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The page below is a sample from the LabCE course Precision Medicine-Molecular Mechanisms of Cancer Development and Actionable Genes. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

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Tumorigenesis

Tumors arise from normal cells in a multistep process. A cancer cell has to overcome all of the cells defenses in order to develop. Cancer cells are able to do this by imparting genetic instability to the genome. The cell will begin down the cancerous pathway by first either knocking out a tumor suppressor or by activating an oncogene. Eventually the cancer cell must also stop responding to signals in the cell cycle where the cell checks the integrity of the DNA before proceeding with replication. Because the cell no longer stops for checkpoints, the cancerous cell’s DNA becomes mutated at an increased frequency, called genetic instability. The unstable nature of the cancerous DNA allows the cancer cell to evolve much faster than normal cells. It will become increasingly different from the normal cell that it once was. If one of these mutations gives the cell a survival advantage they will replicate much faster and eventually outnumber normal cells in the local area. This clonal expansion (expansion from one cell) is how tumor formation occurs.