Recently, a strong mutational bias toward A and T generating mutations was observed in mutation accumulation lines of Caenorhabditis nematodes (Denver et al. 2012).
A similar rate of VHL mutations was observed when we assessed the mutational burden of each individual core, revealing mutations in 29/47 cores (62%).
A significant increase in the accumulation of mutations was observed in cells exposed to Mn2+, using two distinct mutator assays.
Recently, a high frequency of somatic mutations was observed in the PIK3CA gene in various cancer types, including oral squamous cell carcinoma (OSCC).
A similar correlation between the sites of formation of depurinating DNA adducts and H-ras mutations was observed in mouse skin and rat mammary glands treated with E2-3,4-Q [64] 64].
No evidence of point mutations was observed when acrylic acid or over 60 acrylates and methacrylates were investigated in Salmonella bacterial tests or in hprt mutation tests mammalian cells, and no evidence of a mutagenic effect was seen when tested in whole animal clastogenicity and/or aneuploidy (chromosomal aberration/micronucleus) studies.
Shorter time to dominance for reverse mutations was observed in 6 of 23 (26%) comparable subjects.
Unexpectedly, the lowest frequency of mutations was observed with CCC DNA that was not gel purified (experiment 1, Table 2).
In contrast to treated subjects, however, no significant change in the numbers of private mutations was observed between any of the three time points (Figure 3B and C).
Transmitted resistance in the form of major drug resistant mutations was observed in 11.7% (95% confidence interval 7.6 to 17.6%) of the samples.
However, a slight increase, albeit significant, number of mutations was observed at these three hotspots in NBS patients (11.2% vs. 8.0% of total mutations, χ2 test, p<0.05).
