Prostate Problems: Genetic reasons and research on solutions

Prostate cancer is one of the most common cancers in men. In the US and EU, it is the second most common cancer diagnosis —  and the second highest cause of cancer-related deaths in males. (Lung cancer is the most common cause of cancer deaths.)[ref] Currently, 1 in 8 men can expect to be diagnosed with prostate cancer in their lifetime, but the good news is that the 5-year survival rate is 99% when caught early.[ref]

Part of the susceptibility to prostate cancer and other benign prostate problems is genetic. This article explains the genetic variants that increase your risk of prostate problems. Importantly, some of the prostate risk genetic variants are related to environmental toxins that you can mitigate.

What causes prostate problems?

This article dives into all things prostate – from benign prostate hyperplasia (BPH) to prostate cancer. Before going any further, I want to reiterate that I’m simply presenting information from research studies. Please talk with your doctor for medical advice.

Prostate problems are common in older men and can include:

  • prostatitis (inflammation of the prostate)
  • benign prostate hyperplasia (enlarged prostate that is not malignant)
  • prostate cancer

Prostate-specific antigen (PSA) levels are used to screen for prostate issues. High PSA levels can indicate prostatitis, BPH, or prostate cancer. The name prostate-specific is a bit of a misnomer since women also produce PSA at lower levels.

What does the prostate do?

The prostate is a gland in the male reproductive system that surrounds the urethra just below the bladder. It secretes a part of the fluid that becomes semen and protects sperm. Additionally, it acts as a muscle important in controlling urination. When the prostate is enlarged, it can push on the bladder and decrease urine flow through the urethra.

Oxidative stress at the heart of prostate cancer and BPH:

One of the most critical molecular pathways in the development of prostate cancer involves a complex interaction between oxidative stress, chronic inflammation, and androgen receptor (AR) driven signaling. Additionally, it has been suggested that oxidative stress is essential for the formation of the aggressive phenotype in addition to being fundamental to PC growth.

Oxidative stress is the state in a cell when reactive oxygen species (ROS) is higher than normal. ROS are molecules with free radicals derived from oxygen through redox reactions. Examples of reactive oxygen species include hydrogen peroxide, superoxide, and hydroxyl radicals. ROS at low levels has important signaling properties within a cell, but a higher levels, ROS is very detrimental.

Oxidative stress can cause vascular tissue damage, interfere with the way that proteins in cells are supposed to work and cause damage to the nuclear DNA. Oxidative stress can also negatively impact stem cells and a cell’s ability to repair the damage.[ref]

What causes oxidative stress in the prostate?

Oxidative stress increases in aging as well as through exposure to toxicants and dietary choices.

Oxidative stress from diet: For example, omega-6 fats are found in large quantities in our modern diet (corn oil, fried foods, mayo and sauces, etc.). The peroxidation of these omega-6 fatty acids causes inflammation in the prostate, and higher levels of these peroxidation metabolites are found in men with BPH and high PSA levels.[ref] The modern diet has a lot higher intake of omega-6 fats than humans have eaten historically. It may be one possible explanation for the increase in prostate problems since the 1950s.[ref]

Prostate cells turn over rapidly and have fewer DNA repair enzymes, thus leaving them vulnerable to damage from oxidative stress. This damage then leads to the activation of inflammatory pathways.[ref]

Decreased antioxidants: In men with BPH, research shows they have a decrease in antioxidant defenses. In other words, the excess of ROS in the prostate can’t be countered by the body’s built-in antioxidant defenses.[ref] This could be due to a lack of micronutrients in the diet or continuing exposure to a toxicant that causes oxidative stress.

Age is an important factor: One reason that aging is associated with oxidative stress is an increase in cellular senescence. Senescent cells are at the end of their cellular life and unable to divide. This process is normal, and senescent cells are cleared out throughout life. But in older people, there is an increase in senescence above what can be easily cleared out. It is a problem because senescent cells give off inflammatory cytokines (which normally are the signal that causes the immune system to clear them out). An excess of senescent cells then leads to elevated inflammation, which is directly linked in research to the development of BPH.[ref]

cellular senescence = increased inflammation in the prostate = BPH

Toxins: Exposure to toxicants also increases oxidative stress in the prostate. Here are just a few examples:

  • Farmers exposed to high levels of pesticides are at a four-fold increased risk of prostate cancer.[ref]
  • Dioxins are persistent organic pollutants that increase the risk of prostate cancer.[ref]
  • Phthalates are chemicals found in artificial fragrances (think air fresheners, laundry detergents, shampoo) and plastics. Phthalates act as endocrine disruptors and are associated with oxidative stress in BPH and prostate cancer.[ref]
  • Exposure to trace metals, such as cadmium, mercury, or nickel, is also associated with prostate diseases.[ref]
  • BPA, an estrogen mimic found in plastics, is linked to enlarged prostate and prostate cancer risk.[ref][ref]

How do cells take care of oxidative stress?

Cells can respond to excess reactive oxygen species (ROS) with several built-in antioxidant defenses. Essentially, molecules that contain free oxygen are highly reactive. ROS isn’t completely bad and is utilized by cells in specific ways for cell signaling. However, the level of ROS is tightly controlled in cells. Excess reactive oxygen species (ROS), termed oxidative stress, can lead to cell damage, including DNA damage or cell death.

Cells have multiple ways of controlling the level of ROS, including endogenous antioxidants such as glutathione, superoxide dismutases (SOD), and catalase.

One way cells control oxidative stress is through the Nrf2 pathway. Activation of Nrf2 calls up antioxidant response genes, including the glutathione transferase enzyme (GSTs). As part of Phase II detoxification, GSTs are the enzymes responsible for causing the reaction between glutathione and other substances, such as toxicants, for making them water-soluble and able to be excreted.[ref]

I’ll come back to these oxidative stress enzymes in the genetics section…

Related article: Nrf2 Pathway: Increasing the body’s ability to get rid of toxins

What causes prostate cancer?

Essentially, cancer is caused by out-of-control cell growth. Mutations or breaks in cellular DNA in specific genes are the driving factors in cancerous cells. The mutations occur either in genes that promote cancer (oncogenes) or in genes that stop cell growth is what causes cancer cells to replicate. While mutations happen all the time during DNA replication, we have built-in DNA repair mechanisms that usually catch and correct the mutations. Excessive damage to DNA, such as from genotoxic substances or radiation, can result in cancer-causing mutations that replicate and result in tumors.[ref]

Commonly, mutations found in prostate cancer cells are in the TP53 (tumor protein p53) gene.[ref] TP53 is a tumor suppressor gene that keeps cells from dividing and growing uncontrolled. Mutations that prevent TP53 from working can lead to cancer.

Hormones, testosterone, and the prostate:

Let’s dig into how and why hormones impact the prostate.

Androgen hormones are the steroid hormones responsible for male characteristics (lower voice, facial hair, muscle mass, Adam’s apple). Androgens include testosterone, dihydrotestosterone (DHT), Dehydroepiandrosterone (DHEA), and Dehydroepiandrosterone sulfate (DHEA-S). Women also produce these hormones, just at lower levels than men do. Likewise, men produce estrogen, just at much lower levels than women.

Prostate cancer is considered ‘androgen-dependent’ cancer, meaning that initial cancer cell proliferation and survival depend on the androgen hormones.

Estrogens, on the other hand, are protective against prostate cancer due to their anti-androgenic effects. Women produce estrogen mainly in the ovaries, but for men, estrogen is created through the conversion of androgen precursors by an enzyme called aromatase. The aromatase enzyme is encoded by the CYP19A1 gene (coming back to that in the genetics section), and aromatase is produced in the gonads and prostate.[ref]

Hormones in Cancer vs. BPH: One difference between benign prostate hyperplasia (BPH) and prostate cancer is the production of aromatase (and thus estrogen) in the prostate cells. Researchers found that in BPH cells, aromatase was produced, creating estrogens from testosterone. But in the prostate cancer biopsies, very little aromatase was present, thus making no detectable estrogens.[ref]

One thing to note here is that circulating levels of androgens and estrogens don’t necessarily show what is happening in the prostate cells. Researchers are finding that the tissue-specific levels of androgens and aromatase in the prostate drive the difference between BPH and prostate cancer.[ref]

Genetic variants related to prostate cancer:

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Genetic variants can increase the risk of prostate cancer in a couple of ways. Listed first are genetic variants that increase the risk of prostate cancer (purely genetic). Next, are the variants linked to prostate cancer being more aggressive. Finally, I’ll list the variants in the oxidative stress and detoxification genes (likely related to environmental exposure) that are associated with an increase in prostate cancer risk. Please note that not all genetic risk factors are included here — many are not covered in 23andMe or AncestryDNA, and some are not replicated in multiple population groups.

8q24: region of chromosome 8 detected in several studies and a GWAS to increase the risk of prostate cancer significantly while not affecting the risk of other cancers.

Check your genetic data for rs188140481 (23andMe v4, v5)

  • A/A: 8-fold+ increased risk of prostate cancer[ref][ref][ref]
  • A/T: > 4-fold increased risk of prostate cancer
  • T/T: typical

Members: Your genotype for rs188140481 is .

HOXB13 gene: Hox genes are important in the formation of the prostate gland.[ref]

Check your genetic data for rs138213197 G84E (23andMe v4, v5; AncestryDNA):

  • C/C: typical
  • C/T: ~5-fold increase in relative risk of prostate cancer[ref][ref][ref]
  • T/T: (really rare) significantly higher risk of prostate cancer

Members: Your genotype for rs138213197 is .

FGFR4 gene: Fibroblast growth factor receptor 4

Check your genetic data for rs2011077 (23andMe v4; AncestryDNA):

  • T/T: typical
  • C/T: increase in the relative risk of prostate cancer and BPH
  • C/C: in Japanese populations, a 6-fold increase in prostate cancer risk and a 5-fold increase in BPH[ref]; increased risk in other population groups (just not as high as the Japanese study)[ref]

Members: Your genotype for rs2011077 is .

 

Additive risk: These milder risk factors for prostate cancer are considered additive. It means that your relative risk of prostate cancer is higher if you carry more than one of the risk alleles below. (Alternatively, if you carry none of the risk alleles, you are likely at a lower risk of prostate cancer)

CASC8 gene: a long-coding RNA gene associated with cancer susceptibility

Check your genetic data for rs1447295 (23andMe v4, v5; AncestryDNA):

  • A/A: increased relative risk of prostate cancer[ref]
  • A/C: increased relative risk of prostate cancer
  • C/C: typical

Members: Your genotype for rs1447295 is .

HNF1B gene: encodes a protein called hepatocyte nuclear factor-1 beta (HNF-1β), a transcription factor that regulates other genes.

Check your genetic data for rs4430796 (23andMe v4, v5; AncestryDNA):

  • A/A: increased relative risk of prostate cancer, more likely to be diagnosed at an earlier age[ref][ref]
  • A/G: typical risk (or slightly increased risk, depending on the study)[ref]
  • G/G: typical

Members: Your genotype for rs4430796 is .

CASC17 gene: a long-coding RNA gene associated with cancer susceptibility

Check your genetic data for rs1859962 (23andMe v4, v5; AncestryDNA):

  • G/G: increased relative risk of prostate cancer[ref][ref]
  • G/T: increased relative risk of prostate cancer
  • T/T: typical

Members: Your genotype for rs1859962 is .

8Q24 region: a region on chromosome 8 identified in studies as impacting prostate cancer risk.

Check your genetic data for rs16901979 (23andMe v4, v5)

  • A/A: increased relative risk of prostate cancer[ref][ref]
  • A/C: increased relative risk of prostate cancer
  • C/C: typical

Members: Your genotype for rs16901979 is .

Check your genetic data for rs6983267 (23andMe v4, v5; AncestryDNA):

  • G/G: increased relative risk of prostate cancer[ref][ref]
  • G/T: increased relative risk of prostate cancer
  • T/T: typical

Members: Your genotype for rs6983267 is .

 

Aggressiveness of prostate cancer: Prostate cancer is usually a slow-growing cancer, with some doctors adopting an active surveillance approach to treatment. But not everyone has slow-growing cancers, and genetics may be key here. Several studies have identified variants associated with prostate cancer progressing more rapidly.[ref]

DAB2IP gene:

Check your genetic data for rs1571801 (23andMe v4, v5; AncestryDNA):

  • G/G: typical
  • G/T: increased risk of aggressive prostate cancer
  • T/T: increased risk of aggressive prostate cancer[ref]

Members: Your genotype for rs1571801 is .

17p12 region:

Check your genetic data for rs4054823 (AncestryDNA):

  • C/C: typical
  • C/T: typical risk
  • T/T: somewhat higher risk of aggressive prostate cancer[ref]

Members: Your genotype for rs4054823 is .

8q24 region:

Check your genetic data for rs1447295 (23andMe v4, v5; AncestryDNA):

  • A/A: increased risk of prostate cancer, increased risk of aggressiveness (unfavorable pathological characteristics)[ref][ref]
  • A/C: increased risk of unfavorable pathological characteristics in prostate tumors
  • C/C: typical

Members: Your genotype for rs1447295 is .

11Q13 region:

Check your genetic data for rs11228565 (23andMe v5; AncestryDNA):

  • A/A: increased risk of aggressiveness (unfavorable pathological characteristics)[ref]
  • A/G: increased risk of aggressiveness (unfavorable pathological characteristics)
  • G/G: typical

Members: Your genotype for rs11228565 is .

Oxidative stress and diet-related variants:

ESR2 gene: estrogen receptor

Check your genetic data for rs2987983 (23andMe v4, v5; AncestryDNA):

  • A/A: typical genotype, no decrease in prostate cancer from adding phytoestrogens
  • A/G: increased risk of prostate cancer, but risk mitigated by adding phytoestrogens or isoflavonoids to the diet
  • G/G: increased risk of prostate cancer, but risk mitigated by adding phytoestrogens or isoflavonoids to the diet[ref]

Members: Your genotype for rs2987983 is .

COX2 gene: encodes an enzyme key to the production of inflammatory eicosanoids

Check your genetic data for rs5275 (23andMe v4, v5; AncestryDNA):

  • A/A: typical
  • A/G: decreased risk of prostate cancer with salmon consumption, fish oil
  • G/G: decreased risk of prostate cancer with salmon consumption, fish oil[ref]

Members: Your genotype for rs5275 is .

GSTM1 gene: glutathione s-transferase mu 1, significant in detoxifying many different compounds.

Not everyone has a functioning copy of this gene, and the non-functioning (null) genotype links to susceptibility to several types of cancer.[ref] The deletion is fairly common, with 50 – 78% of people, depending on ethnic group, having the null genotype for GSTM1.

Check your genetic data for rs366631 (23andMe v4 only):

  • A/A: deletion (null) GSTM1 gene; increased risk of prostate cancer in Caucasians[ref][ref] (common genotype in many population groups)
  • A/G: GSTM1 present
  • G/G: GSTM1 present

Members: Your genotype for rs366631 is .

GSTP1 gene: glutathione s-transferase pi, important in detoxifying many different compounds.

Check your genetic data for rs1138272 (23andMe v4, v5; AncestryDNA):

  • C/C: typical
  • C/T: increased prostate cancer risk
  • T/T: increased prostate cancer risk[ref]

Members: Your genotype for rs1138272 is .

Check your genetic data for rs1695 (23andMe v4, v5; AncestryDNA):

  • A/A: typical
  • A/G: typical risk
  • G/G: reduced function, increased risk of certain cancers[ref][ref][ref] increased prostate cancer risk[ref]

Members: Your genotype for rs1695 is .

CYP3A4 gene: part of the phase I detoxification system and also involved in estrogen metabolism

Check your genetic data for rs2740574 (23andMe v4, v5; AncestryDNA)

  • C/C: CYP3A4*1B; significantly increased risk of aggressive prostate cancer in African Americans[ref]
  • C/T: carrier of one CYP3A4*1B alleles; increase risk of aggressive prostate cancer in African Americans
  • T/T: typical

Members: Your genotype for rs2740574 is .

GPX4 gene: glutathione peroxidase gene

Check your genetic data for rs3746165 (23andMe v4; AncestryDNA):

  • G/G: 35% lower risk of prostate cancer lethality; higher gamma-tocopherol (specific form of vitamin E) intake decreases the risk even more[ref]
  • A/G: typical risk
  • A/A: typical

Members: Your genotype for rs3746165 is .

Hormone related variants:

CYP1B1 gene: phase I detoxification of estrogen into 4-OHE1(E2), an estrogen metabolite

Check your genetic data for rs1056836 Leu432Val (23andMe v4, v5; AncestryDNA):*

  • G/G: (Leu/Leu – slower); decreased estradiol metabolism[ref]
  • C/G: intermediate/decreased estradiol metabolism[ref]
  • C/C: (Val/Val – faster); decreased risk of prostate cancer[ref][ref]

Members: Your genotype for rs1056836 is .

*Note that these are referred to in the plus orientation to match 23andMe data. This variant is prone to confusion because the variant is very common, and the orientation is often switched in studies.

CYP19A1 gene (aromatase): converts androstenedione and testosterone into estrogen

Check your genetic data for rs700518 (23andMe v4, v5; AncestryDNA):

  • T/T: increased risk of benign prostate hyperplasia[ref]
  • C/T: typical risk
  • C/C: typical risk

Members: Your genotype for rs700518 is .

 


Lifehacks:

Everything presented here is for informational purposes only. Talk with your doctor, of course, if you have any medical questions or questions about interactions with supplements. Prostate cancer or BPH isn’t a DIY healthcare situation.

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References:

Antczak, Andrzej, et al. “The Variant Allele of the Rs188140481 Polymorphism Confers a Moderate Increase in the Risk of Prostate Cancer in Polish Men.” European Journal of Cancer Prevention: The Official Journal of the European Cancer Prevention Organisation (ECP), vol. 24, no. 2, Mar. 2015, pp. 122–27. PubMed, https://doi.org/10.1097/CEJ.0000000000000079.

Apte, Shruti A., et al. “A Low Dietary Ratio of Omega-6 to Omega-3 Fatty Acids May Delay Progression of Prostate Cancer.” Nutrition and Cancer, vol. 65, no. 4, 2013, pp. 556–62. PubMed, https://doi.org/10.1080/01635581.2013.775316.

Bangsi, Dieudonne, et al. “Impact of a Genetic Variant in CYP3A4 on Risk and Clinical Presentation of Prostate Cancer among White and African-American Men.” Urologic Oncology, vol. 24, no. 1, Feb. 2006, pp. 21–27. PubMed, https://doi.org/10.1016/j.urolonc.2005.09.005.

Beuten, Joke, et al. “CYP1B1 Variants Are Associated with Prostate Cancer in Non-Hispanic and Hispanic Caucasians.” Carcinogenesis, vol. 29, no. 9, Sept. 2008, pp. 1751–57. PubMed, https://doi.org/10.1093/carcin/bgm300.

Chang, Wei-Hsiang, et al. “Sex Hormones and Oxidative Stress Mediated Phthalate-Induced Effects in Prostatic Enlargement.” Environment International, vol. 126, May 2019, pp. 184–92. PubMed, https://doi.org/10.1016/j.envint.2019.02.006.

Chang, Wei-Hsiung, et al. “Oxidative Damage in Patients with Benign Prostatic Hyperplasia and Prostate Cancer Co-Exposed to Phthalates and to Trace Elements.” Environment International, vol. 121, no. Pt 2, Dec. 2018, pp. 1179–84. PubMed, https://doi.org/10.1016/j.envint.2018.10.034.

Cheng, Iona, et al. “8q24 and Prostate Cancer: Association with Advanced Disease and Meta-Analysis.” European Journal of Human Genetics: EJHG, vol. 16, no. 4, Apr. 2008, pp. 496–505. PubMed, https://doi.org/10.1038/sj.ejhg.5201959.

Dragovic, Sanja, et al. “Effect of Human Glutathione S-Transferase HGSTP1-1 Polymorphism on the Detoxification of Reactive Metabolites of Clozapine, Diclofenac and Acetaminophen.” Toxicology Letters, vol. 224, no. 2, Jan. 2014, pp. 272–81. PubMed, https://doi.org/10.1016/j.toxlet.2013.10.023.

Duggan, David, et al. “Two Genome-Wide Association Studies of Aggressive Prostate Cancer Implicate Putative Prostate Tumor Suppressor Gene DAB2IP.” Journal of the National Cancer Institute, vol. 99, no. 24, Dec. 2007, pp. 1836–44. PubMed, https://doi.org/10.1093/jnci/djm250.

Grin, Boris, et al. “A Rare 8q24 Single Nucleotide Polymorphism (SNP) Predisposes North American Men to Prostate Cancer and Possibly More Aggressive Disease.” BJU International, vol. 115, no. 1, Jan. 2015, pp. 101–05. PubMed, https://doi.org/10.1111/bju.12847.

GSTM1 Glutathione S-Transferase Mu 1 [Homo Sapiens (Human)] – Gene – NCBI. https://www.ncbi.nlm.nih.gov/gene?cmd=Retrieve&dopt=full_report&list_uids=2944. Accessed 14 July 2022.

Gudmundsson, Julius, et al. “A Study Based on Whole-Genome Sequencing Yields a Rare Variant at 8q24 Associated with Prostate Cancer.” Nature Genetics, vol. 44, no. 12, Dec. 2012, pp. 1326–29. PubMed, https://doi.org/10.1038/ng.2437.

Hedelin, Maria, Ellen T. Chang, et al. “Association of Frequent Consumption of Fatty Fish with Prostate Cancer Risk Is Modified by COX-2 Polymorphism.” International Journal of Cancer, vol. 120, no. 2, Jan. 2007, pp. 398–405. PubMed, https://doi.org/10.1002/ijc.22319.

Hedelin, Maria, Katarina Augustsson Bälter, et al. “Dietary Intake of Phytoestrogens, Estrogen Receptor-Beta Polymorphisms and the Risk of Prostate Cancer.” The Prostate, vol. 66, no. 14, Oct. 2006, pp. 1512–20. PubMed, https://doi.org/10.1002/pros.20487.

Javed, Saqib, and Stephen E. M. Langley. “Importance of HOX Genes in Normal Prostate Gland Formation, Prostate Cancer Development and Its Early Detection.” BJU International, vol. 113, no. 4, Apr. 2014, pp. 535–40. PubMed, https://doi.org/10.1111/bju.12269.

Kabir, Ali, et al. “Dioxin Exposure in the Manufacture of Pesticide Production as a Risk Factor for Death from Prostate Cancer: A Meta-Analysis.” Iranian Journal of Public Health, vol. 47, no. 2, Feb. 2018, pp. 148–55.

Levin, Albert M., et al. “Chromosome 17q12 Variants Contribute to Risk of Early-Onset Prostate Cancer.” Cancer Research, vol. 68, no. 16, Aug. 2008, pp. 6492–95. PubMed, https://doi.org/10.1158/0008-5472.CAN-08-0348.

Minciullo, Paola Lucia, et al. “Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review.” Urologia Internationalis, vol. 94, no. 3, 2015, pp. 249–54. www.karger.com, https://doi.org/10.1159/000366210.

Ragin, Camille, et al. “Farming, Reported Pesticide Use, and Prostate Cancer.” American Journal of Men’s Health, vol. 7, no. 2, Mar. 2013, pp. 102–09. PubMed, https://doi.org/10.1177/1557988312458792.

Severi, Gianluca, et al. “The Common Variant Rs1447295 on Chromosome 8q24 and Prostate Cancer Risk: Results from an Australian Population-Based Case-Control Study.” Cancer Epidemiology, Biomarkers & Prevention: A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology, vol. 16, no. 3, Mar. 2007, pp. 610–12. PubMed, https://doi.org/10.1158/1055-9965.EPI-06-0872.

Stevens, Victoria L., et al. “HNF1B and JAZF1 Genes, Diabetes, and Prostate Cancer Risk.” The Prostate, vol. 70, no. 6, May 2010, pp. 601–07. PubMed, https://doi.org/10.1002/pros.21094.

Van Blarigan, Erin L., et al. “Plasma Antioxidants, Genetic Variation in SOD2, CAT, GPX1, GPX4, and Prostate Cancer Survival.” Cancer Epidemiology, Biomarkers & Prevention: A Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology, vol. 23, no. 6, June 2014, pp. 1037–46. PubMed, https://doi.org/10.1158/1055-9965.EPI-13-0670.

Vital, Paz, et al. “The Senescence-Associated Secretory Phenotype Promotes Benign Prostatic Hyperplasia.” The American Journal of Pathology, vol. 184, no. 3, Mar. 2014, pp. 721–31. PubMed, https://doi.org/10.1016/j.ajpath.2013.11.015.

Wei, Jun, et al. “Germline HOXB13 G84E Mutation Carriers and Risk to Twenty Common Types of Cancer: Results from the UK Biobank.” British Journal of Cancer, vol. 123, no. 9, Oct. 2020, pp. 1356–59. www.nature.com, https://doi.org/10.1038/s41416-020-01036-8.

Xu, Bin, et al. “FGFR4 Gly388Arg Polymorphism Contributes to Prostate Cancer Development and Progression: A Meta-Analysis of 2618 Cases and 2305 Controls.” BMC Cancer, vol. 11, Feb. 2011, p. 84. PubMed, https://doi.org/10.1186/1471-2407-11-84.

Xu, Jianfeng, et al. “Inherited Genetic Variant Predisposes to Aggressive but Not Indolent Prostate Cancer.” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 5, Feb. 2010, pp. 2136–40. PubMed, https://doi.org/10.1073/pnas.0914061107.

Xu, Zongli, et al. “GWAS SNP Replication among African American and European American Men in the North Carolina-Louisiana Prostate Cancer Project (PCaP).” The Prostate, vol. 71, no. 8, June 2011, pp. 881–91. PubMed, https://doi.org/10.1002/pros.21304.

Zhang, Yixiang, et al. “Association between GSTP1 Ile105Val Polymorphism and Urinary System Cancer Risk: Evidence from 51 Studies.” OncoTargets and Therapy, vol. 9, 2016, pp. 3565–69. PubMed, https://doi.org/10.2147/OTT.S106527.

Zheng, S. Lilly, et al. “Cumulative Association of Five Genetic Variants with Prostate Cancer.” New England Journal of Medicine, vol. 358, no. 9, Feb. 2008, pp. 910–19. Taylor and Francis+NEJM, https://doi.org/10.1056/NEJMoa075819.

Zhou, Tian-Biao, et al. “GSTT1 Polymorphism and the Risk of Developing Prostate Cancer.” American Journal of Epidemiology, vol. 180, no. 1, July 2014, pp. 1–10. PubMed, https://doi.org/10.1093/aje/kwu112.


About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.