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The Molecular Genetics OF DNA Methylation in Colorectal Cancer
Published in Leonard H. Augenlicht, Cell and Molecular Biology of Colon Cancer, 2019
We were in fact able to identify and isolate pretransformed cells prior to transformation. Thus, cryopreserved ancestral cells of 5-azaCdR-induced transformants displayed a normal morphology and anchorage-dependence after thawing and replating, but after an additional 2 to 4 weeks in culture developed morphological transformation and anchorage independence.111 This experimental model system should allow us to identify genes activated at the earliest stages in cellular transformation. Whether these genes are specifically induced by 5-azaCdR or indirectly by effects on other genes will need to be determined. Nevertheless, I believe that our studies of altered DNA methylation in cancer and transformation, should lead us to an understanding of the earliest events in transformation.
Breast cancer epigenetic targets for precision medicine
Published in Debmalya Barh, Precision Medicine in Cancers and Non-Communicable Diseases, 2018
Among these defects, epigenetic changes involved in altering gene expression play an essential role in cancer development and progression. Recent studies described the existence of breast cancer–specific DNA methylation profiles (Cancer Genome Atlas Network, 2012) that can help in identifying breast cancer specific pathways, which could be modified by targeted interventions, leading to reduced breast cancer incidence. These methylation signatures can also help in refining breast cancer screening to achieve early detection and can help in clinical care by determining personalized cancer treatments and predicting disease-free and overall survival (Terry et al., 2016). Thus, these epigenetic biomarkers could play an essential role for primary, secondary, and tertiary prevention.
Epigenetic Effects of Blackberry Extract on Human Colorectal Cancer Cells
Published in Nutrition and Cancer, 2022
Mohsen Tatar, Masoumeh Varedi, Fakhraddin Naghibalhossaini
Epigenetic alterations, including histone modifications, and DNA methylation affect the expression of genes without changing the DNA sequence. Aberrant changes in the epigenetic profile of cells are early events in tumor development that contribute to the initiation and progression of cancer. Most cancer cells with perturbed DNA methylations, display global DNA hypomethylation, but hypermethylation in the promoter regions of specific tumor suppressor genes (1). CpG island methylator phenotype (CIMP) is a characteristic of a subgroup of colorectal cancer (CRC) cells with extensive DNA methylation at the promoter regions of several tumor suppressor genes (2). Three groups of DNA methyl transferase (DNMT) enzymes (DNMT1, DNMT3A, and DNMT3B) are involved in methyl group transfer from S-adenosylmethionine to the C-5 position of cytosine in CpG dinucleotides of DNA (3). DNMT1 is the “maintenance” enzyme that acts on hemi-methylated DNA duplex to faithfully transmit methylation profile from maternal to daughter cells following cell division. De novo methylation of DNA is mediated by DNMT3A and DNMT3B enzymes that methylate DNA during development and establish tissue-specific DNA methylation patterns. However, all known DNMTs are engaged in both de novo and maintenance methylation activities (4,5). Aberrant DNA methylation in cancer cells has been linked to the dysregulated expression levels of cellular DNMTs in human cancers (6–9).
Epigenetic therapy: azacytidine and decitabine in acute myeloid leukemia
Published in Expert Review of Hematology, 2018
Stephan R. Bohl, Lars Bullinger, Frank G. Rücker
Hansen and colleagues provided that there are differences in DNA methylation between healthy tissue and its malignant counterpart [5]. It has been demonstrated that in malignant cells genes involved in important regulatory pathways, like e.g. DNA repair, cell cycle regulation, and tumor suppression, show increased hypermethylation of promotor-associated CpG islands, short stretches of DNA with a high concentration of CpG dinucleotides [6]. This epigenetic change can lead to transcriptional silencing of TSGs. However, it seems that aberrant DNA methylation patterns outside of CpG islands may be equally important in carcinogenesis and that hypomethylation is as essential as hypermethylation [7]. In addition, it has been suggested that aberrant DNA methylation in cancer occurs at defined genomic locations, so-called cancer-specific differentially methylated regions [5]. For example, in AML, several ‘epigenome analyses’ pinpoint to a small common set of genes exhibiting consistent aberrant methylation among hundreds of leukemia samples [8,9].
Epigenetic modification in 4T1 mouse breast cancer model by artificial light at night and melatonin – the role of DNA-methyltransferase
Published in Chronobiology International, 2019
Sahar Agbaria, Abraham Haim, Fuad Fares, Abed E. Zubidat
BC-cells proliferation which is triggered by ALAN could be explained at least partly by inducing DNA damage. This possibility was assessed in this study by examining both DNMT activity and GDM levels. DNA methylations, which are a reversible modification in genes, triggered by MLT are a promising mechanism linking between environmental exposures like ALAN and hormonal/cellular pathway mediating carcinogenic activities like metastasis activity, tumor cell proliferation, and estrogen-related responses (Zhu et al. 2011). DNMTs were found to be involved in abnormal DNA methylation in cancer cells (Ballestar and Esteller 2008). These enzymes were shown to be over-expressed in a variety of tumors which it considered the major epigenetic alteration in cancer cells (Korkmaz et al. 2009).