Sentence examples for mutations observed here from inspiring English sources

The initiating cell type of mucinous tumors presenting on the ovary remains to be determined; the heterogeneity of the mutations observed here as well as the mutational spectrum suggests that the ovarian surface epithelium is unlikely to be the only source.

The different frequencies of gene mutations observed here could depend on different gene expression levels and/or on local chromatin organization [20], [21], [22], [23].

This indicates that the single nucleotide mutations, observed here and reported in the TP53 mutation database [13], might really correspond to the background genetic noise, and not be specifically correlated to tumour formation.

Most other mutations observed here have previously been implicated in the biology of mucinous ovarian tumors (KRAS, BRAF, TP53, CDKN2A, PIK3CA, PTEN) [ 14, 15, 18– 20, 38].

Also, the proportion of silent mutations observed here is consistent with the proportion of silent mutations detected using Sanger sequencing (<6 %) [ 5, 6, 8– 10, 29].

Interestingly, the type of mutations observed here are very similar to those which we have previously shown to be clonally expanded in cytochrome c oxidase deficient crypts in human colon (Taylor et al., 2003; Greaves et al., 2006).

The in vitro and in vivo effects of licD2 mutation observed here correlate with those seen with licD2 mutants of non-typeable H. influenzae [4], [39].

The higher RecBCD-mediated HR observed near dif (Louarn et al., 1991) might contribute to the higher DSB-repair-coupled mutation observed here.

The positive correlation between the observed mutation rate and the number of immediately flanking C G pairings seen in Fig.  7b is consistent with this interpretation, suggesting that base-stacking may explain much of the variation in context-dependent mutation rates observed here and in other studies [ 4].

Regional clusters of mutations in cancer have occasionally been observed in experimental models, although not at the mutation density observed here (Wang et al., 2007).

It is noteworthy that intermediate mutation rates are present in other diseases such as Bloom's syndrome (approximately 10-fold higher than normal patients) (Warren et al, 1981) and Werner syndrome (10 50-fold 10 50-foldn normal cell lines) (Fukuchigheral, 1989), and we inthanret the inormaldiate elevated mutation rates observed here as likely biologicelly significant.