Risk Factors for Prostate Cancer

A man’s lifetime risk of prostate cancer is one in seven. Some men with prostate cancer go undiagnosed and die of causes unrelated to the disease. Cancer strikes a guy when he is already advanced in his illness, and the tumor develops slowly. Treatment can be given when it becomes symptomatic, and while it may not be cured, it can be managed. However, because the sickness is more severe and the person is older, they may succumb to it. The number of men with prostate cancer that is present but not found or diagnosed during their lifetime is believed to be larger than the number of men with the illness clinically recognized. Many tests have been developed to understand better the genetic and molecular pathways that underlie why some prostate tumors go undiagnosed while others become severe, life-threatening conditions. Data from the National Cancer Institute has been modified; Age, race, and a family history of prostate cancer are the three most well-known risk factors.

Age

Prostate cancer is a disease in which age is a significant risk factor. It is pretty uncommon among guys under the age of 40. For males 49 years or younger, being diagnosed with prostate cancer is 1 in 325. One in every four males in their 50s and 60s. 1 in 17 males in their 60s and 70s. The risk is one in ten for males aged 70 and older, with a lifetime risk of one in seven.

Race

The risk of developing and dying from prostate cancer is higher among blacks, intermediate among whites, and lowest among Asians. Differences in incidence among populations worldwide further address race.

Family History

Prostate cancer, like breast and colon cancer, runs in families. Prostate cancer is thought to be caused by high-risk inherited genetic factors five to ten percent of the time. A person’s prostate cancer risk increases if he has a sibling or parent who has the disease. A person having a sibling who has prostate cancer has a relative risk of 3.14. When he has a father with prostate cancer, it is 2.35, and 2.25 when he has any other family with prostate cancer. This information was gathered from a Swedish population-based family cancer database, including over 11.8 million males. Prostate cancer was found in 26,651 males, with 5,623 from connected families.

When a father and two brothers are affected, the RR rises to 8.5; when three brothers are diagnosed with prostate cancer, it rises to 17.7. The risk increases with age in afflicted families, reaching around 5% at 60, 15% at 70, and 30% at 80 years old. At the same time, in the general population, the risk is 0.45%, 3%, and 10%, respectively, compared to the typical population. Prostate cancer risk is also increased in males with a mother or sister who has breast cancer. In some families, hereditary abnormalities may cause these prostate cancer clusters in the BRCA1 and BRCA2 genes. Genetic counseling may be beneficial to members of such families.

Differences in Incidence Among Populations Worldwide

Prostate cancer manifests itself in various ways in different communities throughout the world. When comparing nations with low rates of prostate cancer to countries with high rates of prostate cancer, there is a 60 to 100-fold variation in cancer incidence. For example, men in Asia have 2 to 10 cases per 100,000 age-adjusted incidence rate. Prostate cancer is more common in African American males than white men, with a 60 percent greater incidence. White men in Northern European nations have a greater frequency than in other countries. These discrepancies might be related to various variables, including genetics, environmental factors, healthcare access, and screening and treatment differences. Screening practices may influence a prostate cancer diagnosis.

For example, a study utilizing Swedish population-based data found that a diagnosis of prostate cancer in one brother leads to an early diagnosis of prostate cancer in the other brother using PSA screening. This might explain why younger men are diagnosed with prostate cancer, as seen by national incidence data.

Other Modifiers of Prostate Cancer Risk

Certain dietary risk factors may influence prostate cancer risk. Consumption of fat and/or meat, lycopene, and nutritional items such as calcium and vitamin D are all examples. Plant-derived substances and phytochemicals may have a role in prostate cancer prevention. Asian males are more likely to consume phytoestrogen-rich soy products, contributing to a lower prevalence. Prostate cancer is not increased by drinking alcohol. Smoking, on the other hand, may raise the risk. Obesity has also been linked to an increased risk of prostate cancer.

Risk of Developing a Second Cancer after Developing Prostate Cancer

After prostate cancer, there’s a chance you’ll have a second cancer. Radiation therapy for prostate cancer as a first-line treatment has been linked to increased bladder and rectal cancers and carcinoid malignancies. In addition, there is an increased risk of pancreatic cancer and melanoma. In a Swedish study of 18,207 men with prostate cancer, 560 had second cancer, with the risk of colorectal, kidney, bladder, and squamous cell carcinoma all increasing. In addition, prostate cancer was linked to an increased risk of bladder cancer, myeloma, and squamous cell skin cancer in people with a family history of the disease.

Inheritance of Prostate Cancer Risk

According to specific research, a rare 0.003 autosomal dominant, highly penetrant gene allele might explain family clustering of illness among males with early-onset prostate cancer.

Prostate cancer genes were anticipated to account for nearly half of all patients diagnosed with prostate cancer at 55 or younger.

Reduce Overdiagnosis and Detect Aggressive Cancer with the 4K Test

If a patient has an abnormal DRE or a high PSA, the 4K score can help determine whether or not a biopsy should be performed. In addition, it can predict aggressive cancer and metastases 20 years in advance. Depending on age, life expectancy, and health, patients can also set customized boundaries for themselves and their healthcare practitioners.

PSA velocity, density, and age-specific PSA were previously utilized to increase PSA’s specificity in detecting prostate cancer. On the other hand, PSA density appears to be an intrusive method that requires a rectal ultrasound, according to recent research. Moreover, it does not add much to the information provided by PSA alone.

The 4K Test uses an algorithm that integrates four prostate-specific kallikrein test findings with clinical data to quantify a patient’s % risk of aggressive prostate cancer. The 4Kscore Test outperformed PSA, PHI, and PCA3 in predicting aggressive prostate cancer in a prospective, blinded, multicenter research in the United States.

Patients must be informed about their family history, whether there are any cancer syndromes in their family, comorbidities, age, and have an annual PSA test. Because the objective is to discover cancer early and find the best approach to control these risks, RI every 3 to 5 years is beneficial. Genetic counselors can assist in counseling so that patients know their actual dangers and how to manage them. In addition, patients concerned about their cancer risk might benefit from a home genetic test.

Patients hear they’re at increased risk of malignancy but don’t understand the degree of risk. For example, sometimes, patients are told they have a 15% lifetime risk of prostate cancer and are concerned. however, ‘that’s everybody’s risk.’ They’re not at high risk; that’s an average risk. Those tests are associated with an increased risk of prostate cancer but not necessarily an increased risk of aggressive prostate cancer. That’s cancer we want to diagnose—not nonaggressive prostate cancer. Are patients at risk of developing cancer when they’re 75 or 55? Your evaluation and management will differ depending on the clinical scenario. There will be clear genetic tests in the future, and we’ll need to design clinical care to alter the identified risks. If we tell patients they have increased the risk of disease but don’t do anything to change that risk and have not improved patients’ lives, we’ve made their lives worse.

Genetic Testing: Up to 10% of patients with metastatic or advanced prostate cancer and 3% of localized prostate cancer carry a disease-causing variant in a DNA repair gene and other genes conferring risk for hereditary cancer disorders. Invitae’s Detect Hereditary Prostate Cancer is a sponsored, no-charge genetic testing program that uses the Invitae Multi-Cancer Panel. His comprehensive cancer panel tests genes associated with hereditary cancer syndromes, including all known prostate cancer genes. Determining the germline genetic etiology of prostate cancer provides eligibility for precision medical and surgical treatment options and eligibility to participate in clinical trials. his information can also be used to enable surveillance for and early detection of other DNA repair-related cancers in the patient and provide recommendations for early detection in
at­-risk relatives.

Genetic test results may have implications for medical management, including therapy, surveillance, counseling, and identifying at-risk family members. Positive germline results: 8.8% occur in genes with FDA-approved treatment for prostate cancer (PDL-1 inhibitors). 6 % occur in genes implying eligibility for open clinical trials for therapeutic agents for prostate cancer or advanced solid tumors. 8 % occur in genes with consensus management guidelines for surveillance and risk reduction for prostate and other cancers. I Vitae’s Detect Hereditary Prostate Cancer program offers no-charge, sponsored genetic testing and counseling for individuals diagnosed with prostate cancer, stage II and above.

Patient’s guide for Prolaris:
After being informed that you have prostate cancer, you may feel overwhelmed and unsure of the best action. However, knowing the specifics of your tumor might give you and your doctor more confidence when you choose a course of therapy. Prolaris is a genetic test that assesses the aggressiveness of your cancer and the most effective treatment method for newly diagnosed males and patients under active surveillance. By giving you tailored information on your tumor, Prolaris clears any misunderstanding. Prolaris also predicts the course of prostate cancer and determines whether men may safely be treated with active monitoring or need more aggressive measures.
For providers, visit www.myriadpro.com; for patients, see www.mysupport360.com.

References:

  1. Ruijter E, van de Kaa C, Miller G, et al.: Molecular genetics and epidemiology of prostate carcinoma. Endocr Rev 20 (1): 22-45, 1999.
  2. Stanford JL, Stephenson RA, Coyle LM, et al., eds.: Prostate Cancer Trends 1973-1995. Bethesda, Md: National Cancer Institute, 1999. NIH Pub. No. 99-4543.
  3. Miller BA, Kolonel LN, Bernstein L, et al., eds.: Racial/Ethnic Patterns of Cancer in the United States 1988-1992. Bethesda, Md: National Cancer Institute, 1996. NIH Pub. No. 96-4104. 
  4. American Cancer Society: Cancer Facts and Figures 2016. Atlanta, Ga: American Cancer Society, 2016.Available online.Exit Disclaimer Last accessed January 14, 2016.
  5. Altekruse SF, Kosary CL, Krapcho M, et al.: SEER Cancer Statistics Review, 1975-2007. Bethesda, Md: National Cancer Institute, 2010. Also available online. Last accessed February 2, 2016.
  6. Bunker CH, Patrick AL, Konety BR, et al.: High prevalence of screening-detected prostate cancer among Afro-Caribbeans: the Tobago Prostate Cancer Survey. Cancer Epidemiol Biomarkers Prev 11 (8): 726-9, 2002.
  7. Steinberg GD, Carter BS, Beaty TH, et al.: Family history and the risk of prostate cancer. Prostate 17 (4): 337-47, 1990.
  8. Carter BS, Beaty TH, Steinberg GD, et al.: Mendelian inheritance of familial prostate cancer. Proc Natl Acad Sci U S A 89 (8): 3367-71, 1992.
  9. Ghadirian P, Howe GR, Hislop TG, et al.: Family history of prostate cancer: a multicenter case-control study in Canada. Int J Cancer 70 (6): 679-81, 1997.
  10. Stanford JL, Ostrander EA: Familial prostate cancer. Epidemiol Rev 23 (1): 19-23, 2001.
  11. Matikaine MP, Pukkala E, Schleutker J, et al.: Relatives of prostate cancer patients have an increased risk of prostate and stomach cancers: a population-based, cancer registry study in Finland. Cancer Causes Control 12 (3): 223-30, 2001.
  12. Brandt A, Bermejo JL, Sundquist J, et al.: Age-specific risk of incident prostate cancer and risk of death from prostate cancer defined by the number of affected family members. Eur Urol 58 (2): 275-80, 2010.
  13. Agalliu I, Karlins E, Kwon EM, et al.: Rare germline mutations in the BRCA2 gene are associated with early-onset prostate cancer. Br J Cancer 97 (6): 826-31, 2007.
  14. Edwards SM, Kote-Jarai Z, Meitz J, et al.: Two percent of men with early-onset prostate cancer harbor germline mutations in the BRCA2 gene. Am J Hum Genet 72 (1): 1-12, 2003.
  15. Ford D, Easton DF, Bishop DT, et al.: Risks of cancer in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. Lancet 343 (8899): 692-5, 1994.
  16. Gayther SA, de Foy KA, Harrington P, et al.: The frequency of germ-line mutations in the breast cancer predisposition genes BRCA1 and BRCA2 in familial prostate cancer. The Cancer Research Campaign/British Prostate Group United Kingdom Familial Prostate Cancer Study Collaborators. Cancer Res 60 (16): 4513-8, 2000.
  17. Kolonel LN: Fat, meat, and prostate cancer. Epidemiol Rev 23 (1): 72-81, 2001.
  18. Giovannucci E, Rimm EB, Liu Y, et al.: A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst 94 (5): 391-8, 2002.
  19. Chan JM, Giovannucci EL: Vegetables, fruits, associated micronutrients, and risk of prostate cancer. Epidemiol Rev 23 (1): 82-6, 2001.
  20. Chan JM, Giovannucci EL: Dairy products, calcium, and vitamin D and risk of prostate cancer. Epidemiol Rev 23 (1): 87-92, 2001.
  21. Barnes S: Role of phytochemicals in prevention and treatment of prostate cancer. Epidemiol Rev 23 (1): 102-5, 2001.