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Under this model, cancer arises as the result of a single, isolated event, rather than the slow accumulation of multiple mutations. [4] The exact function of some tumor suppressor genes is not currently known (e.g. MEN1, WT1), [5] but based on these genes following the Knudson "two-hit" hypothesis, they are strongly presumed to be suppressor genes.
This gives a wider and more global view of cancer genetics, while these data are usually dispersed. [3] It includes a large iconography of about 35,000 images. Dan van Dyke said "This is one stop shopping that unifies cancer genetics information", and Lidia Larizza said that the Atlas was an "interdisciplinary resource".
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The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).
Genetic architecture is the underlying genetic basis of a phenotypic trait and its variational properties. [1] Phenotypic variation for quantitative traits is, at the most basic level, the result of the segregation of alleles at quantitative trait loci (QTL) . [ 2 ]
Breast cancer type 1 susceptibility protein is a protein that in humans is encoded by the BRCA1 (/ ˌ b r æ k ə ˈ w ʌ n /) gene. [5] Orthologs are common in other vertebrate species, whereas invertebrate genomes may encode a more distantly related gene. [ 6 ]
Cancer is a genetic disease caused by accumulation of DNA mutations and epigenetic alterations leading to unrestrained cell proliferation and neoplasm formation. The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers and new ...