Heritable somatic methylation and inactivation of MSH2 in families with Lynch syndrome due to deletion of the 3′ exons of TACSTD1
By M. Ligtenberg, R. Kuiper, Tsun Leung Chan, M. Goossens, K. Hebeda, M. Voorendt, Tracy Y H Lee, D. Bodmer, E. Hoenselaar, S. Hendriks-Cornelissen and 8 more. Nature Genetics, 2009
831 citations recorded by the source corpus.
Subfields: Cancer Research, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/3e3216918fb747d8a63661fa2ae3d09b92431659
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In Pathology and Forensic Medicine
Citations in the corpus
- Microsatellite instability in colorectal cancer—the stable evidence (2010, background): “A heritable somatic methylation of MSH2 has also been reported that is caused by a deletion of the last exon of EPCAM , which is adjacent to MSH2”
- Gene regulation by the act of long non-coding RNA transcription (2013, background): “In a second example, a subset of Lynch syndrome patients display DNA methylation and inactivation of the mismatch repair MSH2 gene that correlates with aberrant transcription from the flanking EPCAM gene that carries a 3' deletion [72].”
- Microsatellite Instability as a Biomarker for PD-1 Blockade (2016, background): “Patients with a defect in any one of these components, or, in a gene upstream of MSH2 that encodes EPCAM that results in loss of MSH2 expression when mutated (24), develop frameshift mutations leading to truncated protein products.”
- Understanding transgenerational epigenetic inheritance via the gametes in mammals (2012, background): “However, in the case of MSH2 , the epigenetic changes turned out to be associated with mutations in cis”