Sentence examples for mutated in early from inspiring English sources

These genes were selected because of their presence in the overlap between the human datasets and/or their interesting functions; ANXA1 (Annexin 1) is involved in cell proliferation and cytoskeleton regulation; ARMET (Arginine-rich, mutated in early stage tumors) is mutated in cancer; CYR61 (Cysteine-rich, angiogenic inducer, 61) promotes proliferation and angiogenesis.

In previous, we have suggested that oncogenic K-Ras, which is mutated in early adenoma stage, can suppress the p53 function.

High frequent G>T transversions in APC and KRAS2 (mutated in early tumour development) but not in P53 and SMAD4 (implicated in tumour progression) might indicate a predominant MUTYH effect in early carcinogenesis.

The role of mitophagy in Parkinson's disease has been an area of interest following observations that the protein kinase PINK1 and E3 ubiquitin ligase Parkin, both mutated in early onset forms of Parkinson's disease, act to induce mitophagy on mitochondrial membrane depolarization [ 7].

Interestingly, among the most highly up-regulated genes in Matn3 V194D chondrocytes were Armet (arginine-rich, mutated in early stage tumours) and Creld2 (cysteine-rich with EGF-like domains 2); two genes that have only recently been implicated in ER stress and UPR following a variety of physiological and pathological triggers (25– 25).

We examined the mutation status of neighboring genes around these risk loci (Table S2) in the Cancer Genome Project Data of Wellcome Trust Sanger Institute (http://www.sanger.ac.uk/genetics/CGP/cosmic/). CSMD3 in 8q23.3 is a large gene encoding a protein with CUB and sushi multiple domains and is associated with somatic mutations in lung cancer (7 mutated in 11 unique samples).

In colorectal cancer specifically, the pik3ca gene is mutated in 20 25% of CRCs while pik3ca mutations occurring in the hotspots located in exon 9 and exon 20 are oncogenic in CRC cell models [51].

Likewise, TP53 is mutated in 30 60% of IBCs, with most mutations located in exons 5 8, the mutational hot-spot of TP53 [ 17, 25- 27].

BRAF, a serine-threonine kinase in the RAS/RAF/MAPK signalling cascade, is mutated in 60 70% of melanomas and, to date, represents the most common mutation in this disease (Davies et al, 2002; Curtin et al, 2005).

The K-Ras oncogene, mutated in 46 50% of CRC tumors, serves as one molecular marker by which stool samples may be evaluated for early detection of adenocarcinomas.

BRAF encodes a serine/threonine-protein kinase and is the most commonly mutated gene in melanoma (observed to be mutated in 40 70% of melanoma) [7].