A primary tumor is a tumor growing at the anatomical site where tumor progression began and proceeded to yield a cancerous mass.
Cancer is the uncontrolled cell division. This arises when cells escape the normal cell mechanism that limits their growth. When at least one copy of a proto-oncogene (e.g. ras gene) is mutated to form an oncogene, cells divide excessively. The gene product from such oncogene may also be hyperactive. This is a gain-in-function mutation. When both copies of a tumor suppressor gene (e.g. p53 gene) are mutated, cells lose their ability to stop dividing even when they should. The gene product may be defective such that they are unable to activate the other genes that are involved in cell arrest. The lack of contact inhibition and apoptosis leads to the formation of a tumor. The telomerase in cells may also be upregulated. This means that the natural limit of the number of times cells can divide would be higher than normal. All these mutations are observed in a single cell or a line of daughter cells. Rate of mutation increases when the rate of cell division increases. Metastatasis occurs and secondary tumors are formed. Cancer is a multi-step process as it requires all the regulatory checkpoints to be disrupted and this requires an accumulation of mutations.
Weinberg, Robert. The Biology of Cancer, 2007.
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