2023
DOI: 10.1053/j.gastro.2023.01.039
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TET1 and TDG Suppress Inflammatory Response in Intestinal Tumorigenesis: Implications for Colorectal Tumors With the CpG Island Methylator Phenotype

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Cited by 13 publications
(7 citation statements)
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“…Then, the specificity of APE1 was evaluated, as shown in Figure C. The DNA-repair enzymes, such as UDG, TDG, TE, and hAAG, were unable to activate the preprobe, there were minimal fluorescence changes even supplied with high concentrations of miR-21. The sensing specificity of E-DNA walker toward miR-21 was evaluated against miR-429, miR-155, miR-141, miR-31, and let-7a since these related miRNAs are often reported to be overexpressed intracellularly .…”
Section: Resultsmentioning
confidence: 99%
“…Then, the specificity of APE1 was evaluated, as shown in Figure C. The DNA-repair enzymes, such as UDG, TDG, TE, and hAAG, were unable to activate the preprobe, there were minimal fluorescence changes even supplied with high concentrations of miR-21. The sensing specificity of E-DNA walker toward miR-21 was evaluated against miR-429, miR-155, miR-141, miR-31, and let-7a since these related miRNAs are often reported to be overexpressed intracellularly .…”
Section: Resultsmentioning
confidence: 99%
“…Recent work by Tricarico et al demonstrated that inactivation of Tet1-Tdg induced hypermethylation in CpG islands using the Tet1 –/– Tdg N151/+ Apc Min/+ mutant mouse model. 69 TET family inactivation by the oncometabolite, D-2-hydroxyglutarate (D-2HG), resulting from IDH1/2 mutation, is a well-known cause of CIMP in glioma. 6 The absence of TET or IDH mutations in CRC CIMP 70 suggests that the gut microbiota may play a role in TET inactivation.…”
Section: Discussionmentioning
confidence: 99%
“…TET dioxygenases are crucial for maintaining DNA methylation levels, as they collaborate with TDG to initiate DNA demethylation. Inactivation of these enzymes leads to the hypermethylation of DNA, resulting in severe disturbances in gene expression and increased incidence of tumor development and embryonic lethality in mice [ 116 , 292 , 293 , 294 ]. As a result, alterations in TETs and TDG have the potential to serve as drivers of cancer, even though only aberrations and mutations in TET family genes have been found in tumors.…”
Section: Inflammation Epigenetics and Cancermentioning
confidence: 99%