Cancer is a complex group of diseases characterized by the uncontrolled growth and division of abnormal cells. These cells can invade surrounding tissues and spread to distant organs (metastasis). Understanding how normal cellular processes go awry is central to comprehending this disease, which represents a breakdown in cell regulation and repair.
The Cellular Basis of Cancer
Normal cells grow, divide, and die in a regulated manner, maintaining tissue balance. This ensures new cells are produced only when needed. Cancer originates when this control falters, typically from DNA damage leading to genetic alterations called mutations.
Mutations often affect genes regulating cell behavior. Proto-oncogenes stimulate cell growth. When mutated, they become oncogenes, acting like an accelerator promoting uncontrolled cell proliferation. For example, a growth factor receptor might signal for division even without a growth factor present.
Conversely, tumor suppressor genes act as brakes, slowing cell division, repairing DNA damage, and initiating programmed cell death (apoptosis) if a cell is irreparably damaged. When genes like TP53 or BRCA1/2 mutate, they lose this protective function, allowing cells to grow unchecked. Activated oncogenes and inactivated tumor suppressor genes cause cells to ignore normal growth signals, divide continuously, and evade programmed cell death.
Factors That Increase Cancer Risk
Various factors induce DNA damage and mutations that initiate cancer. Environmental carcinogens directly damage DNA. Examples include chemicals in tobacco smoke, asbestos, formaldehyde, and air pollution.
Ionizing and ultraviolet (UV) radiation are significant factors. Ionizing radiation (e.g., medical scans) breaks DNA strands. UV radiation from the sun causes DNA damage leading to skin cancers. Both induce specific mutational patterns.
Lifestyle choices also play a substantial role. An unhealthy diet (processed foods, red meat), excessive alcohol, physical inactivity, and obesity link to increased cancer risk. Obesity is a major factor after tobacco use.
Infectious agents, including certain viruses and bacteria, can contribute to cancer development. Human Papillomavirus (HPV) is a primary cause of cervical cancer and is also linked to anal and head and neck cancers. Hepatitis B and C viruses are major contributors to liver cancer, while Helicobacter pylori is associated with stomach cancer. Epstein-Barr virus (EBV) is linked to certain lymphomas.
Inherited genetic predispositions mean some individuals are born with mutations in genes like BRCA1 and BRCA2, which are tumor suppressor genes. While these mutations significantly increase the likelihood of developing cancers such as breast and ovarian cancer, they do not guarantee disease development. Age is also a prominent risk factor, as the accumulation of DNA damage and declining repair mechanisms over time increase cancer incidence with advancing years.
The Body’s Defense and Cancer Progression
The human body possesses sophisticated defense mechanisms to protect against cancer. Immune surveillance is a process where the immune system constantly monitors and identifies abnormal cells, including those with cancerous potential, and eliminates them before they can cause harm. Immune cells, such as cytotoxic T lymphocytes and natural killer cells, recognize distinctive markers on the surface of rogue cells and destroy them.
Beyond immune responses, cells have DNA repair mechanisms that actively correct errors or damage in the genetic code. These processes work to maintain genomic integrity, preventing mutations from accumulating. If DNA damage is too extensive to repair, these mechanisms can trigger programmed cell death, removing the damaged cell from the body.
Cancer develops when these defense systems fail. Mutated cells might evade detection by the immune system, perhaps by altering their surface markers or releasing immunosuppressive molecules. Similarly, if DNA repair mechanisms become overwhelmed or dysfunctional, damaged cells can survive and continue to divide. This unchecked proliferation leads to the formation of a primary tumor, a mass of abnormal cells.
As the tumor grows, it requires nutrients and oxygen, prompting it to stimulate the formation of new blood vessels from existing ones in a process called angiogenesis. This newly formed blood supply sustains the tumor’s rapid growth. In advanced stages, cancer cells can break away from the primary tumor, enter the bloodstream or lymphatic system, and travel to distant parts of the body, forming new tumors in a process known as metastasis. This spread to new sites is a major cause of cancer-related mortality.