Cancer cells represent a deviation from the normal behavior of cells within the body. These abnormal cells have lost the controls over growth and function, leading to unpredictable and harmful behavior. Understanding these distinct characteristics provides insight into the nature of the disease.
Uncontrolled Growth and Division
Normal cells exhibit a regulated pattern of growth and division, typically dividing only when necessary for repair or replacement and stopping when they come into contact with other cells, a phenomenon known as contact inhibition. Cancer cells disregard these controls and continue to divide rapidly and continuously. This unchecked proliferation leads to the formation of cell masses, commonly referred to as tumors.
The deregulation of the cell cycle is a defining feature of this uncontrolled growth. Healthy cells possess checkpoints that monitor for DNA damage or incomplete replication before allowing progression to the next stage of division. In cancer cells, these checkpoints are compromised, allowing damaged or abnormal cells to continue multiplying.
Proteins such as cyclins and cyclin-dependent kinases (CDKs) orchestrate cell cycle progression, while tumor suppressor proteins like p53 and retinoblastoma (Rb) protein can halt the cycle. In cancer, these regulatory proteins are often disrupted, contributing to continuous cell division. Additionally, cancer cells can sustain proliferative signaling even without external growth factors, enabling them to enter the cell cycle independently.
Evading Normal Cell Death
Programmed cell death, or apoptosis, is a natural process that removes damaged, old, or abnormal cells to maintain tissue health and prevent uncontrolled growth. Cancer cells develop mechanisms to resist this self-destruction, enabling their survival and accumulation despite being abnormal or damaged. This evasion allows cancerous cells to persist and expand.
A family of proteins known as BCL-2 plays a significant role in regulating apoptosis, with some members promoting cell death and others inhibiting it. In many cancers, there is an increased expression of pro-survival BCL-2 proteins. These proteins prevent the cell’s self-destruction process. Consequently, even when faced with signals that would normally trigger apoptosis, cancer cells can survive, contributing to tumor growth and resistance to therapies.
Ability to Invade and Spread
A key characteristic of cancer cells is their capacity to invade surrounding tissues and spread to distant parts of the body, a process known as metastasis. This ability distinguishes malignant tumors from benign ones, as benign tumors typically remain localized. Cancer cells acquire the capacity to detach from the primary tumor and migrate through the body.
This metastatic process involves epithelial-to-mesenchymal transition (EMT), where cancer cells lose their epithelial features and gain mesenchymal characteristics, including increased motility and invasiveness. During EMT, there is a downregulation of epithelial markers like E-cadherin and an upregulation of mesenchymal markers such as N-cadherin. These changes allow cancer cells to break free from the primary tumor, reorganize their cytoskeleton, and move through the extracellular matrix. Once detached, these circulating tumor cells (CTCs) can enter the bloodstream or lymphatic system, travel to new locations, and establish secondary tumors.
Fueling Growth: New Blood Vessel Formation
For a tumor to grow beyond a small size, it requires a constant supply of oxygen and nutrients, as well as a way to remove waste products. Cancer cells stimulate the formation of new blood vessels, a process called angiogenesis, to meet these demands. Without this new vasculature, tumors are limited in their growth and cannot expand significantly.
Vascular Endothelial Growth Factor (VEGF) is a signaling protein that promotes angiogenesis in tumors. Cancer cells release VEGF, which binds to its receptors on endothelial cells lining existing blood vessels. This binding triggers a signaling cascade that stimulates the proliferation and migration of these endothelial cells, leading to the sprouting and formation of new capillaries that extend into the tumor mass. VEGF also increases vascular permeability, supporting the development of new vessels. This newly formed, often chaotic, network of blood vessels efficiently delivers the resources necessary for the tumor’s rapid expansion and survival.
Genetic Instability and Mutations
Genetic instability is central to cancer cell characteristics, referring to an elevated rate of changes in the cell’s DNA. Cancer cells accumulate numerous mutations in their genetic material, leading to errors during cell division and the acquisition of abnormal behaviors like uncontrolled growth and evasion of cell death. These mutations can affect various types of genes that regulate normal cellular processes.
Oncogenes, which are mutated versions of proto-oncogenes, become activated and promote cell growth and proliferation. Tumor suppressor genes, conversely, normally inhibit cell growth and trigger DNA repair or apoptosis; mutations in these genes can render them non-functional, removing a critical brake on cell division. For example, mutations in the p53 tumor suppressor gene are frequently observed in human cancers, impairing its ability to halt the cell cycle or induce cell death in response to DNA damage. This genetic instability can manifest as chromosomal instability, involving large-scale changes like gains or losses of entire chromosomes, or as microsatellite instability, characterized by alterations in repetitive DNA sequences due to defects in DNA mismatch repair mechanisms. The continuous accumulation of these genetic alterations drives the evolution of cancer cells, allowing them to acquire and refine the abnormal behaviors that define the disease.