Increased expression of Drosophila Tailless (TLX homologue) reverts intermediate progenitors to neural stem cells, inducing tumourigenesis via Asense repression and reflecting mutually exclusive TLX and ASCL1 expression in human glioblastoma.
Overexpression of BAG2—a novel mutant p53 binding protein—in tumors inhibits MDM2-mediated mutant p53 degradation, which leads to the accumulation of mutant p53 protein and promotes tumorigenesis.
The retromer complex serves as a bomb squad to retrieve and disarm the potentially harmful pool of Notch receptors in a timely manner and thereby safeguards against brain tumor formation.
A newly discovered feedback amplification loop between stem cells and their immediate daughter progenitor cells drives epithelial regeneration and tumor development.
Dual FAK/PYK2 kinase inhibition disrupts GSK3β phosphorylation and may present a new treatment for colorectal cancer in patients carrying APC mutations.
The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.
miR-31 drives proliferation of intestinal stem cells, and protects intestinal stem cells against apoptosis both during homeostasis and regeneration in response to ionizing radiation injury, and promotes intestinal tumorigenesis through regulation of multiple signaling pathways.
The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.
Genetic analyses reveal how CDX2 and BRAF defects seen in serrated colorectal cancer (CRCs), a poor prognosis CRC subset, cooperate in tumorigenesis in humans and in a mouse cancer model.
