Pregnancy, Primary Aldosteronism, and Adrenal CTNNB1 Mutations.
Cambridge, United Kingdom. In N Engl J Med, Nov 2015
Their aldosterone-producing adenomas harbored activating mutations of CTNNB1, encoding β-catenin in the Wnt cell-differentiation pathway, and expressed LHCGR and GNRHR, encoding gonadal receptors, at levels that were more than 100 times as high as the levels in other aldosterone-producing adenomas.
Targeting the Wnt signaling pathway in colorectal cancer.
Kōbe, Japan. In Expert Opin Ther Targets, Nov 2015
The great majority of colorectal cancers have mutations in one of two genes involved in the Wnt signaling pathway: the adenomatous polyposis coli (APC) and β-catenin (CTNNB1) genes.
TERT promoter mutations in primary liver tumors.
Paris, France. In Clin Res Hepatol Gastroenterol, Oct 2015
UNASSIGNED: Next-generation sequencing has drawn the genetic landscape of hepatocellular carcinoma and several signaling pathways are altered at the DNA level in tumors: Wnt/β-catenin, cell cycle regulator, epigenetic modifier, histone methyltransferase, oxidative stress, ras/raf/map kinase and akt/mtor pathways.
Gene mutations in gastric cancer: a review of recent next-generation sequencing studies.
Shanghai, China. In Tumour Biol, Sep 2015
Mutations in genes relating to genome integrity (TP53, BRCA2), chromatin remodeling (ARID1A), cell adhesion (CDH1, FAT4, CTNNA1), cytoskeleton and cell motility (RHOA), Wnt pathway (CTNNB1, APC, RNF43), and RTK pathway (RTKs, RAS family, MAPK pathway, PIK pathway) are discussed.
Analysis of differentially expressed genes based on microarray data of glioma.
Nanjing, China. In Int J Clin Exp Med, 2014
In addition, the transcription factor analysis showed these DEGs were regulated by the binding sites of transcription factors GLI2, SP1, SMAD7, SMAD3, RELA, STAT5B, CTNNB1, STAT5A, TFAP2A and SP3.
Integrated genomic characterization of adrenocortical carcinoma.
Paris, France. In Nat Genet, 2014
We performed exome sequencing and SNP array analysis of 45 ACCs and identified recurrent alterations in known driver genes (CTNNB1, TP53, CDKN2A, RB1 and MEN1) and in genes not previously reported in ACC (ZNRF3, DAXX, TERT and MED12), which we validated in an independent cohort of 77 ACCs.