According to a recent study, p53 mutation prevalence estimates were 45, 5 and 1%, respectively, for invasive, LMP and benign ovarian tumours (Reles et al, 2001; Kmet et al, 2003).
For the purposes of this study, we analyzed mutation prevalence rates only within subtypes A, B, C, D, F, G, CRF01_AE, and CRF02_AG.
Similar to our study's 7271T>G mutation prevalence of 0.08% (one out of 1149), Chenevix-Trench et al (2002) observed one mutation among 525 cases and 381 controls (0.11%); all women included in the study were under age 40.
In conclusion, the extensive mutation frequency data summarized in this paper provides a useful context in which mutation prevalence data from population-based surveillance studies of transmitted resistance can be interpreted.
Previous studies have estimated mutation prevalence in clinical referrals for primary ovarian insufficiency, but these are likely to be biased as compared with cases in the general population.
However, the number of p53 mutation positive cases (n = 34, mutation prevalence = 11%) was substantially smaller than in our study (n = 128, mutation prevalence = 15%) or in the study by Conway et al. (2002; n = 108, mutation prevalence = 24%), and the results appeared to be unstable.
Overall these studies suggest that 816 c-kit mutation prevalence is high in adult patients and low in pediatrics patients.
In this study, the relationship between lesion growth and mutation prevalence within a lesion was investigated.
Other studies have estimated higher frequencies of BRCA1 mutation prevalence but these did not allow for the presence of other genetic effects (Whittemore et al, 2004).
The computed mutation prevalence for the known cancer genes overlapped with those of previous studies.
