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Diwakar Kumar Singh

Abstract

Through the use of epigenome-wide association studies (EWAS), scientists can identify epigenetic alterations throughout the genome that are related to cancer. The term "epigenetics" describes the mechanisms by which mitotically heritable changes in DNA and chromatin control the expression of genes without altering the nucleotide sequence. Epigenetic regulatory pathways may malfunction in cancer cells may be due to secretion and accumulation of metabolite. According to the recent findings, epigenetic changes, specifically DNA methylation, histone acetylation and deacetylation, and miRNA expression, may contribute to the genesis of cancer. DNA methylation is one epigenetic modification that is becoming recognised as a critical regulator of gene transcription with both heritable and acquired characteristics. Genomic methylation patterns are frequently altered in tumour cells, and this is frequently accompanied by global hypomethylation and nitric oxide generation. The associated gene's expression may be suppressed when the promoter of a tumour suppressor gene is hypermethylated. Atypical DNA methylation patterns are one of the earliest and most common aspects of carcinogenesis. The small molecules which inhibit the epigenetic reprogramming may fill the gap in scientific literature and become more influential area of research in cancer therapy.

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