Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer

By Hiromu Suzuki, D. N. Watkins, K. Jair, Kornel E. Schuebel, Sanford D. Markowitz, Wei Chen, T. P. Pretlow, Bin Yang, Y. Akiyama, M. Engeland and 6 more. Nature Genetics, 2004

1,111 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8fd6650b6ef2770845e9b3d2581196cf3d79551f

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Citations in the corpus

Tissue repair and stem cell renewal in carcinogenesis (2004, background): “The possibility of Wnt ligand dependent pathway activation in cancer is suggested by a recent study demonstrating that epi-genetic silencing of SFRPs (secreted frizzled-related proteins), which encode an extracellular ligand-binding pathway antagonist, may have a critical role in the early establi”
Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease (2008, background): “, 1998), possibly predisposing to pre-malignant changes (Suzuki et al., 2004).”
Epigenetics and Colorectal Cancer (2011, background): “The idea of epigenetic alterations being only passenger events in cancer has since been disproven over the past decade by innovative studies that have led to a richer understanding of the driver role of epigenetic alterations in the development of cancer”
Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast (2011, background): “Second, gene expression of the secreted frizzledrelated protein 1 (SFRP1), which sequesters both canonical and noncanonical Wnt ligands in the extracellular space (Suzuki et al., 2004), was downregulated in HTwist and undetectable in MSP relative to HMLE24+ cells (Figure 2H).”
Colorectal cancer and genetic alterations in the Wnt pathway (2006, background): “The best evidence that such changes have functional consequences comes from study of the secreted frizzled-related proteins (SFRPs) (Suzuki et al., 2004).”
Epigenetic Determinants of Cancer. (2016, background): “Persistence of both epigenetic and genetic alterations seems to complement one another in further driving progression of the disease (Suzuki et al. 2004).”
WNT and β-catenin signalling: diseases and therapies (2004, background): “Intriguingly, despite the observation that mutations in the β-catenin pathway generally activate the pathway downstream of WNT, and usually at the level of the destruction complex, recent evidence indicates that epigenetic inactivation of sFRP genes occurs early in colorectal cancer, and restoring s”
Notch signalling in solid tumours: a little bit of everything but not all the time (2011, background): “; the silencing of genes that express inhibitory WNT ligand”
Wnt signaling in the intestinal epithelium: from endoderm to cancer. (2005, background): “Taking into account the results from Bafico et al. (2004), it is more likely that silencing of SFRPs would only provide a growth advantage before mutations in APC and -catenin have occurred.”
Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “Plasticity of the resultant populations for self-renewing properties may still be present, but the EMT phenotypes involved might be of the more mixed EMT-epithelial types proposed recently in the range of breast cancer cell phenotypes (Tam and Weinberg, 2013).”