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Tumor promotion is a process in carcinogenesis by which various factors permit the descendants of a single initiated cell to survive and expand in number, i.e. to resist apoptosis and to undergo clonal growth. [1] This is a step toward tumor progression. [2] [3]
Cancers and tumors are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat. Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells.
A series of mutations is required in the process of carcinogenesis for a cell to transition from being normal to pre-malignant and then to a cancer cell. [86] The mutated genes usually belong to classes of caretaker, gatekeeper, landscaper or several other genes.
If, through mutation, normal genes promoting cellular growth are up-regulated (gain-of-function mutation), they predispose the cell to cancer and are termed oncogenes. Usually, multiple oncogenes, along with mutated apoptotic or tumor suppressor genes , act in concert to cause cancer.
Colon cancer provides one example of the mechanisms by which diet, the top factor listed in the table, is an external factor in cancer. The Western diet of African Americans in the United States is associated with a yearly colon cancer rate of 65 per 100,000 individuals, while the high fiber/low fat diet of rural Native Africans in South Africa is associated with a yearly colon cancer rate of ...
Lung cancer is the No. 1 cause of cancer-related deaths worldwide. vladwel/iStock via Getty Images PlusThere are many types of cancer treatments. But which ones work best varies from patient to ...
Tumor initiation is defined as "a process in which normal cells are changed so that they are able to form tumors". [1] It is the first phase in tumor development. [2] Mutagens, substances that cause cancer can be tumor initiators.
The SWI/SNF ATPase BRG1 (or SMARCA4) is the most frequently mutated chromatin remodeling ATPase in cancer. [27] Mutations in this gene were first recognized in human cancer cell lines derived from lung. [28] In cancer, mutations in BRG1 show an unusually high preference for missense mutations that target the ATPase domain.