Sentence examples for mutation prevalence has from inspiring English sources

In a genetic counseling TNBC cohort, BRCA1 and BRCA2 mutation prevalence has been reported to differ by populations [ 32]; 50 % in Ashkenazi Jewish women, 33.3 % in Caucasian women, and 20.4 % in African American women which is consistent with what we found in this study.

Higher KRAS2 mutation prevalences have been reported in pancreatic or duodenal juice (63 to 87%), due probably to higher DNA tumour content in pancreatic juice as compared to plasma (Wilentz et al, 1998; van Laethem et al, 1998; Watanabe et al, 1999).

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.

All these genes had a mutation prevalence of ≥5% and about a quarter of patients with CRC in our cohort harboured at least one mutation in these five genes.

According to this approach, the top driver oncogenes having a mutation prevalence over 5%% included AKT1, TRANK1, TRAPPC10, RPGR, COL6A2, RAPGEF4, ATG2B, CNTRL, NAA38, OSBPL10, POTEF, SCLT1, SUN1, VWDE, MTUS2, and PIK3CA, and the top tumor suppressor genes included PHEX, TP53, GGA3, RGS22, PXDNL, ARFGEF1, BRCA2, CHD8, GCC2, and ARMC4.

Titin (TTN) was also selected as a non-cancer gene because it has a high mutation prevalence probably due to its massive size.

However, BRCA2 mutation prevalence in sporadic male breast cancer has been found to be as high as 33 and 21% in the Hungarian and Swedish population (Haraldsson et al, 1998; Csokay et al, 1999).

It was decided that any mutation that has prevalence <0.1% should be removed from the screening panel, but that henceforth, decisions would be based on the benefits and costs of incremental gain in the performance characteristics of the screening test as defined here.

Microsatellite unstable gastric cancer were observed to have a higher mutation prevalence of both C > T transitions and C > A transversions [ 71].

We found that while the PI3K_p85B domain, which is responsible for binding the PI3K p85 subunit to form a heterodimer [ 29], was identified as a significant domain peak in both cancer types, the domain only had a high mutation prevalence (threshold of 0.04) in the colon cancer set.

We have presented estimates of mutation prevalence, and described infections as harbouring two, three or more mutations.