How Does Prostate Cancer Develop?

The difference between a risk factor and a cause

When talking about developing a condition, it is important to distinguish between a risk factor and a cause. Risk factors can be modifiable or non-modifiable, and contribute to an increased risk in developing a condition. While risk factors increase a person’s risk of developing a condition, they are not the cause of the condition’s presence. For example, while exposure to environmental dangers like Agent Orange (a chemical used to destroy crops during the Vietnam War) can increase a person’s risk of developing prostate cancer, it alone does not cause prostate cancer. Being exposed to the chemical could lead to genetic mutations which can then go on to contribute to prostate cancer. While the specific cause of prostate cancer is unknown, basic cancer cell biology can provide insight into how and why this condition develops.1

Cancer development

No matter where a cancer is within the body, how far it has spread, or how long it’s been present, it always stems from the same issue: uncontrolled cell growth. More specifically, cancer is produced from malfunctions within our body’s growth and development process. Our DNA is comprised of genes that provide instructions on how certain processes should be carried out.

Under healthy circumstances, our body has an intricate system of checks and balances, that alerts cells as to when they should divide or die, as well as when they are damaged. Genes that participate in this system include oncogenes and tumor suppressor genes. Oncogenes are genes that tell our body to divide and make new cells. Tumor suppressor genes normally sense mutations or mistakes in the DNA of faulty cells, and either repair these mistakes, or signal for the mutated cell’s death. Mutations in these genes can lead to oncogenes being continuously activated or turned on, and tumor suppressor genes being deactivated or turned off. These mutations allow cells to avoid the normal checking system, and grow faster and live longer than healthy, normal cells.

The accumulation of excess or damaged cells can then create a primary tumor. The most common form of prostate cancer is considered an adenocarcinoma, meaning it arises from the cells lining the prostate gland that will secrete fluid which will end up in the semen. In theory, an oncogene, tumor suppressor gene, or another gene that is involved in the checks and balances system within this region malfunctioned, causing a tumor to grow.1-3

How does cancer spread?

For prostate cancer, a primary tumor has the potential to grow to take up the entirety of the prostate, or break through the wall of the gland. When this happens, it is called extracapsular extension, and the tumor makes its way beyond the prostate. Eventually, tumor cells can break off from the primary tumor and travel into the blood stream or lymph fluid. When this happens, the cancer is able to metastasize, or invade other parts of the body. When the cancer finds a new home, it can continue its faulty growth process to create secondary tumors far away from where it started.1

Potential genetic mutations specific to prostate cancer

As mentioned earlier, cancer is a direct result of mutated genes that can no longer participate in the healthy development and growth and development process. For every type of cancer, there is a specific set of genes thought to contribute to it. Having mutations or abnormal variants of these genes doesn’t necessarily mean that a person will develop an associated condition or type of cancer, but rather, means that their risk is increased. For this reason, possessing these mutations is considered a risk factor until the mutations start to cause a disruption in healthy gene function. When the function of a gene is altered and it begins to contribute to cancer growth, then it develops into a cause.

For prostate cancer, there are several genes that have been linked to the potential development of the condition. In 5-10% of prostate cancer cases, these mutated genes are inherited, while other mutations can be individual-specific and acquired through exposure to environmental factors, such as cigarette smoke, Agent Orange, or radiation. Further research is ongoing to investigate the number of prostate cancer-associated genes, as well as to determine the link between those that have already been identified. Some examples of these include:

  • BRCA1 and BRCA2: These genes are also associated with breast and ovarian cancer in women. They are tumor suppressor genes that normally repair DNA damage or mutations in cells, as well as signal an unhealthy cell to die. Mutations in these genes are typically inherited.
  • MSH2 and MLH1: These genes work to repair mismatches in the DNA base-pairing process. This process is how a cell replicates all of its DNA to pass on to new cells. Individuals with mutations in these genes also tend to have Lynch Syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC), and have an increased risk of prostate cancer.
  • RNASEL: Also known as HPC1, mutations in this gene are typically inherited. RNASEL is a tumor suppressor gene that tells cells when it’s time for them to die, especially when something is wrong.
  • HOXB13: Mutations in the HOXB13 gene have been linked to the very rare early-onset prostate cancer. The healthy HOXB13 gene plays a role in the development of the prostate gland itself. This mutation is not common.2,4,5
Written by: Casey Hribar | Last reviewed: October 2017
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