A genomic screen for genes upregulated by demethylation and histone deacetylase inhibition in human colorectal cancer

By Hiromu Suzuki, E. Gabrielson, Wei Chen, R. Anbazhagan, M. Engeland, M. Weijenberg, J. Herman, S. Baylin. Nature Genetics, 2002

888 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/41a15d5fd03452c4660fb3f0da5806f3e19521e3

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Citations in the corpus

Cancer epigenomics: DNA methylomes and histone-modification maps (2007, methodology): “This method involves comparing mRNA levels from cancer cell lines before and after treatment with a demethylating drug”
Secreted antagonists of the Wnt signalling pathway (2003, background): “It is not known whether the structural similarity between colipases and Dkks implies a common function such as lipid interaction.”
Wnt signaling in cancer. (2012, background): “Indeed, genome-wide analysis of promotor DNA methylation in human medulloblastoma, colon, and pancreatic cancers showed that Wnt pathway inhibitors are common targets of this mechanism of gene repression (Kongkham et al. 2010; Vincent et al. 2011; Suzuki et al. 2002).”
Epigenetic gene silencing in cancer: the DNA hypermethylome. (2007, background): “Chromatin immunoprecipitation using antibodies against MBDs associated with microarray hybridization (ChIP-on-CHIP) (33), DNA immunoprecipitated with an antibody against 5-methylcytosine hybridized to genomic microarray platforms (methyl-DIP) (65,75), and the comparison of mRNA levels from cancer ce”
Beyond Wnt inhibition: new functions of secreted Frizzled-related proteins in development and disease (2008, background): “These sequences have been reported to be hypermethylated in many types of carcinoma, particularly colorectal, gastric mammary and renal cell (Caldwell et al., 2004; Lee, A. et al., 2004; Stoehr et al., 2004; Suzuki et al., 2002; Takada et al., 2004; Zhou et al., 1998), possibly predisposing to pre-m”
Epigenetic Determinants of Cancer. (2016, background): “In terms of the older drugs, the approach has been to exploit preclinical data showing that blocking HDAC activity subsequent to inhibiting DNA methylation can additively lead to the reexpression of DNA hypermethylated genes (Cameron et al. 1999; Suzuki et al. 2002; Cai et al. 2014).”
DNA methylation and gene silencing in cancer (2005, methodology): “Initial treatment with azacitidine or decitabine, followed by HDAC inhibitors, can produce additive or synergistic effects for re-expression of transcriptionally silenced genes”
Specific activation of microRNA-127 with downregulation of the proto-oncogene BCL6 by chromatin-modifying drugs in human cancer cells. (2006, background): “…effect of DNA demethylation and HDAC inhibition was investigated in greater detail by Cameron et al. and Suzuki et al. (Cameron et al., 1999; Suzuki et al., 2002), who showed that silenced genes with unmethylated promoters can often be activated by HDAC inhibitors, whereas these agents are…”
Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer (2004, background): “We previously identified frequent promoter hypermethylation and gene silencing of the genes encoding secreted frizzled-related proteins (SFRPs) in colorectal cance”