160f15cbc4454785a997705640254b802dd995d451124cf189360f54b9a55c2879df37ffe1bc473fa113b499c00c66a38edac01dd53f4e6d8834bd43aa26d4899143a432075841c19ba3a12f08bd16af95bc6e59c17842c990ff6bc66dd8a6f49ddfb00f6ab6488289f4512d1ec61dd09ed450cd968443389fdc99d2eb43c755a7c0ec7896bb4cb5a95d5bb46d0a3499ae737137d4b0466296e0bdfa84211409babd87e7af694bc8ab26e7220cdc66bac1e085714bfd49f3983c391d060e7047f813a25531184ee0a181fd14d4157749
agent
p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epitheliumIntestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like propertiesThe Lgr5 intestinal stem cell signature: robust expression of proposed quiescent '+4' cell markersFocal adhesion kinase is required for intestinal regeneration and tumorigenesis downstream of Wnt/c-Myc signalingActomyosin-mediated cellular tension drives increased tissue stiffness and beta-catenin activation to induce epidermal hyperplasia and tumor growthSpindle orientation bias in gut epithelial stem cell compartments is lost in precancerous tissueRapid loss of intestinal crypts upon conditional deletion of the Wnt/Tcf-4 target gene c-Myc.Cyclin D1 is not an immediate target of beta-catenin following Apc loss in the intestine.Myc deletion rescues Apc deficiency in the small intestineCrypt stem cells as the cells-of-origin of intestinal cancer.Loss of Apc in vivo immediately perturbs Wnt signaling, differentiation, and migrationCyclin D2-cyclin-dependent kinase 4/6 is required for efficient proliferation and tumorigenesis following Apc lossInactivation of Apc perturbs mammary development, but only directly results in acanthoma in the context of Tcf-1 deficiency
author
type
label
O.J. Sansom