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Early mathematical modeling of cancer, by Armitage and Doll, set the stage for the future development of the somatic evolutionary theory of cancer. Armitage and Doll explained the cancer incidence data, as a function of age, as a process of the sequential accumulation of somatic mutations (or other rate limiting steps). [13]
The COSMIC (Catalogue of Somatic Mutations in Cancer) database was designed to collect and display information on somatic mutations in cancer. It was launched in 2004, with data from just four genes, HRAS, KRAS2, NRAS and BRAF. [6] These four genes are known to be somatically mutated in cancer. Since its creation, the database has expanded rapidly.
According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by interfering with the programming regulating the processes, upsetting the normal balance between proliferation and cell death.
Somatic mutations accumulate within an organism's cells as it ages and with each round of cell division; the role of somatic mutations in the development of cancer is well established, and the accumulation of somatic mutations is implicated in the biology of aging. [4]
Conceptual workflow of somatic mutational signatures identification. Diverse mutagenesis processes shape the somatic landscape of tumors. Deciphering the underlying patterns of cancer mutations allows to uncover relationships between these recurrent patterns of mutations and infer possible causal mutational processes.
Human somatic variations are somatic mutations (mutations that occur in somatic cells) both at early stages of development and in adult cells. These variations can lead either to pathogenic phenotypes or not, even if their function in healthy conditions is not completely clear yet.