Oncogenes and Cancer
Oncogenes: A broad category on possible cancer formation.
Cancer is where the cells have lost their ability to control cell division. Tumors are the cells that divide uncontrollably but can be benign (can usually be cured) and malignant (cells that pose a threat to health). The formation of cancer is very rare. It is said that the millions of years of evolution has endowed human beings with the ability under selective pressures to combat tumors from forming. This is prominent during human reproductive lives and this protection may decrease with age. Age-dependent cancers such as invasive carcinoma are thought to undergo more than six mutations in a cell in order for it to be converted in to a malignant tumor. Mechanisms that may provide a window of opportunity for cells to develop into tumors lies in oncogenes.
A proto-oncogene is a gene that promotes normal cell proliferation. Mutations may occur to turn the cell into a oncogene whose normal activity to promote cell proliferation is impaired. These oncogenes can be activated by amplification, point mutation, chromosomal rearrangement, and translocations. There are also five broad classes that oncogenes control in a cell cycle that would be expected to be disrupted in cancer cells. They include secreting growth factors, cell surface receptors, components of intracellular signal transduction systems, DNA-binding nuclear proteins, and components of cyclins.
The activation of oncogenes that affect the five broad areas are a gain in function. Amplification can be looked as multiplying several copies of a gene like the ERBB2 oncogene that contributes to breast cancer. Point mutations are when a particular amino acid that codes for a protein is replaced such as a substitution of BRAF which permanently activates kinases involved in transcription and is prominent in many malignant melanomas. Translocations are a rearrangement of non-homologous chromosomes. A prominent example is the translocation gene fusion between chromosome 22 and chromosome 9 in the human genome. This produces the Philadelphia chromosome responsible for active tryosine kinases in myeloid luekemia. Lastly, translocations other than chromosome rearrangement can occur that do not create chimeric cells such as the Philadelphia chromosome. Translocations of chromosome 8 and 14 signal increased levels of MYC expression in B-cells because the gene for MYC is translocated from chromosome 14 to chromosome 8 that influences B-cells. As B-cells, the makers of antibodies are produced, MYC is also transcribed which is a transcription factor that allows expression of other genes.
Oncogenes are the not sole reason for activating tumors, but shows some possible steps that cells fail to correct with their innate defense over multiple generations to produce such abnormal effects.