Prostate cancer is a type of cancer that develops in men and that affects the prostate (Ramon & Denis, 2007). Prostate is a gland that secretes seminal fluid that is necessary for the nourishment and transport of sperm cells. In the United States alone, more than 2 million men have been victims of this type of cancer (Ramon & Denis, 2007). Its risk factors include race/ethnicity, age, geography, family history, genetics, sedentary life, chronic inflammation, hormones, obesity, and gender (Ramon & Denis, 2007). In its early stages, the cancer is not very dangerous because it is confined only to the prostate gland. However, if not detected and treated early, it can spread to other parts and cause serious damage. Successful treatment is achieved if the cancer is detected early while it is still confined to the prostate gland. This paper will discuss genetics as a major risk factor for prostate cancer based on its pathogenesis, extent of contribution to cancer etiology, prevention, and methods of early detection.
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Numerous studies have found out that prostate cancer is a disease that emanates primarily from the interaction between genetic and non-genetic factors. These factors are responsible for the disease’s initiation and progression. Statistics released by the American Cancer society show that 1 in every 6 American males will be diagnosed with the cancer at a certain stage in their life (Ramon & Denis, 2007).
Prostate cancer develops when mutations repeatedly occur in genes that control processes such as cell division and cell growth (Tewari, 2013). In addition, it results from the genetic mutation of cells that repair damaged DNA. Prostate cells undergo genetic changes referred to as somatic mutations. Some people become exposed to the disease through the inheritance of mutated genes such as BRCA1, BRCA2, and HOXB13 (Pestell & Nevalainen, 2008). Mutations in these genes increase the risk of developing prostate cancer. BRCA1 and BRCA2 are responsible for secreting proteins that fix damaged DNA and suppress tumors (Pestell & Nevalainen, 2008). DNA is critical in the maintenance of cell’s genetic information.
Therefore, existence of mutations in the aforementioned genes prevents the production of BRCA1 and BRCA2 proteins (Pestell & Nevalainen, 2008). These proteins control the division and growth of cells. Changes in BRCA1 and BRCA2 genes prevent them from fixing damaged DNA thus facilitating the persistence of dangerous mutations (Tindall, 2013). Continued mutation of genes triggers rapid growth and division of prostate cells thus causing cancer. Mutations in the HOXB13 gene stop the secretion of a protein that regulates the activity of other genes thus impairing the proteins’ ability to suppress tumors (Pestell & Nevalainen, 2008). This leads to uncontrolled division and growth of prostate cells thus leading to cancer.
Extent of the contribution of genetics to prostate cancer etiology
Several studies have established that genetics play a key role in the etiology of prostate cancer. For example, approximately 5-10% of all prostate cancer cases are attributed to genes that are highly susceptible to cancer (Tewari, 2013). This explains why family history is an important risk factor for prostate cancer because susceptible genes are passed from parents to the offspring. Examples of genes that are associated with prostate cancer include RNASEL (HPC1), BRCA1, BRCA2, and DNA mismatch repair genes (Tindall, 2013). RNASEL’s role is to facilitate the death of cells whenever something goes wrong during the process of cell division or growth (Pestell & Nevalainen, 2008).
Mutations in this gene let cells that are supposed to be destroyed live longer thus increasing an individual’s risk of developing cancer (Tindall, 2013). Majority of gene mutations that have been associated with prostate cancer are acquired and occur during the lifetime of an individual (Pestell & Nevalainen, 2008). Very few cases of prostate cancer are as a result of inherited gene mutations. Therefore, all cases of prostate cancer linked to heredity have a genetic background because they involve the transfer of genes from parents to the offspring. Other genes that are associated with prostate cancer include AR, CD82, CDH1, CHEK2, EHBP1, ELAC2, EP300, GNMT, MED12, EZH2, HPCX, FGFR4, MAD1L1, FGFR2, IGF2, and KLF6 (Pestell & Nevalainen, 2008).
Prevention of the risk factor
It is not possible to prevent genetics from initiating the development of prostate cancer because mutations occur in genes and are not easily detected. However, men who possess mutations in the BRCA1 and BRCA2 genes should undergo screening to determine whether they have prostate cancer. Genetic mutation is a biological process that cannot be stopped. The only remedy is early screening, detection, and treatment.
Methods of early detection
Genetic testing is the most common method of determining the presence of genetic mutations that can predispose men to the risk of developing prostate cancer. It is mainly recommended for men who belong to families that have a history of prostate cancer. Genetic testing involves studying an individual’s DNA to determine whether the molecules are arranged properly (Ramon & Denis, 2007). There are two variations of genetic testing. The first involves looking at the specific DNA in cancerous cells and the second involves looking at the DNA of normal cells in order to identify inherited susceptible genes (Ramon & Denis, 2007).
Whole genome sequencing identifies variations in DNA sequences (Tewari, 2013). In many cases, genetic testing for prostate cancer involves the identification of specific mutations that are associated with prostate cancer (Ramon & Denis, 2007). Men at risk of prostate cancer undergo regular measures of prostate-specific antigen (PSA) and digital rectal exam (DRE). A PSA test is a way of measuring the level of prostate-specific antigens in the blood to determine whether they have prostate cancer or not (Ramon & Denis, 2007). In men with cancer, the levels of PSA are very high compared to those in men without the disease. A DRE is conducted to establish the presence or absence of enlargements or unusual lumps in the prostate (Ramon & Denis, 2007).
Closely related risk factors
Other risk factors related to genetics include heredity and family history. Heredity is related to genetics because the risk of developing prostate cancer due to heredity involves the transmission of mutated or susceptible genes from parents to the offspring (Tewari, 2013). Men who belong to families with history of prostate cancer are at a high risk of developing the cancer due to the interaction between genetic and biological factors that are responsible for inherited genes that are mutated or susceptible (Ramon & Denis, 2007). A man whose father had prostate cancer is more likely to develop the cancer than a man whose dad never developed the cancer. The risk is lower in men with a second-degree relative such as an uncle or nephew who has or had prostate cancer.
Prostate cancer is one of the most common types of cancer that affects men. It affects the prostate and it is so common that statistics project that 1 in 6 American men will be diagnosed with the disease before they come to the end of their life. Genetics is one of the major risk factors that increase the risk of men developing prostate cancer. Mutations on BRCA1, BRCA2, and HOXB13 genes stop the production of proteins that fix damaged DNA and that control the division and growth of cells. These mutations encourage the persistence of mutations that facilitate rapid division and growth of prostate cells thus causing cancer. Genetics as a risk factor of prostate cancer cannot be stopped. However, early screening, detection, and treatment can cure the disease. Genetic testing, PSA test, and DRE test are the most common methods used to detect prostate cancer during its early stages for successful treatment. Heredity and family history are other risk factor closely related to genetics. Men with parents or close relatives who have or had prostate cancer are at high risk of developing the disease.
Pestell, R. G., & Nevalainen, M. T. (2008). Prostate Cancer: Signaling Networks, Genetics, and New treatment Strategies. New York, NY: Springer Science & Business Media.
Ramon, J., & Denis, L. J. (2007). Prostate Cancer. New York, NY: Springer Science & Business Media.
Tewari, A. K. (2013). Prostate Cancer: A Comprehensive Perspective. New York, NY: Springer Science & Business media.
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Tindall, D. J. (2013). Prostate Cancer: Biochemistry, Molecular Biology and Genetics. New York, NY: Springer Science & Business Media.