by Aston University. Department of Pharmaceutical Sciences. in Birmingham .
Written in English
Thesis (PhD) - Aston University, 1990 awarded in 1991.
Background: Genome-wide association studies (GWASs) have identified dozens of loci associated with gout, but for most cases, the risk genes and the underlying molecular mechanisms contributing to these associations are unknown. This study sought to understand the molecular mechanism of a common genetic variant, rs, in the development of gout, both in vitro and in by: 4. During the last decade, quantitative measurement of the methylation status in white blood cells (WBCs) has been used as a potential biomarker in a variety of diseases. Long interspersed nucleotide element-1 (LINE-1) has been used widely as a surrogate marker of global DNA methylation. Altered maternal DNA methylation is suggested to be an underlying mechanism in the trisomy 21 Author: Aleksandra Stanković. NBL2 is a tandem kb DNA repeat, whose hypomethylation in hepatocellular carcinomas was shown previously to be an independent predictor of disease progression. Here, we examined methylation of all cytosine residues in a kb subregion of NBL2 in ovarian carcinomas, Wilms' tumors, and diverse control tissues by hairpin-bisulfite PCR. This new genomic sequencing Cited by: Aberrant DNA methylation changes have been detected in several diseases, particularly cancer where genome-wide hypomethylation coincides with gene-specific hypermethylation. DNA methylation patterns can be used to detect cancer at very early stages, to classify tumors as well as predict and monitor the response to antineoplastic treatment.
Accordingly, another DNA methylation pan-cancer study focused on promoters found that thyroid carcinoma exhibited one of the lowest frequencies in both hypomethylation and hypermethylation events. And ATC exhibits a high frequency of DNA methylation . Considering the effects of DNMT inhibitor agents on major methylation enzymes in the absence of toxicity and chemical stability, it has been shown that the learning and memory of certain DNA methylation enzymes can be genetically altered through DNA methylation mechanisms [51, 52, 53]. Some studies have demonstrated that memory organisation and. DNA methylation and demethylation, two of the most widely studied epigenetic mechanisms, represent an attractive target for pain diagnosis, prognosis, and treatment. The understanding of alterations in DNA methylation homeostasis in chronic pain has rapidly increased due to the emergence of more sensitive high-throughput technologies. DNA methylation is an important characteristic of plant genomes [1, 2], and can occur in all cytosine contexts (CG, CHG and CHH, where H = A, C or T) .The effect of DNA methylation variants on plant development has been demonstrated through methylation alteration tests, which led to plant abnormalities [4, 5].Furthermore, DNA methylation has been reported to vary from tissue to tissue in.
DNA methylation, an epigenetic mechanism, has been associated with cancer initiation and progression. Greenlandic Inuit have some of the highest reported POP levels worldwide. Objective: Our aim in this study was to evaluate the relationship between plasma POPs concentrations and global DNA methylation (percent 5-methylcytosine) in DNA. DNA hypomethylation refers to the loss of the methyl group in the 5-methylcytosine nucleotide. Methylation is a natural modification of DNA, and mainly affects the cytosine base (C) when it is followed by a guanosine (G) in mammals (Methylation).The term hypomethylation can be applied to describe the unmethylated state of most CpG sites in a specific sequence that is normally . DNA methylation is the only genetically programmed DNA modification in mammals. This postreplication modification is found almost exclusively on the five position of the pyrimidine ring of cytosines in the context of the dinucleotide sequence CpG, with approximately 29 million CpGs present in the human genome (Rollins et al., ). 5-Methylcytosine accounts for approximately 1% of all bases. Targeting DNA methylation for cancer therapy has had a rocky history. The first reports on DNA methylation changes in cancer described global loss of methylation, which has been suggested to drive tumorigenesis through activation of oncogenic proteins or induction of chromosomal instability. In this context, reducing DNA methylation was viewed as a tumor-promoting event rather than a promising.