Wnt signaling and cancer.

By Paul Polakis. Genes & Development, 2000

3,367 citations recorded by the source corpus.

The regulation of cell growth and survival can be subverted by a variety of genetic defects that alter transcriptional programs normally responsible for controlling cell number. High throughput analysis of these gene expression patterns should ultimately lead to the identification of minimal expression profiles that will serve as common denominators in assigning a cancer to a given category. In the course of defining the common denominators, though, we should not be too surprised to find that cancers within a single category may nevertheless exhibit seemingly disparate genetic defects. The wnt pathway has already provided an outstanding example of this. We now know of three regulatory genes in this pathway that are mutated in primary human cancers and several others that promote experimental cancers in rodents (Fig. 1). In all of these cases the common denominator is the activation of gene transcription by -catenin. The resulting gene expression profile should provide us with a signature common to those cancers carrying defects in the wnt pathway. In this review, the wnt pathway will be covered from the perspective of cancer, with emphasis placed on molecular defects known to promote neoplastic transformation in humans and in animal models.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/95cc5189fde120c50990f7dd9cb11bacfb60148e

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Citations in the corpus

Mouse models of human breast cancer: evolution or convolution? (2003, positive): “pro-oncogenic roles (Wnt, β-catenin) or tumour-suppressor activities (APC, TCF-1, axin) (Polakis 2000).”
The ins and outs of APC and β‐catenin nuclear transport (2002, background): “Wnt activation inhibits the phosphorylation of β-catenin by glycogen synthase kinase 3 (GSK-3), thus also preventing its ubiquitylation and subsequent proteasomal degradation (Morin, 1999; Polakis, 2000).”
Negative Feedback Loop of Wnt Signaling through Upregulation of Conductin/Axin2 in Colorectal and Liver Tumors (2002, background): “Colon carcinomas and liver tumors show active Wnt signaling because of mutation of APC or -catenin (25, 33, 44).”
Function and biological roles of the Dickkopf family of Wnt modulators (2006, background): “The Wnt pathway plays an important role in cancer (Polakis, 2000; Moon et al., 2004) and thus it is not surprising that Wnt modulators, including Dkks, are also involved.”
TSC2 integrates Wnt and energy signals via a coordinated phosphorylation by AMPK and GSK3 to regulate cell growth. (2006, background): “*Contact: kunliang@umich.edu DOI 10.1016/j.cell.2006.06.055”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, neutral): “Detailed information about Wnt signaling and its functions can be found in Barker and Clevers (2000), Huelsken and Behrens (2002), Lustig and Behrens (2003), Polakis (2000), Willert and Nusse (1998) (see also Fig.”
BMP‐2 Controls Alkaline Phosphatase Expression and Osteoblast Mineralization by a Wnt Autocrine Loop (2003, background): “Dysfunction of the Wnt/ -catenin pathway has been implicated in several diseases such as cancer and Alzheimer’s disease.((5,6)) More recently, it has been shown that loss of function of the Wnt coreceptor, LRP5, in both humans and mice leads to decreased bone formation postnatally, and a point mutat”
The cadherin-catenin adhesion system in signaling and cancer. (2002, background): “, adenomatous polyposis coli [APC] or Axin) (Figure 1), as well as N-terminal mutations in β-catenin itself that compromise the protein’s degradation, have been found in a variety of human cancers (18).”