A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts - Test2 - elhamkhani - TriplyDB

A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts

A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts

http://www.wikidata.org/entity/Q28709909

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Wnt Signaling in Cancer Stem Cell Biology Understanding phenotypic variation in rodent models with germline Apc mutations Heterogeneity of the level of activity of lgr5+ intestinal stem cells Brg1 loss attenuates aberrant wnt-signalling and prevents wnt-dependent tumourigenesis in the murine small intestine Wnt Drug Discovery: Weaving Through the Screens, Patents and Clinical Trials In Vitro Polarization of Colonoids to Create an Intestinal Stem Cell Compartment Investigation of the atypical FBXW7 mutation spectrum in human tumours by conditional expression of a heterozygous propellor tip missense allele in the mouse intestines Canonical Wnt signals combined with suppressed TGFβ/BMP pathways promote renewal of the native human colonic epithelium.Prognostic Significance of β-Catenin, E-Cadherin, and SOX9 in Colorectal Cancer: Results from a Large Population-Representative Series.Colorectal cancer stem cells and their implications for novel anticancer therapy.Host-microbiota interaction and intestinal stem cells in chronic inflammation and colorectal cancer.Cited1 deficiency suppresses intestinal tumorigenesis.Cell organisation in the colonic crypt: a theoretical comparison of the pedigree and niche concepts.Distribution of LGR5+ cells and associated implications during the early stage of gastric tumorigenesis.Integrated β-catenin, BMP, PTEN, and Notch signalling patterns the nephron.Wnt activity and basal niche position sensitize intestinal stem and progenitor cells to DNA damage.E-cadherin can limit the transforming properties of activating β-catenin mutations.Apc Restoration Promotes Cellular Differentiation and Reestablishes Crypt Homeostasis in Colorectal Cancer.A hypermorphic epithelial β-catenin mutation facilitates intestinal tumorigenesis in mice in response to compounding WNT-pathway mutations.Data resources for the identification and interpretation of actionable mutations by clinicians.Serrated polyposis associated with a family history of colorectal cancer and/or polyps: The preferential location of polyps in the colon and rectum defines two molecular entities Different APC genotypes in proximal and distal sporadic colorectal cancers suggest distinct WNT/β-catenin signalling thresholds for tumourigenesis.Major signaling pathways in intestinal stem cells.Location-specific effect of microbiota and MyD88-dependent signaling on Wnt/β-catenin pathway and intestinal stem cells.Characterization of LGR5 stem cells in colorectal adenomas and carcinomas.Anti-inflammatory activity of Wnt signaling in enteric nervous system: in vitro preliminary evidences in rat primary cultures Cancer: leaping the E-cadherin hurdle.Brg1 is required for stem cell maintenance in the murine intestinal epithelium in a tissue-specific manner.Wnt disruption in colorectal polyps - the traditional serrated adenoma enters the fray.Chir99021 and Valproic acid reduce the proliferative advantage of Apc mutant cells.Wnt ligands influence tumour initiation by controlling the number of intestinal stem cells.Distribution of intestinal stem cell markers in colorectal precancerous lesions.Wnt Signalling in Gastrointestinal Epithelial Stem Cells.

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A basal gradient of Wnt and stem-cell number influences regional tumour distribution in human and mouse intestinal tracts

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2013年の論文

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Ian P M Tomlinson

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P2860

Lgr5 homologues associate with Wnt receptors and mediate R-spondin signalling

Intestinal polyposis in mice with a dominant stable mutation of the beta-catenin gene

Identification of stem cells in small intestine and colon by marker gene Lgr5

Organizing cell renewal in the intestine: stem cells, signals and combinatorial control

APC mutations occur early during colorectal tumorigenesis

Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migration

Wnt activity defines colon cancer stem cells and is regulated by the microenvironment

Lithium inhibits glycogen synthase kinase-3 activity and mimics wingless signalling in intact cells

Sustained in vitro intestinal epithelial culture within a Wnt-dependent stem cell niche.

Location in the large bowel influences the APC mutations observed in FAP adenomas.

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