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The consequences of these mutations are currently being examined.
Most mutations are currently identified by conventional methods of polymorphism detection and DNA sequencing [ 12].
By contrast, the clinical implications of identifying low levels of drug-sensitizing mutations are currently unknown.
All of these mutations are currently believed to represent secondary events and are known to coexist.
A number of sequencing and PCR-based methods for detecting KRAS mutations are currently in clinical use.
Larger epigenetic studies of smoking, diet and co-morbidities and associations with known genetic mutations are currently underway.
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Whether these previously unreported NPM-1 mutations will confer the same better outcome as previously reported mutations is currently unknown and warrants a larger study.
The detection of these mutations is currently performed by the reverse dot blot (RDB) hybridization technique, which could detect only known mutations.
The K70Q/Q151Mc set of mutations is currently rare among HIV-infected patients.
Interestingly, it has been reported that chicken DT40 B cells deficient for members of the FA pathway show a decrease in SHM [23], [26], although the precise mechanism for the decrease in the accumulation of non-templated mutations is currently unclear.
Based on these findings, repeated testing of RAS mutations is currently not recommended.
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