We found significant mutation frequency in a number of genes previously known to be somatically mutated in colon cancer patients including APC, TP53 and KRAS.
(a) γ-irradiation induced mutation frequency in BaF3 cells treated with or without 1 μM imatinib.
Therefore, we analyzed mutation frequency in cells transfected with an imatinib-resistant bcr-abl mutant (Bcr-AblT315I).
We attempted to develop a therapeutic that would inhibit the CEES-induced increase in mutation frequency in the skin.
(b) HPRT mutation frequency in Bcr-Abl-positive 32D cells (BA+), 32D cells expressing the imatinib-resistant bcr-abl mutant T315I (Bcr-AblT315I), and Bcr-Abl-negative 32D cells (BA−) in the presence or absence of 3 μM imatinib.
In transgenic mice, we have found that locus specific effects can profoundly influence the mutation frequency in a reporter gene, and we have begun to study tissue-dependent variations in the pattern of spontaneous mutagenesis.
The overall c-kit mutation frequency in exons 8, 9, 11, 13, 15 and 17 was determined to be 25.86% (15/58).
We identified alterations in DNA copy number and complex genomic rearrangements and demonstrated a low somatic point mutation frequency in the absence of tobacco mutagens.
We next investigated whether overexpression of the hPolλ W438 variant could affect mutation frequency in vivo.
We found that, similar to a previous report [29], nutrient depletion induced a chronological-age-dependent increase in mutation frequency in wild-type cells (Fig. 5D; "vector").
To evaluate the existence of multiple alleles per locus, we calculated the mutation frequency in 19 targeted genes (Table 1) according to [21].
