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4th¬†International Conference on Epigenetics and Human Diseases, will be organized around the theme “”

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All epigenetic alterations, including as DNA methylation and histone modifications, as well as non-coding RNAs, are included in the epigenome at any given time. The cell epigenome is dynamic, and genetic and environmental factors can influence it. Furthermore, epigenetic modifications can be reversed, making the genome adaptable to environmental changes.



On a daily basis, we are exposed to different environmental pollutants, which might cause alterations in our epigenome, which might influence our health. The toxins produced by Listeria monocytogenes, Clostridium perfringens, and Streptococcus pneumonia have been demonstrated to cause substantial alterations in histone acetylations.



 


Epigenetics is the study of how your behaviour and environment can influence how your genes function. Epigenetic alterations, unlike genetic alterations, are reversible and do not alter your DNA sequence; nevertheless, they can alter how your body interprets a DNA sequence.

Birth defects, childhood disorders, and indications of diseases later in life can all be caused by incorrect epigenetic markers. Epigenetic systems also control an organism's development and adaptations throughout its life, and their disruption can lead to diseases like cancer.


 



Epigenetic abnormalities such as aberrant DNA methylation, histone modifications, or RNA silencing are found in numerous human diseases. Gene mutations that alter the epigenetic profile may also cause pathologies, which can be inherited or acquired somatically.



 



Throughout life, DNA accessibility is epigenetically regulated. In early embryonic stages, histone modifications and demethylation occur in the paternal genome. The maternal genome is also demethylated, followed by embryonic re-methylation, which contributes to the growing embryo's epigenetic profile. For effective gene control, the newly established epigenetic profile must be maintained. Any maintenance error can cause congenital problems and put people at risk for acquired diseases.



 



Global DNA hypomethylation and gene-specific hypermethylation have been observed in human cancer cells obtained from clinical tissue biopsies. During initial studies of cancer epigenetics, the genome of patients with colorectal cancer was reported to be hypomethylated. In these patients, regions that are hypermethylated under normal conditions and silent regions of the genome were found to be demethylated. In some malignancies, however, abnormal gene activity, such as inhibition of tumor-suppressor genes, has been linked to hypermethylation of CpG islands. By hypermethylating DNA, repeating DNA sequences such as microsatellites become functionally abnormal and cause tumorigenesis. microsatellites in colorectal and ovarian cancers are distorted by abnormal epigenetic modulations in the MLH1 promoter (a DNA repair gene).



Cancer epigenetics is the study of epigenetic modifications to the DNA of cancer cells that do not involve a change in the nucleotide sequence, but instead involve a change in the way the genetic code is expressed.



 


The development of type 2 diabetes is aided by epigenetic reprogramming of insulin target organs, islet cells, and immune cells, while gamete reprogramming has transgenerational consequences. Hyperglycemia causes epigenetic alterations in tissues that are affected by diabetic complications.

The development of type 2 diabetes is aided by epigenetic reprogramming of insulin target organs, islet cells, and immune cells, while gamete reprogramming has transgenerational consequences. Hyperglycemia causes epigenetic alterations in tissues that are affected by diabetic complications.



 


Epigenetic mechanisms such as DNA methylation and modifications to histone proteins regulate high-order DNA structure and gene expression. Aberrant epigenetic mechanisms are involved in the development of many diseases, including cancer.

Both patients and healthcare costs are burdened by neurological disorders, particularly neurodegenerative disorders. Despite substantial research, therapy choices for people with these disorders are limited and, in most cases, only give minor symptomatic improvement. Aberrant epigenetic post-translational modifications of proteins are emerging as important elements in the pathogenesis of neurological disease.



 


Natural  and  normal  functions  of  immune  system depend on self-tolerance, and self-tolerance deficiency can  result  in  autoimmunity.  Autoimmune  disease  studies  in  both  monozygotic  and dizygotic  twins  have suggested  a  role for  epigenetic factors. Epigenetic homeostasis  failure, as a  response to  environmental agents, can result in gene expression changes  in  specific  differentiated  cells  leading  to dysregulated self-tolerance.  The immune system and  target organ are two  main players  in  an  autoimmune  disease  process  and  the epigenetic  modifications  of these  players could  have roles  in  disease  development.  Many  functions  of immune  cells  such  as  hematopoietic  lineage, rearrangement  of  antigen-receptor,  allelic  exclusion, and inducible immune responses against pathogens are epigenetically controlled. The alterations of epigenetic mechanisms  regulating  immunological  development could promote autoimmunity disease.


 



 


There are many types of histone modifications, including acetylation, methylation, ubiquitination, citrullination and phosphorylation of specific amino acids within the histone protein, usually towards the C-terminal ('tail') end of the protein.

Histone alterations control gene expression in two ways: by changing the general structure of chromatin and/or by regulating the binding of transcription effector molecules. Histone alterations control gene expression in two ways: by changing the general structure of chromatin and/or by regulating the binding of transcription effector molecules.



 


DNA methylation is a biological process that involves the addition of methyl groups to the DNA molecule. Without affecting the sequence, methylation can modify the activity of a DNA region. When DNA methylation occurs at a gene promoter, it usually suppresses gene transcription. In mammals, DNA methylation is essential for normal development and is associated with a number of key processes including genomic imprinting, X-chromosome inactivation, repression of transposable elements, aging, and carcinogenesis.

Aging, environmental effects, and lifestyle variables such as smoking and food all cause biochemical changes in the DNA over time. These frequently result in DNA methylation, which is the addition of methyl groups to specific DNA sequences without affecting the DNA sequence.



 


Non-coding RNAs (ncRNAs) play a role in transcriptional and post-transcriptional regulation of gene expression. Some ncRNAs appear to play a role in epigenetic regulation. They're involved in heterochromatin formation, histone modification, DNA methylation targeting, and gene silencing, according to the findings.

A non-coding RNA (ncRNA) is a functional RNA molecule that is transcribed from DNA but not translated into proteins. Epigenetic related ncRNAs include miRNA, siRNA, piRNA and lncRNA. In general, ncRNAs function to regulate gene expression at the transcriptional and post-transcriptional level. Abundant and functionally important types of non-coding RNAs include transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), as well as small RNAs such as microRNAs, siRNAs, piRNAs, snoRNAs, snRNAs, exRNAs, scaRNAs and the long ncRNAs such as Xist and HOTAIR



 


The use of medicines or other epigenome-influencing approaches to treat medical diseases is known as epigenetic therapy. Epigenetic pathways play a role in a variety of diseases, including cancer, heart disease, diabetes, and mental problems. Epigenetic therapy may be a technique to directly modify such circuits. it has been proposed that epigenetic drugs may prevent the formation of cancer progenitor cells while also killing drug-resistant cancer cells.

On the other hand, some epigenetic marks can be reversible, and this fact has encouraged many researchers to focus on epigenetic therapy. Epigenetic pathways play a role in a variety of diseases, including cancer, heart disease, diabetes, and mental problems. Epigenetic therapy may be a technique to directly modify such circuits.



 


Various studies and clinical trials have examined epigenetic therapies which shown the potential to decrease the burden of diseases in which abnormal epigenetic mechanisms play a critical role. Numerous therapeutic agents that can modulate epigenetic mechanisms in various disease conditions are under consideration for clinical use. Additional studies of the therapeutic approach to epigenetic therapy are required, as the procedure is not selective for target cells and activating gene expression in normal cells may make them cancerous. Further insight into the molecular mechanisms governing these epigenetic modulators will facilitate the design of more specific and effective drugs. The development of more specific HDAC inhibitors has shown great promise. Increasing target specificity will also significantly affect the development of more effective treatment options. The approval of two epigenetic drugs (Vidaza and romidepsin, HDAC inhibitors) by the US Food and Drug Administration has supported their use in disease treatment. Additionally, epigenetic profiling of patients may have predictive or prognostic value for epigenetic therapy. Thus, epigenetic biomarkers can be used to complement current strategies for diagnosis, prognosis, and prediction of drug responses and assist with therapeutic decision-making