Sentence examples for active mutations of from inspiring English sources

Ligand-independent, constitutively active mutations of PDGFRα occur in about 5-8% of patients [ 7].

For example, constitutively active mutations of epidermal growth factor receptor (EGFR) gene are often associated with well differentiated adenocarcinoma of the lung showing bronchioloalveolar pattern.

A receptor for androgens has been reported to occur in NSCLCs (Beattie et al, 1985; Kaiser et al, 1996) and there may be cooperative interaction between the hormones and active mutations of EGFR during the development of lung cancer.

Recently, active mutations of EGFR have been identified in such cases (Paez et al, 2004; Pao et al, 2004) and may be linked with the sensitivity to gefitinib (Lynch et al, 2004; Paez et al, 2004; Pao et al, 2004).

Originally developed for the treatment of BCR/ABL positive chronic myeloid leukemia, gleevec is also effective for several constitutively active mutations of c-kit found in numerous t(8 21) positive patients [ 34].

EGF treatment of tumour cell lines induces HIF-1 α expression and constitutively active mutations of EGFR potentiate hypoxic induction of other targets of HIF-1 α such as VEGF (Clarke et al, 2001; Semenza, 2002).

Clearly, further studies (e.g., via molecular modeling) will be required to better understand the effect of the active mutations on the stereo- and enantioselectivity of these enzymes, including the apparent context-dependent effect of the T268A mutation in either enhancing or decreasing such selectivity (Table 2).

If TTR-11 functions in axon regeneration upstream of CED-10, we would expect that a constitutively active mutation of the ced-10 gene would suppress the ttr-11 phenotype.

DNA fragments carrying the G12V or equivalent (constitutively active) mutation of human and Dictyostelium Rho GTPases were generated from wild-type cDNA by polymerase chain reaction-based site-directed mutagenesis.

In HEL cells with active mutation of JAK2, phosphorylation of STAT3 and STAT5 was inhibited at early time points when JAK2 phosphorylation was not inhibited, although phosphorylated JAK2 was reduced 24 h after OPB-31121 administration, probably due to cell death-related degradation of JAK2.

These findings suggest that the EGFR-RAC1 axis is more critical in NSCLC cells with EGFR active mutations through the induction of cell cycle arrest and cell death.