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Open AccessJournal ArticleDOI

The beta-catenin/TCF-4 complex imposes a crypt progenitor phenotype on colorectal cancer cells.

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TLDR
The β-catenin/TCF-4 complex constitutes the master switch that controls proliferation versus differentiation in healthy and malignant intestinal epithelial cells.
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This article is published in Cell.The article was published on 2002-10-18 and is currently open access. It has received 1972 citations till now. The article focuses on the topics: Cellular differentiation & Wnt signaling pathway.

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Cancer Genome Landscapes

TL;DR: This work has revealed the genomic landscapes of common forms of human cancer, which consists of a small number of “mountains” (genes altered in a high percentage of tumors) and a much larger number of "hills" (Genes altered infrequently).
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Wnt/beta-catenin signaling in development and disease.

TL;DR: A remarkable interdisciplinary effort has unraveled the WNT (Wingless and INT-1) signal transduction cascade over the last two decades, finding that Germline mutations in the Wnt pathway cause several hereditary diseases, and somatic mutations are associated with cancer of the intestine and a variety of other tissues.
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Identification of stem cells in small intestine and colon by marker gene Lgr5

TL;DR: The expression pattern of Lgr5 suggests that it marks stem cells in multiple adult tissues and cancers, suggesting that it represents the stem cell of the small intestine and colon.
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Wnt signalling in stem cells and cancer

TL;DR: Insights gained from understanding how the Wnt pathway is integrally involved in both stem cell and cancer cell maintenance and growth in the intestinal, epidermal and haematopoietic systems may serve as a paradigm for understanding the dual nature of self-renewal signals.
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Long-term expansion of epithelial organoids from human colon, adenoma, adenocarcinoma, and Barrett's epithelium.

TL;DR: A technology that can be used to study infected, inflammatory, or neoplastic tissues from the human gastrointestinal tract is developed that might have applications in regenerative biology through ex vivo expansion of the intestinal epithelia.
References
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Journal ArticleDOI

CDK inhibitors: positive and negative regulators of G1-phase progression

TL;DR: This work challenges previous assumptions about how the G1/S transition of the mammalian cell cycle is governed, helps explain some enigmatic features of cell cycle control that also involve the functions of the retinoblastoma protein (Rb) and the INK4 proteins, and changes the thinking about how either p16 loss or overexpression of cyclin D-dependent kinases contribute to cancer.
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The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases

TL;DR: In this article, an improved two-hybrid system was employed to isolate human genes encoding Cdk-interacting proteins (Cips) and found that CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2.
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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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Identification of c-MYC as a Target of the APC Pathway

TL;DR: The c-MYC oncogene is identified as a target gene in this signaling pathway and shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c- MYC promoter.
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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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