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The ability of every multicellular organism to fight off dysfunctional, mutated cells (tumors), and/or external factors that can lead to the mutations constitutes an important mechanism controlled by natural selection.
The apurinic sites derived from the loss of these adducts from DNA lead to the mutations that can initiate cancer.
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It has been proposed that the metabolic burden of the Agr cascade leads to the mutations in this locus [ 40], with parallels to the in vitro conversion of mucoid P. aeruginosa strains to non-mucoid [ 93].
RIP is a gene silencing mechanisms that leads to the mutation of repetitive DNA sequences during the sexual cycle, between fertilization and nuclear fusion.
RIP is a gene silencing mechanism that leads to the mutation of repeated DNA sequences during the Neurospora crassa sexual cycle (Selker, 1990).
Possible errors in the repair of these sites can lead to the critical mutations initiating many common human cancers [63, 64].
Incomplete repair of DPX can lead to the formation of mutations, in particular chromosome mutations and micronuclei (MN) in proliferating cells.
These mutations have lead to the genetic variation we see in modern human populations [ 1, 15].
Defects in the MMR system lead to the accumulation of mutations at short repetitive DNA sequences, termed microsatellites.
Conversely, techniques that are too sensitive may lead to the detection of mutations in rare cell clones within heterogeneous tumours.
Different mechanisms lead to the gain-of-function mutations in the HD and the KD.
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