Sentence examples for concurrent mutation from inspiring English sources

One possibility is that such tumours contain a concurrent mutation in another oncogene that activates the same signalling pathway as KRAS.

n.t., not tested Considering the immunocytochemical results, all melanoma cell lines (7/7; 100%) with concurrent mutation of BRAF- NRAS and down-regulation of p16 CDKN 2 A presented high expression levels of the activated pERK1-2 protein.

The concurrent mutation and amplification of PIK3CA frequently occur in all of breast cancer with 42% (18 of 43) of tumors with amplified PIK3CA also harboring a PIK3CA mutation (Additional file 3: Figure S2).

Interestingly, the concurrent mutation of DOF2 and DOF3 (mDOF(2+3)::GUS) resulted in a strong, but yet not complete, inactivation of the promoter activity in guard cells, as 15% of the mDOF(2+3)::GUS lines displayed weak expression of the reporter in stomata.

There was also a higher incidence of concurrent mutation of FLT3/ITD, FLT3/TKD, AML1/RUNX1 or MLL/PTD in CEBPAsingle-mut patients than in CEBPAdouble-mut patients (20.8 vs 10.6%, 12.5 vs 4.3%, 8.3 vs 2.1% and 4.2 vs 0%, respectively), but the difference did not reach statistical significance.

Moreover, no concurrent mutation of the PTEN gene was observed in melanoma cell lines; this is clearly in contrast with previous data from other series, which reported that such a gene is mutated at a rate of about 30% among in vitro melanomas [ 37].

Nearly all NPM1-mutated AML patients showed concurrent mutations in genes involved in regulation of DNA methylation (DNMT3A, TET2, IDH1, IDH2), RNA splicing (SRSF2, SF3B1), or in the cohesin complex (RAD21, SMC1A, SMC3, STAG2).

Two concurrent mutations were identified in 89 (29%) tumors, 3 mutations in 24 (8%), 4 mutations in 6 (2%), and 5 mutations in 1 tumor.

Routine tumor genotyping enables identification of concurrent mutations in tumors and reveals low-frequency mutations that may be associated with a particular tumor phenotype.

Most importantly, the nanoparticles tackle multiple biological pathways found in a broad spectrum of microorganisms which may require many concurrent mutations to achieve resistance against the nanoparticle's antimicrobial activity.

Our findings indicate that routine tumor genotyping is helpful in identifying low-frequency mutations, such as GNAS, that may correlate with a specific morphological phenotype and also reveal multiplicity of concurrent mutations in a significant proportion of CRC that may have significant implications for clinical trial design and personalized therapy.