Linking colorectal cancer to Wnt signaling.

By M. Bienz, Hans Clevers. Cell, 2000

1,597 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/0125da95c9397c0e1cce23c8c290bc892241be68

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Hans Clevers
2. R. Nusse
3. Nick Barker
4. A. Gregorieff
5. E. Batlle
6. W. Birchmeier
7. E. Dejana
8. H. Begthel

In Molecular Biology

1. Hans Clevers
2. R. Nusse
3. Xi He
4. Nick Barker
5. S. Morrison
6. W. Birchmeier
7. K. Tamai
8. M. Clarke

In Pathology and Forensic Medicine

1. R. Nusse
2. E. Dejana
3. W. Birchmeier
4. A. Gregorieff
5. Hans Clevers
6. Angeliki Voulgari
7. A. Pintzas

Citations in the corpus

• Wnt/β-Catenin/Tcf Signaling Induces the Transcription of Axin2, a Negative Regulator of the Signaling Pathway (2002, background): “The proliferation of these stem cells is known to be regulated by the Wnt/ catenin/Tcf4 pathway, and mutations in APC or -catenin (2, 31), as well as Axin2 itself (25), predispose the cells to oncogenic transformation leading to colon cancer.”
• Prominin1 marks intestinal stem cells that are susceptible to neoplastic transformation (2008, neutral): “Mutations that activate aberrant WNT signaling, including mutations in Beta-Catenin ( CTNNB1 ), have been identified in over 80% of human colonic cancers5,24 and this tumor type was reported recently to contain Prom1 + CSC3,4.”
• LDL receptor-related proteins 5 and 6 in Wnt/β-catenin signaling: Arrows point the way (2004, background): “It is widely accepted that in this Wnt pathway β-catenin associates with, and acts as an obligatory nuclear co-activator for, the TCF/LEF (T cell factor/Lymphoid enhancer factor) family of transcription factors (Bienz and Clevers, 2003; Cong et al., 2003; Tolwinski and Wieschaus, 2004).”
• Applying the principles of stem-cell biology to cancer (2003, background): “So, tumorigenesis in the intestinal epithelium seems to be caused, at least initially, by the hyper-self-renewal of intestinal-crypt stem cells, followed by the accumulation of additional mutations that confer malignancy and allow cancer progressio”
• Axin-mediated CKI phosphorylation of beta-catenin at Ser 45: a molecular switch for the Wnt pathway. (2002, background): “A major target of the Wnt pathway is cytoplasmic -catenin, which, when stabilized in response to Wnt signaling, enters the nucleus and serves as a coactivator of TCF/LEF-induced transcription (Willert and Nusse 1998; Bienz and Clevers 2000; Polakis 2000).”
• β-catenin is critical for dendritic morphogenesis (2003, neutral): “β-catenin is also an integral component of the Wnt signal transduction pathway; in response to Wnt signaling, β-catenin enters the nucleus and activates transcription of Wnt target gene”
• Cdks, cyclins and CKIs: roles beyond cell cycle regulation (2013, background): “The most common manifestation of de-regulated Wnt signaling is colorectal cancer, in which loss-of-function mutations in the APC tumor suppressor gene are prevalent, leading to hyperactivation of βcatenin (Bienz and Clevers, 2000).”