Growing evidence suggests that aberrant epigenetic regulation of gene function is strongly related to the genesis of cancer. Unlike genetic mutations, the ability to reprogram the epigenetic landscape in the cancer epigenome is one of the most promising target therapies in both treatment and reversibility of drug resistance. Epigenetic alterations in cancer development and progression may be the basis for the individual variation in drug response. Thus, this review focuses on the emerging area of pharmaco(epi)genomics, specifically highlighting epigenetic reprogramming during tumorigenesis and how epigenetic markers are targeted as a therapy (epidrugs) and the clinical implications of this for cancer treatment.

Epidrugs: targeting epigenetic marks in cancer treatment

Early detection of lung cancer biomarkers through biosensor technology: A review.

Epigenetic alteration has been proposed to give rise to numerous classic hallmarks of cancer. Impaired DNA methylation plays a central role in the onset and progression of several types of malignancies, and DNA methylation is mediated by DNA methyltransferases (DNMTs) consisting of DNMT1, DNMT3A, and DNMT3B. DNMTs are frequently implicated in the pathogenesis and aggressiveness of acute myeloid leukaemia (AML) patients. In this review, we describe and discuss the oncogenic roles of DNMT1, DNMT3A, and DNMT3B in AML. The clinical response predictive roles of DNMTs in clinical trials utilising hypomethylating agents (azacitidine and decitabine) in AML patients are presented. Novel hypomethylating agent (guadecitabine) and experimental DNMT inhibitors in AML are also discussed. In summary, hypermethylation of tumour suppressors mediated by DNMT1 or DNMT3B contributes to the progression and severity of AML (except MLL-AF9 and inv(16)(p13;q22) AML for DNMT3B), while mutation affecting DNMT3A represents an early genetic lesion in the pathogenesis of AML. In clinical trials of AML patients, expression of DNMTs is downregulated by hypomethylating agents while the clinical response predictive roles of DNMT biomarkers remain unresolved. Finally, nucleoside hypomethylating agents have continued to show enhanced responses in clinical trials of AML patients, and novel non-nucleoside DNMT inhibitors have demonstrated cytotoxicity against AML cells in pre-clinical settings.

https://journals.sagepub.com/doi/pdf/10.1177/1177271919846454

Oncogenic Roles and Inhibitors of DNMT1, DNMT3A, and DNMT3B in Acute Myeloid Leukaemia.

MicroRNA: A signature for cancer progression.

Schizophrenia is a severe psychiatric disorder with a complex array of signs and symptoms that causes very significant disability in young people. While schizophrenia has a strong genetic component, with heritability around 80%, there is also a very significant range of environmental exposures and stressors that have been implicated in disease development and neuropathology, such as maternal immune infection, obstetric complications, childhood trauma and cannabis exposure. It is postulated that epigenetic factors, as well as regulatory non-coding RNAs, mediate the effects of these environmental stressors. In this review, we explore the most well-known epigenetic marks, including DNA methylation and histone modification, along with emerging RNA mediators of epigenomic state, including miRNAs and lncRNAs, and discuss their collective potential for involvement in the pathophysiology of schizophrenia implicated through the postmortem analysis of brain tissue. Given that peripheral tissues, such as blood, saliva, and olfactory epithelium have the same genetic composition and are exposed to many of the same environmental exposures, we also examine some studies supporting the application of peripheral tissues for epigenomic biomarker discovery in schizophrenia. Finally, we provide some perspective on how these biomarkers may be utilized to capture a signature of past events that informs future treatment.

https://www.mdpi.com/2073-4409/9/8/1837/pdf

Epigenomic Dysregulation in Schizophrenia: In Search of Disease Etiology and Biomarkers.

The impact of genetic variation on metabolism of heavy metals: Genetic predisposition?

Epigenetics and Epi-miRNAs: Potential markers/therapeutics in leukemia.

Alpha-1 Antitrypsin is one of the Serpins which in fact indicates a Glico protein with 12% carbohydrat e. It contains 394 amino acids with molecular weight of 54 KDa which is synthesized in liver and secretes into plasma . Its original performance is to inhibit Neutrophil Elastase and p rotect the tissues, especially against destructive effects of Elastase during inflammation. Genetic (inherited) s hortage of AAT results in pulmonary and hepatic ill nesses. Emphysema is one of the most important one. Hence, due to their widespread application in medicine and treating the diseases in the perspective of various bacteria l, plant, and yeast sources, great medical companie s pay much attention to the production of recombinants in prot eins. Furthermore, due to Glycosylatedness of this protein and its high molecular weight, every technique which may increase the expression output and recombinant protei ns secretion in yeast can be regarded as a helpful ins trument in producing this medicine. The current stu dy is going to investigate the purity separation and determination of the properties and optimization of the alpha-1 Antitrypsin expression in Saccharomyces cerevisiae. In order to separate and purify this protein, some properties such as molecular mass, the amount and capacity of inhibiti ng are also measured. It is worth mentioning that t he materials and performing technique in the present study have been determined in the following order: strains, pl asmids, cultivation environments, transformation, protein p roperty determination, and expression increase.

/pdf/separation-and-optimization-of-alpha-1-antitrypsin-356iijtiot.pdf

Zeinab Joneidi

Papers

The impact of genetic variation on metabolism of heavy metals: Genetic predisposition?

Epigenetics and Epi-miRNAs: Potential markers/therapeutics in leukemia.

Separation and Optimization of Alpha-1 Antitrypsin Properties in Saccharomyces Yeast