In contrast, our clustering analysis has clearly shown that BRAF mutation is clustered with CIMP-high specific markers, indicating that BRAF mutation is perhaps associated with a non-random pattern of CpG island methylation.
Although these findings appeared to be discrepant, we believe that KRAS mutation is perhaps associated with a random pattern of CpG island methylation, indicated by the non-clustering phenomenon in clustering analysis.
BRAF mutations, which are perhaps one of the most commonly accepted indicator events for CIMP in colorectal cancers, also appear to be relevant in LUAD, but not the other tumor types.
The origins of limits on mutation rates from above are perhaps harder to untangle.
With regard to excitatory synaptic function, mutations in the ProSAP/Shank family are perhaps some of the most exciting given their link to autism spectrum disorders (Durand et al, 2007; Berkel et al, 2010) and Alzheimer's disease (Gong et al, 2009; Roselli et al, 2009; Pham et al, 2010).
The long-lived power of K to detect selection on microsatellites with high mutation rates is perhaps particularly important.
The gatekeeper mutation T790M is perhaps the most common mechanism of resistance in NSCLC, but is rarely, if ever, found in GBM, despite that GBM is often refractory to TKI treatment.
These are unusual for EMS-induced mutations, but it is perhaps the location and frequency of these mutations which is most intriguing.
The finding of TINF2 mutations in DC is perhaps one of the most critical in confirming the role of telomeres in the disease.
