For example, sequencing each mutational hotspot is laborious and detecting mutations outside the hotspots is not feasible.
The seventh and eighth digits distinguish mutations outside the coding region.
The key advantages of this approach include facile amplification, restriction enzyme-free library generation, and a significantly reduced risk of mutations outside the targeted region and wild-type contamination as compared with current methods.
Finding mutations outside the coding sequence may be difficult as regulatory elements of this small gene are scattered over large distances [16], [17].
Carriers of the haplotype should be enriched for relevant mutations outside the MC4R coding region and could thus be used for re-sequencing approaches.
Interestingly, this association for DSS became non-significant when tumors harbouring TP53 mutations affecting the p53 L2/L3 DNA-binding domains were compared to those with wild-type or TP53 mutations outside the L2/L3 domains (p = 0.095).
Sequence data from the cloned SIGLEC 1 consistent with the NCBI sequence with the exception of two single nucleotide polymorphisms (dbSNP: 6037651 and dbSNP: 709012) in the cloned gene, which generated two sense mutations outside the sialic acid-binding domain.
When tumors harboring TP53 mutations affecting the p53 L2/L3 DNA-binding domains were compared to those with wild-type TP53 or TP53 mutations outside the L2/L3 domains, this correlation was further strengthened (p = 0.0136).
The difference in DSS was smaller if patients harbouring TP53 mutations affecting the L2/L3 domain were compared to the combined group of patients revealing TP53 wild-type status or TP53 mutations outside the L2/L3 domain (p>0.5).
Recent reports have stated that AID-mediated deamination on DNA can also lead to the generation of unwanted lesions, namely, mutations outside the Ig genes [27], [28], or DNA breaks and chromosomal translocations [19], [20], [21], [22], whose contribution to lymphoid neoplasia has been demonstrated in several in vivo models [19], [21], [22], [23], [24], [25].
In addition, an earlier study by Cox and colleagues on HCV evolution during the first six months after acute infection showed a comparable rate of 25% of mutations were in detected CD8+ T-cell responses [9], although this number was about 50% when only mutations outside the envelope were included.
