Molecular analysis of driver mutations is standard care in lung cancer in the era of personalized treatment as the presence of a driver mutation can have prognostic and predictive value-targeted therapy [ 1, 2].
Most importantly, all mutations are standard analyzable types.
Because the techniques for measuring BRCA1/2 mutations are standard and relatively inexpensive, the medical care system should consider coverage of BRCA1/2 mutation screening for the high-risk families.
Even for D. melanogaster it is unknown whether the male-infertility phenotype associated with this mutation is specific to the standard nuclear backgrounds in which previous experiments have been conducted (Clancy et al. 2011; Yee et al. 2013) and thus dependent on a mito-nuclear interaction.
The mutation rates thus estimated range from 7×10−4 to 3×10−3 per locus per generation, which are standard mutation rates for microsatellite loci in other species [94].
However, routine screening for LKB1 gene mutations is not standard-of-care practice making it difficult to stratify patients by LKB1 inactivation.
The Q209P mutation was created by standard PCR-directed mutagenesis approaches.
Molecular analyses for MSI and BRAF V600E mutation were performed using standard protocols as described previously (Loughrey et al, 2007; Raptis et al, 2007; Campbell et al, 2010).
The Gria3 tmutationutation was genotyped in standard PCR conditions as above in a 3-primer assays using oligonucleotides designed by Deltagen 39637: 5′- GGTCACGAGGTTCTTCATTGTTGTC-3′, 3196 (neo): 5′- GGGTGGGATTAGATAAATGCCTGCTCT-3′, and 39636: 5′- AGCTGATATAGCTGTTGCTCCACTC-3′, giving a 380 bp product for the targeted allele and a 275 bp product for the endogenous allele.
