Mutator mutations may occur in only a minority of premalignant lesions, but the mutator premalignant lesions are predicted to overwhelmingly be the ones that actually develop into cancers.
Suppressor mutations may occur within the gene carrying the primary mutation (intragenic suppressors) or in another gene, generating a phenotype that counterbalances the effect of the primary mutation.
Unlike inherited variants, cancer mutations may occur at low frequencies because of contamination from normal cells or tumor heterogeneity and can therefore be challenging to detect using common NGS analysis tools, which are often designed for constitutional genomic studies.
Therefore, mitochondrial disorders may be inherited in either a Mendelian (autosomal recessive, autosomal dominant, or X-linked) or maternal (mitochondrial) fashion, because mutations may occur in either the nuclear or mitochondrial genome.
Errors (mutations) may occur at each reproduction event, at each generation (a round of copies).
Random color mutations may occur in the wild, but these are rare.
The Microcystis genome contains two identical rRNA operons, although point mutations may occur occasionally [39], [42], [51].
Mutations may occur at different rates u, from A1 to A2, and v, in the reverse direction.
Furthermore CRC development appears to depend on whole-life nutrition pattern [23], and TP53 mutations may occur years before CRC diagnosis [25], [35].
It appears that in MSI colon cancers ACVR2 mutations may occur early in tumorigenesis and are associated with increased local growth [14].
Because studies of CTL epitopes in CRF01_AE infections are limited, we believe that several other mutations may occur in clade-specific CTL epitopes that have not yet been reported.
