Cancer is characterized by cells that exhibit several distinct properties due to various mutations. These properties include the ability to grow without external growth signals, insensitivity to anti-growth signals, evasion of apoptosis (programmed cell death), unlimited replication, angiogenesis (formation of new blood vessels), invasion and metastasis (spreading to other tissues), and genetic instability, which leads to rapid accumulation of mutations. Each of these characteristics contributes to the uncontrolled growth and spread of cancer cells.
At the genetic level, two main types of genes are involved in cancer development: oncogenes and tumor suppressor genes. Oncogenes are mutated forms of normal genes (proto-oncogenes) that become overexpressed, leading to increased cell proliferation, survival, and tumor development. This overexpression can occur through mutations or gene amplification, resulting in excessive activity that drives cancerous behavior. Common examples of oncogenes include growth factors, growth factor receptors, GTP-binding proteins, and transcription factors. A notable oncogene is RAS, which is mutated in approximately 20% of human cancers, highlighting its significant role in tumorigenesis.
In contrast, tumor suppressor genes function to inhibit cell growth and promote apoptosis. When these genes are mutated, their activity is lost, which can lead to unchecked cell proliferation and survival. A well-known tumor suppressor is p53, a transcription factor that responds to DNA damage by initiating repair processes or triggering apoptosis. When p53 is mutated, cancer cells can accumulate further mutations without the necessary checks, facilitating tumor growth. Another example is the retinoblastoma gene, which regulates the cell cycle and can be inherited in its mutated form, leading to increased cancer risk.
Understanding the roles of oncogenes and tumor suppressors is crucial in cancer biology, as these genes are central to the mechanisms that allow cancer cells to thrive and proliferate despite the body's regulatory systems. The interplay between these two types of genes underscores the complexity of cancer development and the importance of targeted therapies that can address these genetic alterations.