Abstract

ROLE OF JUNK DNA IN ONCOGENETICS

Keyur Parmar*, Apeksha Kadam and Dr. Rajashree Mashru

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Abstract

Junk DNA has long been conceived of by evolutionists as unused DNA from previous evolutionary iterations. According to the selfish or parasitic DNA idea, this DNA survives only due to its ability to duplicate itself, or because it has randomly mutated into a form that is beneficial to the cell. Introns, pseudogenes, mobile or repetitive DNAs are all examples of junk DNA. Many previously discarded DNA sequences have recently gained renewed attention for their roles in genome structure and function, gene control, and fast speciation. On the other hand, there are examples of what appear to be actual junk DNA sequences, or sequences that have lost their activities due to mutational inactivation that could have occurred after the Fall, or by God-ordained temporal restrictions placed on their functions (Walk up, 2000). The preservation of telomere length is required for long-term cell division. Telomerase lengthens telomeres and maintains a telomere length balance that prevents them from becoming dangerously short when they get too short to protect chromosomal ends., and emphysema in people with insufficient telomerase or other telomere gene abnormalities. The ability to annotate enhancers and their activity levels is based on epigenomic characteristics such as the build-up of histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation. BD modules bind to acetylated histones in a variety of transcriptional coregulators, influencing chromatin accessibility and transcriptional activation at active enhancers. Epigenetic is a Greek word that means "above and beyond." Conrad Waddington invented the term in 1939 to describe the process by which a population's response to an environmental stimulus is passed down through the generations.

Keywords: junk DNA, BRD4 inhibitors, Histone proteins, Micro RNA, Breast Cancer, Paediatrics Cancer.