Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer.

By S. Baylin, Manel Esteller, M. R. Rountree, K. Bachman, Kornel E. Schuebel, J. Herman. Human Molecular Genetics, 2001

970 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8a9b3d8dd16a02bd672ea5e99b36ffccd333e005

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Citations in the corpus

Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “Interestingly, genomic analysis of gliomas has shown that TERT promoter mutations occur in 70–80 % of primary GBMs and in more than 70 % of oligodendrogliomas, but are less frequent in IDH1/2 mutant diffuse and anaplastic astrocytomas as well as IDH1/2 mutant (secondary) GBMs that instead carry freq”
CpG island hypermethylation and tumor suppressor genes: a booming present, a brighter future (2002, background): “Demethylating agents such as 5-azacytidine or 5-aza-2-deoxicytidine (Decitabine) (Baylin et al., 2001) inhibits the DNMTs and cause global hypomethylation , and we can not reactivate solely the particular gene we would wish to.”
Social Exchange and Micro Social Order (2008, background): “Mounting evidence shows that the silencing of tumor suppressor genes by DNA methylation is a typical process in cancer development (Baylin et al. 2001).”
5-Azacytidine and 5-aza-2′-deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy (2002, background): “…loss of methylation induced by ZCyd or ZdCyd treatment can lead to reactivation of the same genes whose inactivation was selected for during development of a specific tumor and has stimulated interest in revisiting the use of ZdCyd and other Cyd analogs in anticancer therapy (Baylin et al., 2001).”
Cancer as an epigenetic disease: DNA methylation and chromatin alterations in human tumours (2002, background): “In cultured cancer cell lines, we have been able for years to re-express genes silenced by methylation using demethylating agents such as 5azacytidine or 5-aza-2-deoxycytidine [5,51].”
Characterization of DOK1, a candidate tumor suppressor gene, in epithelial ovarian cancer (2011, background): “Promoter hypermethylation often leads to inactivation of different TSGs and is associated with many important pathways involved with cancer, such as DNA repair, cell cycle regulation, apoptosis, carcinogen metabolism, hormonal response, and cell adherence (Baylin et al., 2001; Momparler, 2003).”
The Integration of Genetic Propensities into Social-Control Models of Delinquency and Violence among Male Youths (2008, background): “Mounting evidence shows that the silencing of tumor suppressor genes by DNA methylation is a typical process in cancer development (Baylin et al. 2001).”
Mapping and elucidating the function of modified bases in DNA (2017, background): “For example, atypical methylation patterns at specific CpG islands and in tumor suppressor genes is a hallmark of cancer.(100,101,102) In addition, certain genes are hypermethylated in a number of neurodegenerative disorders, including Alzheimer’s disease.”