Analysis of these loop 3 mutations has indicated that certain substitutions induce drastic changes in channel properties due to the presence of bulky or differentially charged residues [20] [22].
Previous mutation screening studies have indicated that mis-sense mutations in the ATM gene – rather than protein-truncating mutations – are over-represented in patients with breast cancer compared with the general population [ 72, 75- 79].
Of the remaining non-synonymous mutations, previous studies have indicated that the majority are actually background population variation [30], [31].
Several studies focusing on mutations in mitochondrial genes have indicated dysfunction of mitochondrial ATP production, dysregulation of DSB repair gene expression, and genomic instability.
Motif mutation studies in rats have indicated that nuclear respiratory factor 1 (NRF-1), NRF-2 and Sp1 promote basal Tfam gene transcription.
However, recent studies have indicated that mutations of these genes might play distinct roles in tumor initiation and/or maintenance [10], [14].
Several studies [32], [33] have indicated the mutations in the NA gene that confer resistance to known NA inhibitors such as Oseltamivir and Zanamivir.
Mutations in buried polar groups have indicated a role for these groups in the reduction potential as well.
Previous studies have indicated that mutations in TP53 are associated with a poor prognosis and a poor response to systemic therapy (see [ 46] for references).
Some studies have indicated that mutations are acquired during fetal development, 69, 70 but the principle of the difference in the number of mutations required for adulthood and childhood cancers remains to be determined.
