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As a result, a woman with one of those mutations is estimated to have a 60%to70%0% chance of developing breast cancer at some point in her life.

In women with early-onset breast carcinoma unselected for family history, the prevalence of BRCA1 mutations is estimated to be between four and nine percent [16] [23].

The frequency of FUS mutations is estimated at 4% in familial ALS and 1% in sporadic ALS.

The ovarian cancer relative risk for carriers of RAD51D mutations is estimated to be 6.3, while the relative risk for breast cancer is not statistically significant [ 120].

The number of nonsynonymous mutations is estimated on every codon position in the alignment and regions with overabundant mutation rate are reckoned using Faster software [ 18].

Under this approach, the DFE of amino acid mutations is estimated by maximum likelihood based on their site-frequency spectrum and that of sites assumed to be evolving neutrally (synonymous sites).

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In 1997, the lifetime risk of breast cancer in women with BRCA mutations was estimated in the range of 85percentt.

Therefore, the lower limit of detection of minor resistance mutations was estimated to be 0.5 3.0% in the previous studies [12], [18], [19], [30], [31].

The fractions of sites in the coding regions for synonymous, nonsynonymous, and nonsense mutations were estimated to be 28.5%, 68.1%, and 3.4%, respectively.

Overall, the sensitivity of the microarray was estimated to be 73.3%, while the sensitivity of the microarray with respect to missense mutations was estimated to be 95.65% (22/23 detected; Table 2).

The A32V and Δ152 164 mutations were estimated to be present in the R6 (pH 5.6) cell population at frequencies of 18.6%, and 11.2%, respectively (Fig. 2A) while 3.3% contained both mutations (Fig. 2A).

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