Dysfunctional transforming growth factor-β signaling with constitutively active Notch signaling in Barrett's esophageal adenocarcinoma

Cancer

Volumn 118, Issue 7, 2012, Pages 1957-

  Masuda, Shigeo ^a  

^a JICHI MEDICAL UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

GAMMA SECRETASE INHIBITOR; NOTCH RECEPTOR; PROTEIN P15; PROTEIN P16; PROTEIN P21; SMAD4 PROTEIN; TRANSFORMING GROWTH FACTOR BETA;

APOPTOSIS; BARRETT ESOPHAGUS; CELL CYCLE ARREST; DRUG TARGETING; ESOPHAGEAL ADENOCARCINOMA; GENE SILENCING; HETEROZYGOSITY LOSS; LETTER; PRIORITY JOURNAL; PROTEIN DOMAIN; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION;

EID: 84858699558     PISSN: 0008543X     EISSN: 10970142     Source Type: Journal    
DOI: 10.1002/cncr.26444     Document Type: Letter

References (5)

1. Mendelson J, Song S, Li Y, et al. Dysfunctional transforming growth factor-β signaling with constitutively active Notch signaling in Barrett's esophageal adenocarcinoma. Cancer. 2011;117:3691-3702.
2. Rao P, Kadesch T. The intracellular form of notch blocks transforming growth factor β-mediated growth arrest in Mv1Lu epithelial cells. Mol Cell Biol. 2003;23:6694-6701. (Pubitemid 37075778)
3. Carlson ME, Hsu M, Conboy IM. Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells. Nature. 2008;454:528-532.
4. Masuda S, Kumano K, Shimizu K, et al. Notch1 oncoprotein antagonizes TGF-β/Smad-mediated cell growth suppression via sequestration of coactivator p300. Cancer Sci. 2005;96:274-282. (Pubitemid 40895075)
5. Hage M, Siersema PD, Vissers KJ, et al. Genomic analysis of Barrett's esophagus after ablative therapy: persistence of genetic alterations at tumor suppressor loci. Int J Cancer. 2006;118:155-160. (Pubitemid 41681592)