ReadYourDNA

Prostate Cancer

Where your DNA places you among other people, and the studies behind it.

General information

Not tailored to your result, and not medical advice

Quit or Avoid Smoking: A meta-analysis of 51 prospective cohorts covering 11,823 prostate cancer deaths found current smokers had about 24 percent higher prostate cancer mortality than never smokers (RR 1.24, 95% CI 1.18 to 1.31), with a dose-response by cigarettes smoked per day. The association with simply being diagnosed is weak and actually runs slightly the other way in the PSA screening era (RR 0.90 for incidence), which reflects who gets screened more than biology. The honest summary is that smoking looks more connected to how aggressively prostate cancer behaves than to whether it appears at all. European Urology (PubMed)

Make Room for Vigorous Exercise: The Health Professionals Follow-up Study tracked 49,160 men for 26 years. Men in the highest fifth of vigorous activity had a 30 percent lower risk of advanced prostate cancer (HR 0.70, 95% CI 0.53 to 0.92) and a 25 percent lower risk of lethal prostate cancer (HR 0.75, 95% CI 0.59 to 0.94) than men in the lowest fifth, and the pattern held in a heavily screened subgroup. Total activity of any intensity showed no association with prostate cancer overall, so the signal sat with intensity rather than general movement. This is observational data, so it shows association rather than proof of cause. European Urology (PMC)

Be Skeptical of Prostate Supplements: SELECT randomised 34,887 men to vitamin E, selenium, both, or placebo, and the updated results found vitamin E alone increased prostate cancer incidence by 17 percent (HR 1.17, 99% CI 1.004 to 1.36), an absolute excess of about 1.6 cases per 1,000 person-years. Selenium alone gave no benefit (HR 1.09), and neither did the combination (HR 1.05). Antioxidant supplements marketed for prostate health have not been shown to prevent this cancer, and one of the most studied measurably raised risk. The trial tested supplements, not ordinary food. JAMA (PMC)

Know What Cannot Be Changed: The strongest established prostate cancer risk factors are not behavioral: increasing age, having a father or brother with the disease, and being African American, among whom it occurs more often. NCI's prevention review is blunt about the rest, stating it is not known whether decreasing fat or increasing fruit and vegetables in the diet lowers risk, and that lycopene results are inconsistent across studies. Folic acid supplements raised risk in one trial while adequate dietary folate was associated with lower risk. It is more honest to treat prostate cancer as largely not lifestyle-preventable and to put the effort into general health and into knowing your family history. NCI (PDQ)

Get Urinary Changes Looked At: Prostate cancer often has no symptoms at first, because it usually starts growing in the outer part of the gland and does not press on the urethra until it has grown or spread. Changes worth noticing include difficulty starting or straining to urinate, a weak or stop-start flow, needing to urinate more often at night, and blood in urine or semen, while lower back pain and unexplained weight loss are listed as possible signs the cancer has spread. These symptoms do not always mean cancer and are often caused by something else, commonly a non-cancerous enlarged prostate, but they are worth taking to a clinician rather than waiting out. A PSA blood test exists, and it, along with any family history, is a reasonable thing to raise in that conversation. NHS

Genetics vs Environment

How much of this is genetic?

Genetics explains 57% of why people differ in this trait. The rest is environment, daily habits and chance.

Heritability estimate: Mucci et al. 2016, JAMA

About Prostate Cancer

Background and further reading

Prostate cancer arises in the prostate, a small gland below the bladder that produces seminal fluid. It is one of the most commonly diagnosed cancers in men worldwide, and incidence rises steeply with age, with most cases diagnosed after 65. The great majority of prostate cancers are slow-growing and confined to the gland, and many men with the disease never experience symptoms from it; a minority are aggressive and can spread. Early disease is usually silent, while advanced disease can cause urinary changes, blood in the urine or semen, or bone pain. This score is educational and reflects inherited predisposition only; it is not a diagnosis or a measure of whether cancer is present.

Genetic basis: Prostate cancer is among the most heritable common cancers. The Nordic Twin Study of Cancer estimated its heritability at roughly 57%, higher than for most other cancer types [1]. The bulk of that heritability is polygenic, spread across many common variants each of small effect. Large trans-ancestry genome-wide association studies have identified well over 250 risk loci, including strong and repeatedly replicated signals in the 8q24 gene desert, and at TERT, MSMB, and KLK3 (the gene encoding PSA) [2]. Polygenic scores built from these variants stratify predisposition across a wide range. Separately, rare higher-penetrance variants, most notably the HOXB13 G84E variant [3] and mutations in BRCA2, contribute to a smaller share of cases, often clustering in families; those monogenic variants are not what this common-variant score captures.

Other factors: Age, family history, and ancestry are the most established non-genetic correlates: risk roughly doubles with a first-degree relative affected, and men of African ancestry have higher incidence and mortality on average, only part of which is explained by known genetics. Modifiable and lifestyle associations are more modest and less certain, but obesity and smoking are more consistently linked to aggressive or fatal disease than to slow-growing tumors. Because most prostate cancers are indolent, this common-variant score is educational context only and is not a substitute for medical assessment; age, family history, and personal preferences matter more than a polygenic score alone.

How this was calculated

The published research behind your score, and the variants it draws on.

Study Details

39 published scores from 11 studies

The prostate cancer score combines 39 polygenic scores drawn from 11 published studies.

Tanha HM (2025). Polygenic risk scores for prostate cancer: Comparative evaluations in UK and Australian cohorts. HGG Adv: 3.8M

Fritsche LG (2020). Cancer PRSweb: An Online Repository with Polygenic Risk Scores for Major Cancer Traits and Their Evaluation in Two Independent Biobanks. Am J Hum Genet: 1.1M

Hu J (2024). Using clinical and genetic risk factors for risk prediction of 8 cancers in the UK Biobank. JNCI Cancer Spectr: 1.0M

Mars N (2020). Polygenic and clinical risk scores and their impact on age at onset and prediction of cardiometabolic diseases and common cancers. Nat Med: 6.6M

Mars N (2022). Genome-wide risk prediction of common diseases across ancestries in one million people. Cell Genom: 6.5M

Monti R (2024). Evaluation of polygenic scoring methods in five biobanks shows larger variation between biobanks than methods and finds benefits of ensemble learning. Am J Hum Genet: 1.1M

Youssef O (2024). High-Resolution Genotyping of Formalin-Fixed Tissue Accurately Estimates Polygenic Risk Scores in Human Diseases. Lab Invest: 1.1M

Jermy B (2024). A unified framework for estimating country-specific cumulative incidence for 18 diseases stratified by polygenic risk. Nat Commun: 766k

Namba S (2022). Common germline risk variants impact somatic alterations and clinical features across cancers. Cancer Res: 169k

Truong B (2024). Integrative polygenic risk score improves the prediction accuracy of complex traits and diseases. Cell Genom: 922k

Privé F (2022). Portability of 245 polygenic scores when derived from the UK Biobank and applied to 9 ancestry groups from the same cohort Am J Hum Genet: 451k

Sources

Mucci LA, et al. Familial Risk and Heritability of Cancer Among Twins in Nordic Countries. JAMA (2016)

Conti DV, et al. Trans-ancestry genome-wide association meta-analysis of prostate cancer identifies new susceptibility loci and informs genetic risk prediction. Nature Genetics (2021)

Ewing CM, et al. Germline mutations in HOXB13 and prostate-cancer risk. New England Journal of Medicine (2012)

Related Traits

These traits are influenced by some of the same genes and variants as this one

Leukemia: A cancer of the blood-forming tissues, represented here mainly by lymphoid leukemia.

Benign Prostatic Hyperplasia: A non-cancerous enlargement of the prostate gland, common with age, that can cause urinary symptoms.

Systolic Blood Pressure: The pressure in your arteries when the heart contracts and pushes blood out.

Back to All Traits

Content updated August 2026.

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