Cancer arises from the accumulation of multiple mutations within a single cell, leading to uncontrolled cell growth and proliferation. These mutations can be categorized into two main classes: passenger mutations and driver mutations. Passenger mutations are those that accumulate without contributing directly to cancer development; they do not promote cell growth or inhibit apoptosis. Instead, they represent random DNA damage that does not affect the cancerous phenotype.
In contrast, driver mutations are critical to cancer progression. They enable cancer cells to grow abnormally, proliferate uncontrollably, or evade programmed cell death. Within the category of driver mutations, there are two primary types: oncogenes and tumor suppressor genes. Oncogenes are mutated forms of normal genes, known as proto-oncogenes, which typically regulate cell growth. When proto-oncogenes mutate, they act dominantly, meaning that even a single mutated allele can lead to a cancerous phenotype. An example of an oncogene is the RAS GTPase, which plays a significant role in signal transduction pathways.
On the other hand, tumor suppressor genes function to inhibit cell division and prevent tumor formation. When these genes are mutated, they lose their ability to suppress tumor growth. Notable examples include the retinoblastoma gene and the p53 gene, both of which are transcription factors. The normal function of p53 is to regulate the expression of multiple genes involved in cell cycle control and apoptosis. When mutated, p53 can lead to widespread dysregulation of these genes, contributing to tumorigenesis. While mutations in p53 are typically somatic and not inherited, retinoblastoma mutations can be inherited and often require both alleles to be mutated for the cancer phenotype to manifest.
Understanding the distinction between oncogenes and tumor suppressor genes is crucial, as questions regarding their differences frequently appear in examinations. In summary, the interplay between these mutations, particularly the activation of proto-oncogenes and the inactivation of tumor suppressor genes, is fundamental to the development of cancer.
