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Journal ArticleDOI

WNT signalling pathways as therapeutic targets in cancer

Jamie N. Anastas, +1 more
- 01 Jan 2013 - 
- Vol. 13, Iss: 1, pp 11-26
TLDR
This work has shown that WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumour initiation, tumour growth, cell senescence, cell death, differentiation and metastasis, and improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can alter WNT signalling in preclinical models.
Abstract
Since the initial discovery of the oncogenic activity of WNT1 in mouse mammary glands, our appreciation for the complex roles for WNT signalling pathways in cancer has increased dramatically. WNTs and their downstream effectors regulate various processes that are important for cancer progression, including tumour initiation, tumour growth, cell senescence, cell death, differentiation and metastasis. Although WNT signalling pathways have been difficult to target, improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can alter WNT signalling in preclinical models, thus setting the stage for clinical trials in humans.

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Journal ArticleDOI

Glycogen synthase kinase-3 (GSK3): Regulation, actions, and diseases

TL;DR: Glycogen synthase kinase-3 (GSK3) must be particularly adaptable for incorporating new substrates into its repertoire, and the distinct properties of GSK3 that may contribute to its capacity to fulfill its roles in multiple signaling pathways are discussed.
Journal ArticleDOI

Exosomes in Cancer Development, Metastasis and Drug Resistance: A Comprehensive Review

TL;DR: It is proposed that the successful combination of cancer treatments to tackle exosome-mediated drug resistance requires an interdisciplinary understanding of these cellular exclusion mechanisms, and how secreted biomolecules are involved in cellular cross-talk within the tumor microenvironment.
Journal ArticleDOI

Genetic Landscape and Biomarkers of Hepatocellular Carcinoma.

TL;DR: Data from genomic profiling enabled a proposal of HCC in 2 major molecular clusters (proliferation and non Proliferation), with differential enrichment in prognostic signatures, pathway activation and tumor phenotype, which helps define some of the core deregulated pathways in HCC.
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The multifaceted roles of fatty acid synthesis in cancer

TL;DR: This Review explores how different aspects of FA synthesis promote tumorigenesis and tumour progression and strategies to target this pathway have not yet translated into clinical practice.
Journal ArticleDOI

Can we safely target the WNT pathway

TL;DR: The problems and potential solutions to the vexing situation of aberrant regulation of the WNT pathway are examined and a attempt is made to bring them into perspective.
References
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Journal ArticleDOI

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Donna M. Muzny, +320 more
- 19 Jul 2012 - 
TL;DR: Integrative analyses suggest new markers for aggressive colorectal carcinoma and an important role for MYC-directed transcriptional activation and repression.
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Lessons from Hereditary Colorectal Cancer

TL;DR: The authors are grateful to the members of their laboratories for their contributions to the reviewed studies and to F. Giardiello and S. Hamilton for photographs of colorectal lesions.
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Activation of β-Catenin-Tcf Signaling in Colon Cancer by Mutations in β-Catenin or APC

TL;DR: Results indicate that regulation of β-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or β- catenin.
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Complex networks orchestrate epithelial–mesenchymal transitions

TL;DR: Understanding how mesenchymal cells arise from an epithelial default status will also have a strong impact in unravelling the mechanisms that control fibrosis and cancer progression.
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Constitutive Transcriptional Activation by a β-Catenin-Tcf Complex in APC−/− Colon Carcinoma

TL;DR: Constitutive transcription of Tcf target genes, caused by loss of APC function, may be a crucial event in the early transformation of colonic epithelium.
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