (within and around the prostate):

2. Regional spread (to nearby lymph nodes):

3. Distant spread (metastasis):

A critical point: Even when prostate cancer spreads to the bones, liver, or lungs, it is still prostate cancer — not bone cancer, liver cancer, or lung cancer. The cells still look and behave like prostate cancer cells under the microscope, and they are treated with prostate cancer therapies. The cancer may accumulate new genetic mutations as it spreads, but its identity remains prostate cancer.

How prostate cancer spreads
1. Local 2. Regional 3. Distant Through the capsule (ECE), into the seminal vesicles, toward bladder or rectum Cancer cells travel through lymph channels to pelvic lymph nodes Bones (spine, pelvis, ribs) are the most common site; liver and lungs less often Even when it reaches bone, it is still prostate cancer, not bone cancer, and it is treated with prostate cancer therapies.
Prostate cancer spreads in three stages: local, then to lymph nodes, then to distant organs.

How Common Is Prostate Cancer?

Prostate cancer is extremely common. Here are the key numbers:

In the United States:

Worldwide:

By age:

By race and ethnicity (in the US):

These racial disparities are complex and not fully understood. They likely reflect a combination of biological differences (genetics, tumor biology), social determinants of health (access to care, insurance, education), and screening patterns. Importantly, studies show that when Black patients receive equitable treatment, their outcomes improve significantly.⁶

Trends over time:

Prostate cancer incidence has had a roller-coaster pattern:⁴

Prostate cancer by the numbers (US)
How common? ~313,000 new cases every year 1 in 8 Survival 95%+ survive More than 95% of men diagnosed do not die from prostate cancer. Incidence by race and ethnicity (per 100,000 men) Black173.0 White97.1 Hispanic~75 Asian / PI~50 Black men: 67% higher incidence and about 2x higher mortality. Median age at diagnosis: 67.
Common but rarely fatal, with a striking gap in incidence across racial and ethnic groups.

What Causes Prostate Cancer?

The exact cause of prostate cancer is not known in most cases. However, research has identified several factors that increase or decrease the risk. These are divided into factors you cannot change (non-modifiable) and factors you may be able to change (modifiable).

Non-Modifiable Risk Factors (You Cannot Change These)

1. Sex:

Only people with a prostate can get prostate cancer. This includes cisgender men and transgender women.

2. Age:

Age is the strongest risk factor. Prostate cancer is rare before 40, uncommon before 50, and becomes increasingly common with each decade of life. By age 80, autopsy studies show that the majority of men have some cancer cells in their prostate.¹

3. Family history:

Having a first-degree relative (father or brother) with prostate cancer approximately doubles your risk. The risk increases further if:⁸ ⁹

Men with a strong family history should discuss earlier screening with their doctor. The NCCN recommends that men with a concerning family history consider beginning shared decision-making about PSA screening at age 40.⁹

4. Genetics:

Prostate cancer is one of the most heritable cancers. Twin studies suggest that more than 50% of prostate cancer risk is attributable to genetic factors.¹ Specific genes associated with increased risk include:

Men with known or suspected hereditary cancer syndromes should be referred to a genetic counselor.⁹

5. Race/Ethnicity:

As discussed above, Black men have the highest risk, followed by White men, Hispanic men, and Asian men. The reasons are complex and include both biological and social factors.¹ ⁶

Modifiable Risk Factors (You May Be Able to Change These)

1. Diet:

2. Obesity:

Being overweight or obese is associated with an increased risk of advanced and aggressive prostate cancer, though not necessarily overall prostate cancer risk.¹⁵ Central obesity (belly fat) appears to be particularly important. Obesity may also worsen outcomes after diagnosis.

3. Smoking:

The relationship between smoking and prostate cancer is complex. Current smoking may be associated with a lower overall incidence of prostate cancer (possibly due to lower PSA levels and less screening), but smoking is consistently associated with higher risk of aggressive, fatal prostate cancer and worse outcomes after treatment.¹⁵ ¹⁶

4. Physical activity:

Regular physical activity, particularly vigorous exercise, appears to reduce the risk of advanced prostate cancer. A large umbrella review found that occupational physical activity was associated with a 13% reduction in prostate cancer risk.¹⁶

5. Vasectomy:

Some studies have suggested a small increase in prostate cancer risk with vasectomy, but this remains controversial and may be due to detection bias (men who have vasectomies may be more health-conscious and get screened more).¹⁵

6. Environmental exposures:

Risk factors you can and cannot change
Cannot Change May Be Able to Change AgeFamily historyGenetics (BRCA2)Race / ethnicitySex Risk rises each decade after 50 Father or brother doubles risk BRCA2 raises risk 4.5 to 8.6x Black men highest, Asian lowest Only people with a prostate DietWeightExerciseSmokingExposures Less red meat and fat; more fish Obesity raises aggressive risk 150 min/week of activity Linked to fatal prostate cancer Agent Orange, radiation at work You cannot change your age, race, or genes, but you can eat well, stay active, keep a healthy weight, and avoid smoking. Heart-healthy is prostate-healthy.
Some risk factors are fixed; several important ones are within your control.

Prevention: Can You Reduce Your Risk?

While there is no guaranteed way to prevent prostate cancer, several strategies may help reduce risk:

Diet and Lifestyle

The best evidence supports a "heart-healthy equals prostate-healthy" approach:¹⁷

Finasteride: The Prostate Cancer Prevention Trial (PCPT)

The most important prostate cancer prevention study ever conducted was the Prostate Cancer Prevention Trial (PCPT), published in the New England Journal of Medicine in 2003.²¹

The study: 18,882 men aged 55 or older with normal PSA (≤3.0 ng/mL) and normal DRE were randomly assigned to take either finasteride (5 mg/day) or placebo for 7 years.²¹

The results:

The paradox: More high-grade cancers (Gleason 7–10) were found in the finasteride group (37% of cancers vs. 22% in placebo). This raised concerns that finasteride might cause aggressive cancer.²¹

The resolution: Subsequent analyses showed that this paradox was likely due to detection bias — finasteride shrinks the prostate, which makes biopsies more accurate at finding cancer, including high-grade cancer. Additionally:²⁴ ²⁵

The REDUCE trial tested dutasteride (another 5-alpha reductase inhibitor) in higher-risk men (PSA 2.5–10 ng/mL with a negative biopsy) and found a similar 23% reduction in prostate cancer.²³

A large Swedish study of over 350,000 men found that 5-ARI use was associated with a 9% reduction in prostate cancer mortality (HR 0.91), with a stronger effect among men who used 5-ARIs for more than 4 years.²⁷ A Canadian study of over 3 million men similarly found that 5-ARI use was associated with a 31% reduction in prostate cancer mortality (HR 0.69).²⁸

Side effects of finasteride include:²¹

Important note: Despite the evidence, the FDA has not approved finasteride for prostate cancer prevention, and in 2011 added a label warning about the potential increase in high-grade cancer. Most experts now believe this concern was overstated based on detection bias.²⁴

Finasteride and mental health:

There has been concern about psychiatric side effects of 5-alpha reductase inhibitors. A large Swedish study of over 2.2 million men found:²⁹

A Canadian study of 93,197 men found similar results: no increased suicide risk, but increased risk of self-harm (HR 1.88) and depression (HR 1.94) during the first 18 months, with the absolute increase being small (237 additional depression cases per 100,000 patient-years).³⁰

A 2025 pharmacovigilance analysis found stronger signals for depression and suicidality with finasteride in younger men (ages 18–44), particularly when used for hair loss rather than BPH.³¹

Bottom line: Men taking finasteride should be aware of the potential for mood changes and should report any symptoms of depression to their doctor promptly.

The finasteride prevention story
PCPT trial:risk down24.8% REDUCE:dutasteridedown 23% No survivaldifference at15 years Mortalitydown 25%(not signif.) Detection biasexplained: betterbiopsy accuracy FDA adds labelwarning on high-grade cancer Sustained 21%reduction; safeafter stopping Swedish study:9% lower death,350,000+ men 2003 2007 2010 2011 2013 2018 2019 2023 Finasteride cuts risk about 25% with no rise in overall mortality, but it is not FDA-approved for prevention.
Two decades of evidence turned an early scare into reassurance about finasteride.

Selenium and Vitamin E: The SELECT Trial

The Selenium and Vitamin E Cancer Prevention Trial (SELECT) was a large randomized trial of 35,533 healthy men testing whether selenium (200 μg/day), vitamin E (400 IU/day), both, or placebo could prevent prostate cancer.³² ³³

The results were disappointing and concerning:

The earlier NPC trial (1983) had suggested selenium might reduce prostate cancer risk (HR 0.48), but this was a secondary endpoint in a smaller study of men who may have been selenium-deficient. The SELECT trial, conducted in a nutritionally replete population, definitively showed no benefit.³²

Bottom line: Men should avoid selenium or vitamin E supplementation at doses exceeding recommended dietary intakes. Getting these nutrients from food is preferred.³⁴

Zinc

The prostate contains the highest concentration of zinc in the male body, and zinc plays important roles in prostate cell function.³⁵ ³⁶ However, the relationship between zinc supplementation and prostate cancer is complex:

Bottom line: Moderate zinc intake from food is likely safe and may be beneficial. However, high-dose zinc supplements (>75 mg/day) should be avoided, as they may increase the risk of aggressive prostate cancer.³⁸

NSAIDs, Statins, and Metformin

These common medications have shown some promise in prostate cancer prevention, though none is approved for this purpose:

Bottom line: These medications should not be taken solely for prostate cancer prevention. However, men who are already taking them for their primary indications (heart disease, diabetes, pain) may derive some additional prostate cancer benefit.¹⁷

Symptom Assessment Tools

Several validated questionnaires are used by doctors to measure and track symptoms related to prostate conditions. Understanding these tools can help you communicate more effectively with your medical team.

IPSS (International Prostate Symptom Score) / AUA Symptom Index

The IPSS is the most widely used questionnaire in urology worldwide.⁴¹ It contains:

How to interpret your score:⁴¹

SHIM (Sexual Health Inventory for Men) / IIEF-5

The SHIM is a 5-question version of the longer International Index of Erectile Function (IIEF) questionnaire.⁴² It is used to diagnose the presence and severity of erectile dysfunction (ED):

EPIC-26 (Expanded Prostate Cancer Index Composite)

The EPIC-26 is a 26-question tool specifically designed for prostate cancer patients. It measures quality of life across four domains:

This questionnaire is particularly important because it captures the side effects of prostate cancer treatment and helps doctors and patients track changes over time. The NCCN recommends measuring baseline function with a tool like EPIC-26 before starting any treatment.

Myth vs. Fact

Fact: While prostate cancer is more common in older men, it can occur in men in their 40s and 50s, especially those with a family history or genetic predisposition. Younger men with prostate cancer sometimes have more aggressive disease.

Fact: Early prostate cancer almost never causes symptoms. By the time symptoms appear, the cancer may be advanced. This is why screening with PSA is important.¹ ²

Fact: More than 95% of men diagnosed with prostate cancer do not die from it. The 5-year relative survival rate for localized and regional prostate cancer is nearly 100%.¹

Fact: The SELECT trial showed that vitamin E supplements actually increased prostate cancer risk by 17%, and selenium provided no benefit. Getting these nutrients from food is safer.³³ ³⁴

Fact: Prostate cancer cannot be transmitted from one person to another. It is not caused by an infection (unlike some other cancers such as cervical cancer).

Fact: Many conditions can raise PSA, including BPH, prostatitis, urinary infections, and even recent sexual activity. PSA is a screening tool, not a diagnostic test.²

Questions to Ask Your Doctor

  1. Based on my age, race, and family history, what is my risk of prostate cancer?
  2. Should I be screened for prostate cancer? At what age should I start?
  3. Are there genetic tests I should consider based on my family history?
  4. What lifestyle changes can I make to reduce my risk?
  5. I am taking finasteride/dutasteride — does this affect my PSA results?
  6. Should I take any supplements for prostate health?
  7. I have urinary symptoms — could these be from cancer or from BPH?

Key Takeaways

  1. Prostate cancer is the most common cancer in men (excluding skin cancer). About 1 in 8 men will be diagnosed, but more than 95% will not die from it.
  2. Early prostate cancer has no symptoms. Screening with PSA is the primary way it is detected early.
  3. The strongest risk factors are age, family history, genetics, and Black race. Modifiable risk factors include diet, obesity, and physical activity.
  4. Finasteride reduces prostate cancer risk by about 25% with no increase in mortality, but it is not FDA-approved for prevention and may cause sexual side effects and depression.
  5. Vitamin E and selenium supplements do not prevent prostate cancer and may increase risk. A diet rich in tomatoes, cruciferous vegetables, and fish is a better approach.
  6. "Heart-healthy equals prostate-healthy" — the same lifestyle that protects your heart also appears to protect your prostate.

Support Resources

References

  1. 1. Raychaudhuri R, Lin DW, Montgomery RB. Prostate cancer: a review. JAMA. 2025;333(16):1433–1446.
  2. 2. Pinsky PF, Parnes H. Screening for prostate cancer. New England Journal of Medicine. 2023;388(15):1405–1414.
  3. 3. Lowrance W, Dreicer R, Jarrard DF, et al. Updates to advanced prostate cancer: AUA/SUO guideline (2023). Journal of Urology. 2023;209(6):1082–1090.
  4. 4. Kratzer TB, Mazzitelli N, Star J, et al. Prostate cancer statistics, 2025. CA: A Cancer Journal for Clinicians. 2025. doi:10.3322/caac.70028.
  5. 5. US Preventive Services Task Force, Grossman DC, Curry SJ, et al. Screening for prostate cancer: US Preventive Services Task Force recommendation statement. JAMA. 2018;319(18):1901–1913.
  6. 6. Saka AH, Giaquinto AN, McCullough LE, et al. Cancer statistics for African American and Black people, 2025. CA: A Cancer Journal for Clinicians. 2025;75(2):111–140.
  7. 7. Du XL, Gao D, Li Z. Incidence trends in prostate cancer among men in the United States from 2000 to 2020 by race and ethnicity, age and tumor stage. Frontiers in Oncology. 2023;13:1292577.
  8. 8. Wei JT, Barocas D, Carlsson S, et al. Early detection of prostate cancer: AUA/SUO guideline part I: prostate cancer screening. Journal of Urology. 2023;210(1):46–53.
  9. 9. National Comprehensive Cancer Network. NCCN Guidelines: Prostate Cancer Early Detection. Version 2.2026; and NCCN Guidelines: Genetic/Familial High-Risk Assessment: Breast, Ovarian, Pancreatic, and Prostate. Version 3.2026.
  10. 10. Cheng HH, Shevach JW, Castro E, et al. BRCA1, BRCA2, and associated cancer risks and management for male patients: a review. JAMA Oncology. 2024;10(9):1272–1281.
  11. 11. Nyberg T, Frost D, Barrowdale D, et al. Prostate cancer risks for male BRCA1 and BRCA2 mutation carriers: a prospective cohort study. European Urology. 2020;77(1):24–35.
  12. 12. Giri VN, Knudsen KE, Kelly WK, et al. Role of genetic testing for inherited prostate cancer risk: Philadelphia consensus conference 2017. Journal of Clinical Oncology. 2018;36(4):414–424.
  13. 13. Ballon-Landa E, Parsons JK. Nutrition, physical activity, and lifestyle factors in prostate cancer prevention. Current Opinion in Urology. 2018;28(1):55–61.
  14. 14. Aune D, Navarro Rosenblatt DA, Chan DS, et al. Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies. American Journal of Clinical Nutrition. 2015;101(1):87–117.
  15. 15. Pernar CH, Ebot EM, Wilson KM, Mucci LA. The epidemiology of prostate cancer. Cold Spring Harbor Perspectives in Medicine. 2018;8(12):a030361.
  16. 16. Solano-Iturri JD, Beitia M, Errarte EG, et al. Modifiable risk factors for prostate cancer: an umbrella review of meta-analyses. Cancers. 2023;15(4):1069.
  17. 17. Murtola TJ, Tammela TL, Lahtela J, Auvinen A. Antidiabetic medication and prostate cancer risk: a population-based case-control study. American Journal of Epidemiology. 2008;168(8):925–931.
  18. 18. Zu K, Mucci L, Rosner BA, et al. Dietary lycopene, angiogenesis, and prostate cancer: a prospective study in the prostate-specific antigen era. Journal of the National Cancer Institute. 2014;106(2):djt430.
  19. 19. Miyata Y, Shida Y, Hakariya T, Sakai H. Anti-cancer effects of green tea polyphenols against prostate cancer. Molecules. 2019;24(1):193.
  20. 20. Kenfield SA, DuPre N, Richman EL, Stampfer MJ, Chan JM, Giovannucci EL. Mediterranean diet and prostate cancer risk and mortality in the Health Professionals Follow-up Study. European Urology. 2014;65(5):887–894.
  21. 21. Thompson IM, Goodman PJ, Tangen CM, et al. The influence of finasteride on the development of prostate cancer. New England Journal of Medicine. 2003;349(3):215–224.
  22. 22. Thompson IM, Tangen CM, Goodman PJ, et al. Finasteride improves the sensitivity of digital rectal examination for prostate cancer detection. Journal of Urology. 2007;177(5):1749–1752.
  23. 23. Andriole GL, Bostwick DG, Brawley OW, et al. Effect of dutasteride on the risk of prostate cancer. New England Journal of Medicine. 2010;362(13):1192–1202.
  24. 24. Thompson IM Jr, Goodman PJ, Tangen CM, et al. Long-term survival of participants in the Prostate Cancer Prevention Trial. New England Journal of Medicine. 2013;369(7):603–610.
  25. 25. Goodman PJ, Tangen CM, Darke AK, et al. Long-term effects of finasteride on prostate cancer mortality. New England Journal of Medicine. 2019;380(4):393–394.
  26. 26. Unger JM, Hershman DL, Till C, et al. Using Medicare claims to examine long-term prostate cancer risk of finasteride in the Prostate Cancer Prevention Trial. Journal of the National Cancer Institute. 2018;110(11):1208–1215.
  27. 27. Wallerstedt A, Strom P, Gronberg H, Nordstrom T, Eklund M. Risk of prostate cancer in men treated with 5α-reductase inhibitors — a large population-based prospective study. Journal of the National Cancer Institute. 2023;115(2):198–205.
  28. 28. Fleshner NE, Lucia MS, Egerdie B, et al. Dutasteride in localised prostate cancer management: the REDEEM randomised, double-blind, placebo-controlled trial. Lancet. 2012;379(9821):1103–1111.
  29. 29. Hagberg KW, Divan HA, Persson R, Nickel JC, Jick SS. Risk of dementia, depression, and suicide in men prescribed 5α-reductase inhibitors: nationwide cohort study in Sweden. Pharmacotherapy. 2024;44(1):47–58.
  30. 30. Welk B, McArthur E, Garg AX, et al. The risk of self-harm and depression in men prescribed 5α-reductase inhibitors. JAMA Internal Medicine. 2017;177(5):683–691.
  31. 31. Nguyen DD, Marchese M, Cone EB, et al. Investigation of suicidality and psychological adverse events in patients treated with finasteride. JAMA Dermatology. 2021;157(1):35–42.
  32. 32. Lippman SM, Klein EA, Goodman PJ, et al. Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2009;301(1):39–51.
  33. 33. Klein EA, Thompson IM Jr, Tangen CM, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA. 2011;306(14):1549–1556.
  34. 34. Kristal AR, Darke AK, Morris JS, et al. Baseline selenium status and effects of selenium and vitamin E supplementation on prostate cancer risk. Journal of the National Cancer Institute. 2014;106(3):djt456.
  35. 35. Costello LC, Franklin RB. A comprehensive review of the role of zinc in normal prostate function and metabolism; and its implications in prostate cancer. Archives of Biochemistry and Biophysics. 2016;611:100–112.
  36. 36. Kolenko V, Teper E, Kutikov A, Uzzo R. Zinc and zinc transporters in prostate carcinogenesis. Nature Reviews Urology. 2013;10(4):219–226.
  37. 37. Epstein MM, Kasperzyk JL, Andrén O, et al. Dietary zinc and prostate cancer survival in a Swedish cohort. American Journal of Clinical Nutrition. 2011;93(3):586–593.
  38. 38. Leitzmann MF, Stampfer MJ, Wu K, Colditz GA, Willett WC, Giovannucci EL. Zinc supplement use and risk of prostate cancer. Journal of the National Cancer Institute. 2003;95(13):1004–1007.
  39. 39. Gonzalez A, Peters U, Lampe JW, White E. Zinc intake from supplements and diet and prostate cancer. Nutrition and Cancer. 2009;61(2):206–215.
  40. 40. Mahmoud AM, Al-Alem U, Dabbous F, et al. Zinc intake and risk of prostate cancer: case-control study and meta-analysis. PLoS One. 2016;11(11):e0165956.
  41. 41. Barry MJ, Fowler FJ Jr, O'Leary MP, et al. The American Urological Association symptom index for benign prostatic hyperplasia. Journal of Urology. 1992;148(5):1549–1557.
  42. 42. Rosen RC, Cappelleri JC, Smith MD, Lipsky J, Peña BM. Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. International Journal of Impotence Research. 1999;11(6):319–326.