Prof Jesper T Troelsen: CDX2, intestinal master gene regulator and a new biomarker for colon cancer relapse.
Location:Level 2 Conference Room, The Westmead Institute for Medical Research, Hawkesbury Road, Westmead
Homeodomain transcription factor CDX2 is a central player in the differentiation and maintenance of the intestinal epithelium. Reduced expression of CDX2 associates with loss of intestinal cellular identity. CDX2 is furthermore promising biomarker identifying stage 2 and 3 colorectal cancer patients with increased risk of relapse and the effect of adjuvant chemotherapy. High levels of CDX2 expression correlate with improved prognosis and patients with low levels of CDX2 have the best response to adjuvant chemotherapy. The presentation will discuss the role of CDX2 as a driver of differentiation process in the intestinal epithelium and its dual role as a tumor suppressor gene and lineage-survival oncogene.
Jesper T. Troelsen, Professor in Medical Biology. Head of Biology, Dept of Science and Environment, Roskilde University, Denmark.
Research interests: Intestinal gene regulation, nucleotide variation in gene regulatory sequences, molecular mechanisms in inflammatory bowel diseases and colorectal cancer.
Recent selected publications:
Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies. Boyd et al. 2018 Nature Commun., in press.
Precise integration of inducible transcriptional elements (PrIITE) enables absolute control of gene expression. Pinto et al. Nucleic Acids Res. 2017 Jul 27;45(13):e123
Regulation of Laminin γ2 Expression by CDX2 in Colonic Epithelial Cells Is Impaired During Active Inflammation. Coskun et al. J Cell Biochem. 2017 Feb;118(2):298-307.
Escape from epigenetic silencing of lactase expression is triggered by a single-nucleotide change. Swallow DM, Troelsen JT. Nat Struct Mol Biol. 2016 Jun 7;23(6):505-7.
CDX2 downregulation is associated with poor differentiation and MMR deficiency in colon cancer. Olsen et al., Exp Mol Pathol. 2016 Feb;100(1):59-66