Cancer is a complex disease that naturally arises as a consequence of disruptions to the tightly regulated normal mechanisms of cell growth, division, and death. It’s not one single event, but a multi-step process driven by an accumulation of genetic alterations in a cell.
On its roots, cancer begins with damage to a cell’s DNA. Our DNA contains the blueprints, or genes, instructing a cell about its life – when to grow, when to divide, what work to do, and even when to die with programmed cell death (apoptosis). When these genes get changed or damaged, the blueprints inside the cell become confusing, leading to abnormal functioning.
There are several primary categories of genes that contribute to cancer onset:
Proto-oncogenes
These genes normally provide the instruction for the barigen 4 mg cell to grow and proliferate. When they become altered, or mutated, they become oncogenes, which are similar to a stuck accelerator pedal, constantly telling the cell to copy itself, even when it should not.
Tumor suppressor genes: These are the brakes, normally preventing cell growth, repairing DNA errors, and inducing apoptosis when harm is too extensive. Mutation in tumor suppressor genes removes these crucial checks and balances, allowing damaged-DNA cells to proliferate uncontrolled. The TP53 gene, or the so-called “guardian of the genome,” is mutated in about half of all human cancers.
DNA repair genes: These types of genes repair errors occurring during DNA replication or due to environmental insults. The repair function of the cell for its own DNA is lost if the genes are mutated, and the consequence is more mutations are added on, and cancer would be more likely to occur.
The origin of these gene mutations may be diverse:
Inherited mutations: A few cancers (5-10%) follow genetic mutations inherited from parents. These predispose them to certain cancers, i.e., they are born with a higher risk. But the presence of an inherited mutation does not always mean cancer; it typically requires a couple of acquired mutations to trigger off the disease.
Acquired mutations: The vast majority of cancer-causing mutations occur after birth, during one’s lifetime. These could be because of:
Cell division errors
Our cells constantly divide and make copies of their DNA. Even with tight error-checking mechanisms, sometimes there can be an occasional mistake that leads to mutations.
Environmental exposures: Exposures to environmental carcinogens (environmental cancer-causing chemicals) can directly damage DNA. Some examples include chemicals in tobacco smoke, sun’s ultraviolet (UV) radiation, some viruses (e.g., HPV), and some chemicals in industry.
Lifestyle factors: Obesity, chronic inflammation, excessive alcohol consumption, and lack of exercise may also cause genetic damage and propel the growth of cancer.
The development of cancer is most commonly described to occur in stages:
Initiation: This is the first change in the DNA of a cell, making it “initiated.” The cell is not necessarily cancerous immediately, but it has developed a tendency.
Promotion: The initiated cells are then stimulated to grow and develop more rapidly than normal cells. This “promotion” can be caused by continued exposure to carcinogens or to agents inducing chronic inflammation. At this point, the initiated cells gain a growth advantage and form a small lesion or population of abnormal cells.
Progression
As the abnormal cells continue to grow, they also accumulate more mutations. These additional genetic changes add more malignant features, such as increased proliferation, ability to invade nearby tissues, and the ability to evade the immune surveillance of the body. This is when the cells are indeed malignant.
As the cancer cells develop, they accumulate in a quantity known as a tumor. While regular cells will honor boundaries and no longer increase when they meet other cells, cancer cells grow at will and have a tendency to lose adhesion characteristics. This lack of adhesion comes into play with the most destructive aspect of cancer: metastasis.
Metastasis is the process by which cancer cells break away from the primary tumor, enter the circulatory or the lymphatic system, and travel to the other parts of the body to form secondary tumors. This extensive spread is the reason why cancer becomes so tough to treat in its advanced stages.
Briefly, cancer does not start with a sudden switch, but with the gradual addition of genetic errors in a single cell. They disturb the delicate balance of cell growth and division, turning a normal cell into one that grows unrestrained, avoids the immune system, and finally gains the ability to invade and spread, and the cycle starts of a potentially lethal disease.