Causes of Stomach Cancer

Stomach (Gastric) cancer occurs when abnormal cells within the stomach grow uncontrollably. There are also some risk factors that can increase your chances of developing gastric cancer. But have you ever wondered what makes the normal, healthy cells in your stomach lining turn cancerous? Let’s take a deep dive into what causes gastric cancer at a molecular level.

Like all other types of cancer, gastric cancer is caused by mutations (changes or alterations) in your genetic material or DNA. Your DNA carries thousands of genes. These genes provide instructions, telling your cells how to grow, develop and function. They do this by producing different types of proteins that are involved in a wide range of cellular processes.

Cancer is caused by mutations in one or more genes within your cells. In the case of gastric cancer, these mutations occur in the genes of your stomach mucosa cells. When this happens, your mutated genes produce abnormal proteins that can no longer regulate various cellular processes, such as cell division and programmed cell death (apoptosis).

Having a single gene mutation is unlikely to cause cancer. This is because our cells have various mechanisms in place to repair DNA damage or mutations. However, when multiple mutations build up over the years and different cellular processes go haywire, your cells are allowed to grow and divide uncontrollably. This leads to the formation of tumors that turn malignant when they are capable of invading other tissues and organs.

There are mutations in some types of genes that are strongly associated with the formation of cancer, such as tumor suppressor genes, oncogenes and DNA repair genes.

Tumor suppressor genes

Tumor suppressor genes ensure that cells do not multiply too quickly. They do this by regulating certain genes that are involved in cell divisions and apoptosis.

Gene regulation refers to the process by which a cell controls the timing, location and amount in which genes are expressed. It usually involves turning genes on and off. When a mutation occurs in a tumor suppressor gene that could turn the gene off, this would allow the cells to grow and divide unchecked, leading to the formation of a tumor.

The most common tumor suppressor gene that is mutated in people with cancer is the p53 gene, which is faulty in more than half of all cancers. This infamous gene provides instructions for the production of the p53 protein, which is responsible for keeping cell division under control. Therefore, when the gene is mutated, the p53 protein loses its tumor-suppressing function.

Oncogenes

Proto-oncogenes are genes that normally regulate processes, such as cell division and apoptosis, which are needed to maintain healthy tissues and organs in your body. When a mutation occurs in a proto-oncogene, the gene can become permanently activated when it isn’t supposed to be. This turns the proto-oncogene into a malfunctioning gene called an oncogene.

When an oncogene is switched on, cell division and apoptosis are no longer kept in control. This allows the cells to grow and divide uncontrollably, thereby leading to tumorigenesis.

DNA repair genes

The protein products of DNA repair genes are responsible for catching and correcting mistakes that occur when your DNA is being copied during cell division. If they are unable to fix these mistakes, they trigger cell death (apoptosis) to ensure that the mistakes do not cause further problems.

When your DNA repair genes are mutated, their protein products lose their repairing function. Mistakes in the DNA do not get corrected and accumulate. This allows more mutations to build up inside the cell, affecting other genes and cellular processes. Eventually, the cells in your body turn cancerous and cancer starts to form.