The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
The Wnt connection to tumorigenesis
Open accessAbstract
Wnt signaling has been identified as one of the key signaling pathways in cancer, regulating cell growth, motility and differentiation. Because of its widespread activation in diverse human tumor diseases, the Wnt pathway has gained considerable and growing interest in tumor research over recent years. Evidence that altered Wnt signaling is important for human tumor development came from three major findings: (i) the tumor suppressor adenomatous polyposis coli (APC) binds to the Wnt pathway component beta-catenin and is involved in its degradation, (ii) mutations of APC in colon tumors lead to stabilization of the beta-catenin protein and (iii) tumor-associated mutations of beta-catenin in colorectal cancer as well as in other tumor types lead to its stabilisation, qualifying beta-catenin as a proto-oncogene. Here we will describe the biochemical interactions which shape the Wnt pathway and focus on its role in tumorigenesis.
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Cites
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Functional interaction of β-catenin with the transcription factor LEF-1
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Self-citationKremen proteins are Dickkopf receptors that regulate Wnt/β-catenin signalling
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Linking β-Catenin to Androgen-signaling Pathway
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Cited by
Wnt/β-Catenin Is Essential for Intestinal Homeostasis and Maintenance of Intestinal Stem Cells
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Dysregulation of growth factor signaling in human hepatocellular carcinoma
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From signatures to models: understanding cancer using microarrays
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Metadata
- Authors
- Behrens, J., & Lustig, B.
- Venue
- The International Journal of Developmental Biology
- Publisher
- EHU Press
- Published
- 2004
- Volume
- 48
- Issue
- 5-6
- Pages
- 477-487
- ISSN
- 0214-6282 (ISSN-L)
- OpenAlex
- W1990671646
- Cited by
- 194
- References
- 8
- FWCI
- 5.47
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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