The promise of epigenetic therapy: reprogramming the cancer epigenome (2023)

Table of Contents
Section snippets Technologies to interrogate the epigenome Epigenetic modifiers and drugs that target them Combination therapies Conclusions and future directions Disclosures Conflict of interest statement References and recommended reading Cited by (115) Biological and pharmacological aspects of tannins and potential biotechnological applications Use of histone methyltransferase inhibitors in cancer treatment: A systematic review Targeting the epigenome in malignant melanoma: Facts, challenges and therapeutic promises Epigenetics of glioblastoma multiforme: From molecular mechanisms to therapeutic approaches Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-deficient pancreatic cancer Epigenetic regulation of necrosis and pyknosis Recommended articles (6) Demethylation regulation of BDNF gene expression in dorsal root ganglion neurons is implicated in opioid-induced pain hypersensitivity in rats Clinical and biological effects of demethylating agents on solid tumours – A systematic review Genome-wide identification and characterization of glucose transporter (glut) genes in spotted sea bass (Lateolabrax maculatus) and their regulated hepatic expression during short-term starvation Epigenomes as therapeutic targets SHR2554, an EZH2 inhibitor, in relapsed or refractory mature lymphoid neoplasms: a first-in-human, dose-escalation, dose-expansion, and clinical expansion phase 1 trial Epigenetic modifiers as new immunomodulatory therapies in solid tumours FAQs Videos

Section snippets

Technologies to interrogate the epigenome

Our ability to characterize the epigenetic state of tissues relies on a growing number of technologies designed to quantify a particular type of epigenetic mark. A recent analysis comparing DNA methylation assays concluded that amplicon bisulfite sequencing and bisulfite pyrosequencing are the most promising technologies (in terms of accuracy and reproducibility) for clinical applications of DNA methylation [13]. Other higher-throughput methods for measuring DNA methylation include restriction

Epigenetic modifiers and drugs that target them

The epigenome is maintained by sets of proteins that govern DNA methylation, histone modifications, and chromatin states; a set of examples is presented in Figure 1b. DNA methylation and histone modification regulators consist of proteins that ‘write’, ‘read’, or ‘erase’ various chemical groups from chromatin. In recent years there has been an explosion of clinical development of drugs targeting this machinery, as outlined below (Figure 1c). A partial list of epigenetic drugs and relevant

Combination therapies

In recent years many groups have started exploring the possibility that combination regimens involving epigenetic drugs may improve clinical efficacy. Indeed, investigators recognized as far back as 2000 that hypomethylating agents can reverse drug resistance to platinum chemotherapy in vitro [64]. This result has since been confirmed, and synergy has been observed between decitabine and platinum agents [65]. Several combination regimens have subsequently been tested clinically. In one study,

Conclusions and future directions

Epigenetic factors in cancer development are now widely accepted, however, our ability to effectively target the epigenome clinically is not yet mature. Several FDA-approved drugs antagonize various components of the epigenetic machinery, most prominently the DNMT1 and HDAC inhibitors, which have shown clear benefits in specific types of cancer [23, 38, 41•]. Other contributors to epigenome maintenance are also being targeted by novel drugs in clinical trials. Such targets include histone


Jean-Pierre Issa is a consultant for Astex Pharmaceuticals and Teva Pharmaceutical Industries.

Conflict of interest statement

Nothing declared.

References and recommended reading

Papers of particular interest, published within the period of review, have been highlighted as:

  • • of special interest

  • •• of outstanding interest

Cited by (115)

  • Biological and pharmacological aspects of tannins and potential biotechnological applications

    2023, Food Chemistry

    Secondary metabolites are divided into three classes: phenolic, terpenoid, and nitrogenous compounds. Phenolic compounds are also known as polyphenols and include tannins, classified as hydrolysable or condensed. Herein, we explored tannins for their ROS reduction characteristics and role in homeostasis. These activities are associated with the numbers and degree of polymerisation of reactive hydroxyl groups present in the phenolic rings of tannins. These characteristics are associated with anti-inflammatory, anti-aging, and anti-proliferative health benefits. Tannins can reduce the risk of cancer and neurodegenerative diseases, such as cardiovascular diseases and Alzheimer's, respectively. These biomolecules may be used as nutraceuticals to maintain good gut microbiota. Industrial applications include providing durability to leather, anti-corrosive properties to metals, and substrates for 3D printing and in bio-based foam manufacture. This review updates regarding tannin-based research and highlights its biological and pharmacological relevance and potential applications.

  • Use of histone methyltransferase inhibitors in cancer treatment: A systematic review

    2023, European Journal of Pharmacology

    Histone modifications are an epigenetic mechanism, and the dysregulation of these proteins is known to be associated with the initiation and progression of cancer. In the search for the development of new and more effective drugs, histone modifications were identified as possible therapeutic targets. Histone methyltransferase (HMT) inhibitors correspond to the third generation of epigenetic drugs capable of writing or deleting epigenetic information. This systematic review summarized the development and prospect for the use of different HMT inhibitors in cancer therapy. An electronic search was applied across CENTRAL, Clinical Trials, Embase, LILACS, LIVIVO, Open Gray, PubMed, Scopus, and Web of Science. Based on the title and abstracts, two authors independently selected eligible studies. After the complete reading of the articles, based on the eligibility criteria, 11 studies were included in the review. Different inhibitors of HMT have been explored in multiple clinical studies, and have shown considerable anti-tumor effects. However, few phase 2 studies have been completed and/or have available results. The most advanced clinical trials mainly include tazemetostat, an Enhancer of zeste homolog 2 (EZH2) inhibitor approved for follicular lymphoma (FL). The use of HMT inhibitors has presented, so far, concise results in the treatment of hematological cancers, moreover, the adverse effects presented after the use of these medicines (alone or in combination) did not show a high level of risk for the patient. These findings, in addition to ongoing clinical studies, can represent a promising future regarding the use of HMT inhibitors in treating different types of cancer.

    (Video) Targeting Cancer Pathways: The Epigenetics Question
  • Targeting the epigenome in malignant melanoma: Facts, challenges and therapeutic promises

    2022, Pharmacology and Therapeutics

    Malignant melanoma is the most lethal type of skin cancer with high rates of mortality. Although current treatment options provide a short-clinical benefit, acquired-drug resistance highlights the low 5-year survival rate among patients with advanced stage of the disease. In parallel, the involvement of an aberrant epigenetic landscape, (e.g., alterations in DNA methylation patterns, histone modifications marks and expression of non-coding RNAs), in addition to the genetic background, has been also associated with the onset and progression of melanoma. In this review article, we report on current therapeutic options in melanoma treatment with a focus on distinct epigenetic alterations and how their reversal, by specific drug compounds, can restore a normal phenotype. In particular, we concentrate on how single and/or combinatorial therapeutic approaches have utilized epigenetic drug compounds in being effective against malignant melanoma. Finally, the role of deregulated epigenetic mechanisms in promoting drug resistance to targeted therapies and immune checkpoint inhibitors is presented leading to the development of newly synthesized and/or improved drug compounds capable of targeting the epigenome of malignant melanoma.

  • Epigenetics of glioblastoma multiforme: From molecular mechanisms to therapeutic approaches

    2022, Seminars in Cancer Biology

    Citation Excerpt :

    Epigenetic modifications play a vital role in the development and progression of GBM [12,15,16]. Epigenetics represent mitotically heritable alterations in gene expression that are not due to alterations in the sequence of deoxyribonucleic acid (DNA) and is considered a marker of human cancers [17–19]. Undeniably, abnormal epigenetic mechanisms, including histone modifications (HM), altered non-coding ribonucleic acid (RNA) expression, DNA methylation, and chromatin remodeling (CR), are presently documented as related events in tumor formation [20].

    Glioblastoma multiforme (GBM) is the most common form of brain cancer and one of the most aggressive cancers found in humans. Most of the signs and symptoms of GBM can be mild and slowly aggravated, although other symptoms might demonstrate it as an acute ailment. However, the precise mechanisms of the development of GBM remain unknown. Due to the improvement of molecular pathology, current researches have reported that glioma progression is strongly connected with different types of epigenetic phenomena, such as histone modifications, DNA methylation, chromatin remodeling, and aberrant microRNA. Furthermore, the genes and the proteins that control these alterations have become novel targets for treating glioma because of the reversibility of epigenetic modifications. In some cases, gene mutations including P16, TP53, and EGFR, have been observed in GBM. In contrast, monosomies, including removals of chromosome 10, particularly q23 and q25–26, are considered the standard markers for determining the development and aggressiveness of GBM. Recently, amid the epigenetic therapies, histone deacetylase inhibitors (HDACIs) and DNA methyltransferase inhibitors have been used for treating tumors, either single or combined. Specifically, HDACIs are served as a good choice and deliver a novel pathway to treat GBM. In this review, we focus on the epigenetics of GBM and the consequence of its mutations. We also highlight various treatment approaches, namely gene editing, epigenetic drugs, and microRNAs to combat GBM.

  • Glycolysis addiction compensating for a defective pentose phosphate pathway confers gemcitabine sensitivity in SETD2-deficient pancreatic cancer

    2022, Biochemical and Biophysical Research Communications

    Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy driven by genetic mutations and/or epigenetic dysregulation. Gemcitabine chemotherapy is the first-line regimen for pancreatic cancer but has limited efficacy. Our previous study revealed the role of SETD2-H3K36me3 loss in the initiation and metastasis of PDAC, but little is known about its role in tumor metabolism. Here, we found that SETD2-deficient PDAC enhanced glycolysis addiction via upregulation of glucose transporter 1 (GLUT1) to meet its large demand for glucose in progression. Moreover, SETD2 deficiency impaired nucleoside synthesis by directly downregulating the transcriptional level of transketolase (TKT) in the pentose phosphate pathway. The metabolic changes confer SETD2-deficient PDAC cells with increased sensitivity to gemcitabine under glycolysis restriction conditions. Collectively, our study provides mechanistic insights into how SETD2 deficiency reprograms glycolytic metabolism to compensate for insufficient nucleoside synthesis, suggesting that glycolysis restriction combined with gemcitabine might be a potential therapeutic strategy for PDAC patients with SETD2 deficiency.

    (Video) The Cancer Epigenome - Peter Jones, Ph.D., D.Sc.

  • Epigenetic regulation of necrosis and pyknosis

    2022, Epigenetics in Organ Specific Disorders

    Necrosis occurs commonly in many pathological conditions. A stereotypical change of necrotic cell is the rupture of plasma membrane and nuclear shrinkage (also known as pyknosis). The rupture of plasma membrane releases toxic cellular contents such as cytokines and fragmented DNAs, to cause inflammation and death of the surrounding cells. The regulatory machinery of necrosis is variable depending on cell type and stress context. Here, we briefly review our current understanding of epigenetic control of necrosis and pyknosis. Epigenetic alterations such as DNA methylation, histone modification, and noncoding RNA associate with diverse pathological conditions, which may be used as biomarkers of the diseases. Further, many endogenous epigenetic regulators have been identified to regulate necrosis. Therefore, these epigenetic processes may be targetable for disease treatments. In general, our understanding of the epigenetic mechanism of necrosis is still in its early stage.

View all citing articles on Scopus

Recommended articles (6)

  • Repeated administration of morphine may result in opioid-induced hypersensitivity (OIH), which involves altered expression of numerous genes, including brain-derived neurotrophic factor (BDNF) in dorsal root ganglion (DRG) neurons. Yet, it remains unclear how BDNF expression is increased in DRG neurons after repeated morphine treatment. DNA methylation is an important mechanism of epigenetic control of gene expression. In the current study, we hypothesized that the demethylation regulation of certain BDNF gene promoters in DRG neurons may contribute to the development of OIH. Real-time RT-PCR was used to assess changes in the mRNA transcription levels of major BDNF exons including exon I, II, IV, VI, as well as total BDNF mRNA in DRGs from rats after repeated morphine administration. The levels of exon IV and total BDNF mRNA were significantly upregulated by repeated morphine administration, as compared to that in saline control group. Further, ELISA array and immunocytochemistry study revealed a robust upregulation of BDNF protein expression in DRG neurons after repeated morphine exposure. Correspondingly, the methylation levels of BDNF exon IV promoter showed a significant downregulation by morphine treatment. Importantly, intrathecal administration of a BDNF antibody, but not control IgG, significantly inhibited mechanical hypersensitivity that developed in rats after repeated morphine treatment. Conversely, intrathecal administration of an inhibitor of DNA methylation, 5-aza-2′-deoxycytidine (5-aza-dC) markedly upregulated the BDNF protein expression in DRG neurons and enhanced the mechanical allodynia after repeated morphine exposure. Together, our findings suggest that demethylation regulation of BDNF gene promoter may be implicated in the development of OIH through epigenetic control of BDNF expression in DRG neurons.

  • Research article

    Clinical and biological effects of demethylating agents on solid tumours – A systematic review

    Cancer Treatment Reviews, Volume 54, 2017, pp. 10-23

    It is assumed that DNA methylation plays a key role in both tumour development and therapy resistance. Demethylating agents have been shown to be effective in the treatment of haematological malignancies. Based on encouraging preclinical results, demethylating agents may also be effective in solid tumours. This systematic review summarizes the evidence of the effect of demethylating agents on clinical response, methylation and the immune system in solid tumours.

    We conducted a systematic literature search from 1949 to December 2016, according to the PRISMA guidelines. Studies which evaluated treatment with azacitidine, decitabine, guadecitabine, hydralazine, procaine, MG98 and/or zebularine in patients with solid tumours were included. Data on clinical response, effects on methylation and immune response were extracted.

    Fifty-eight studies were included: in 13 studies complete responses (CR) were observed, 35 studies showed partial responses (PR), 47 studies stable disease (SD) and all studies except two showed progressive disease (PD). Effects on global methylation were observed in 11/15 studies and demethylation/re-expression of tumour specific genes was seen in 15/17 studies. No clear correlation between (de)methylation and clinical response was observed. In 14 studies immune-related responses were reported, such as re-expression of cancer-testis antigens and upregulation of interferon genes.

    Demethylating agents are able to improve clinical outcome and alter methylation status in patients with solid tumours. Although beneficial effect has been shown in individual patients, overall response is limited. Further research on biomarker predicting therapy efficacy is indicated, particularly in earlier stage and highly methylated tumours.

    (Video) Epigenetic Reprogramming Within Tumor Microenvironment Impacts Immune-mediated Gene Therapy Efficacy
  • Research article

    Genome-wide identification and characterization of glucose transporter (glut) genes in spotted sea bass (Lateolabrax maculatus) and their regulated hepatic expression during short-term starvation

    Comparative Biochemistry and Physiology Part D: Genomics and Proteomics, Volume 30, 2019, pp. 217-229

    The glucose transporters (GLUTs) are well known for their essential roles in moving the key metabolites, glucose, galactose, fructose and a number of other important substrates in and out of cells. In this study, we identified a total of 21 glut genes in spotted sea bass (Lateolabrax maculatus) through extensive data mining of existing genomic and transcriptomic databases. Glut genes of spotted sea bass were classified into three subfamilies (Class I, Class II and Class III) according to the phylogenetic analysis. Glut genes of spotted sea bass were distributed in 15 out of 24 chromosomes. Deduced gene structure analysis including the secondary structure and the three-dimensional structures, as well as the syntenic analysis further supported their annotations and orthologies. Expression profile in healthy tissues indicated that 9 of 21 glut genes were expressed in liver of spotted sea bass. During short-term starvation, the mRNA expression levels of 3 glut genes (glut2, glut5, and glut10) were significantly up-regulated in liver (P < 0.05), indicating their potential roles in sugar transport and consumption. These findings in our study will facilitate the further evolutionary characterization of glut genes in fish species and provide a theoretical basis for their functional study.

  • Research article

    Epigenomes as therapeutic targets

    Pharmacology & Therapeutics, Volume 151, 2015, pp. 72-86

    Epigenetics is a molecular phenomenon that pertains to heritable changes in gene expression that do not involve changes in the DNA sequence. Epigenetic modifications in a whole genome, known as the epigenome, play an essential role in the regulation of gene expression in both normal development and disease. Traditional epigenetic changes include DNA methylation and histone modifications. Recent evidence reveals that other players, such as non-coding RNAs, may have an epigenetic regulatory role. Aberrant epigenetic signaling is becoming to be known as a central component of human disease, and the reversible nature of the epigenetic modifications provides an exciting opportunity for the development of clinically relevant therapeutics. Current epigenetic therapies provide a clinical benefit through disrupting DNA methyltransferases or histone deacetylases. However, the emergence of next-generation epigenetic therapies provides an opportunity to more effectively disrupt epigenetic disease states. Novel epigenetic therapies may improve drug targeting and drug delivery, optimize dosing schedules, and improve the efficacy of preexisting treatment modalities (chemotherapy, radiation, and immunotherapy). This review discusses the epigenetic mechanisms that contribute to the disease, available epigenetic therapies, epigenetic therapies currently in development, and the potential future use of epigenetic therapeutics in a clinical setting.

  • Research article

    (Video) Epigenetic Editing: towards reprogramming of gene expression

    SHR2554, an EZH2 inhibitor, in relapsed or refractory mature lymphoid neoplasms: a first-in-human, dose-escalation, dose-expansion, and clinical expansion phase 1 trial

    The Lancet Haematology, Volume 9, Issue 7, 2022, pp. e493-e503

    Dysregulation of EZH2 has a crucial role in lymphomagenesis. We did a first-in-human study to assess the safety, pharmacokinetics, pharmacodynamics, and preliminary clinical activity of SHR2554, an oral EZH2 inhibitor, in patients with relapsed or refractory mature lymphoid neoplasms, including B-cell lymphomas, T-cell lymphomas, and classical Hodgkin lymphoma.

    This was a multicentre, dose-escalation, dose-expansion, and clinical expansion phase 1 study done at 13 hospitals in China. Eligible patients had histologically or cytologically confirmed mature lymphoid neoplasms that had relapsed or were refractory to standard systemic therapies or had no standard-of-care. The study included a dose-escalation phase, at doses of SHR2554 from 50 mg to 800 mg twice daily; a dose-expansion phase, at two selected doses; and a subsequent clinical expansion phase at the recommended phase 2 dose in selected tumours. Primary endpoints were the safety, maximum tolerated dose, and recommended phase 2 dose. Objective response rate was a secondary endpoint. Safety and activity were assessed in all patients who received at least one dose of SHR2554 and had at least one post-baseline evaluation. This study is registered with, NCT03603951, and follow-up is ongoing.

    Between Aug 14, 2018, and July 13, 2021, 113 patients received SHR2554. At data cutoff (Sept 10, 2021), the median follow-up duration was 7·0 months (IQR 3·7–12·0). 71 (63%) patients were men and 42 (37%) were women, 110 (97%) were of Han ethnicity and 3 (3%) of other ethnicities, and 53 (47%) had received three or more lines of previous anticancer therapies. Dose-limiting toxicities occurred in two (67%) of three patients who received 400 mg SHR2554 twice daily and one (17%) of six patients who received 350 mg SHR2554 twice daily. The maximum tolerated dose and recommended phase 2 dose was determined to be 350 mg twice daily. The most common grade 3 or 4 treatment-related adverse events in all 113 patients were decreased platelet count (20 [18%]), decreased neutrophil count (ten [9%]), decreased white blood cell count (nine [8%]), and anaemia (seven [6%]). 18 (16%) patients had serious treatment-related adverse events. Two patients (2%) died due to treatment-related adverse events: one (1%) due to skin infection and toxic epidermal necrolysis and one (1%) due to respiratory failure. 107 (95%) of the 113 enrolled patients had post-baseline assessments for tumour response and were included in the activity analysis. 46 (43%; 95% CI 33–53) of these 107 patients had an overall response.

    SHR2554 showed an acceptable safety profile and promising antitumour activity in patients with relapsed or refractory lymphomas, providing evidence for future investigations.

    Jiangsu Hengrui Pharmaceuticals.

    For the Chinese translation of the abstract see Supplementary Materials section.

  • Research article

    Epigenetic modifiers as new immunomodulatory therapies in solid tumours

    Annals of Oncology, Volume 29, Issue 4, 2018, pp. 812-824

    Immune therapies have revolutionized cancer treatment over the last few years by allowing improvements in overall survival. However, the majority of patients is still primary or secondary resistant to such therapies, and enhancing sensitivity to immune therapies is therefore crucial to improve patient outcome. Several recent lines of evidence suggest that epigenetic modifiers have intrinsic immunomodulatory properties, which could be of therapeutic interest.

    We reviewed preclinical evidence and clinical studies which describe or exploit immunomodulatory properties of epigenetic agents. Experimental approaches, clinical applicability and corresponding ongoing clinical trials are described.

    Several epigenetic modifiers, such as histone deacetylase inhibitors, DNA methyl transferase inhibitors, bromodomain inhibitors, lysine-specific histone demethylase 1 inhibitors and enhancer of zeste homolog 2 inhibitors, display intrinsic immunomodulatory properties. The latter can be achieved through the action of these drugs either on cancer cells (e.g. presentation and generation of neoantigens, induction of immunogenic cell death, modulation of cytokine secretion), on immune cells (e.g. linage, differentiation, activation status and antitumor capability), or on components of the microenvironment (e.g. regulatory T cells and macrophages). Several promising combinations, notably with immune checkpoint blockers or adoptive T-cell therapy, can be envisioned. Dedicated clinically relevant approaches for patient selection and trial design will be required to optimally develop such combinations.

    (Video) Clark S (2013): Cancer epigenetics

    In an era where immune therapies are becoming a treatment backbone in many tumour types, epigenetic modifiers could play a crucial role in modulating tumours’ immunogenicity and sensitivity to immune agents. Optimal trial design, including window of opportunity trials, will be key in the success of this approach, and clinical evaluation is ongoing.

© 2017 Elsevier Ltd. All rights reserved.


What does epigenetic therapy do to the cancer cells? ›

Epigenetics and cytotoxic treatments

Studies have shown that the combination of epigenetic therapy and chemotherapy will reinduce the response to chemotherapy and resolve the resistance to cytotoxic agents.

What is the purpose of epigenetic reprogramming? ›

Epigenetic reprogramming is the process by which an organism's genotype interacts with the environment to produce its phenotype and provides a framework for explaining individual variations and the uniqueness of cells, tissues, or organs despite identical genetic information.

What is the epigenetic theory of cancer? ›

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.

What is the idea of epigenetic therapy? ›

Epigenetic therapy is the use of drugs or other epigenome-influencing techniques to treat medical conditions. Many diseases, including cancer, heart disease, diabetes, and mental illnesses are influenced by epigenetic mechanisms. Epigenetic therapy offers a potential way to influence those pathways directly.

What are the benefits of epigenetic therapy? ›

Epigenetic modification has a strong influence on cell regulation and function, like inhibiting genes that are involved in DNA repair, cell cycle regulation, drug resistance, metastasis and angiogenesis (blood vessel growth).

What is the evidence that epigenetic changes are involved in cancer quizlet? ›

What is the evidence that epigenetic changes are involved in cancer? All cancers tested thus far have exhibited a pattern of global hypomethylation, although specific regions are hypermethylated. The genes that are silenced include tumor suppressors.

What is the epigenome and why is it so important? ›

Within the complete set of DNA in a cell (genome), all of the modifications that regulate the activity (expression) of the genes is known as the epigenome. Because epigenetic changes help determine whether genes are turned on or off, they influence the production of proteins in cells.

Where does epigenetic reprogramming occur? ›

The role of epigenetic reprogramming

These marks need to be erased and reset in a sex-specific manner in order to create future functional gametes. Notably, epigenetic reprogramming occurs in the germline prior to the sex differentiation (E12. 5) and the onset of meiosis (E13. 5 in female germline).

How does reprogramming work? ›

In typical cellular reprogramming, cells are first converted into an induced pluripotent stem cell (iPSC) state and are then differentiated down a desired lineage to generate a large quantity of reprogrammed cells [2].

What are examples of epigenetic cancer drugs? ›

They include hydralazine, EGCG, RG108, MG98, and disulfiram, etc. Those epi-drugs have slightly inhibitory effects to multiple cancer cells compared with those cytosine analogue inhibitors.

What is an example of epigenetics? ›

Epigenetics and Reversibility

For example, at certain parts of the AHRR gene, smokers tend to have less DNA methylation than non-smokers. The difference is greater for heavy smokers and long-term smokers. After quitting smoking, former smokers can begin to have increased DNA methylation at this gene.

Which statement about epigenetics is false? ›

The epigenetics does not involve a change in the sequence of DNA. This sequence of DNA cannot be altered permanently. The given statement in this option is false, hence this option is the correct choice.

What is one very important epigenetic process called? ›

In order for this process to occur, the epigenome must be erased through a process called "reprogramming." Reprogramming is important because eggs and sperm develop from specialized cells with stable gene expression profiles. In other words, their genetic information is marked with epigenetic tags.

How does epigenetics affect behavior? ›

Background—Behavioral Epigenetics

Aberrant changes in the epigenetic profile might induce abnormal gene silencing. Subsequently, physiological regulation, such as cellular differentiation, genomic imprinting, genome stability, and even behavior can be potentially affected.

Is epigenetics good or bad? ›

Epigenetic changes are necessary for typical development and health, but they can also cause disease. Understanding the good and the bad epigenetic changes that take place in our bodies could help us develop new treatments for many diseases like cancer, heart disease and HIV.

How can epigenetics affect your health? ›

Disease may be caused by direct changes in epigenetic marks, such as DNA methylation, commonly found to affect imprinted gene regulation. Also described are disease-causing genetic mutations in epigenetic modifiers that either affect chromatin in trans or have a cis effect in altering chromatin configuration.

What are epigenetic drugs? ›

Epigenetic drugs are responsible for tumor suppressor gene reactivation. Therefore, normal cell functioning can be restored. These drugs can be used alone or in combination to produce with synergistic effects [15].

Can epigenetics influence the development of cancer disease? ›

Epigenetic silencing of genes can affect cancer at various stages (19). The epigenetic changes in gene expression and their pathologic correlation is a result of overlapping changes in genes expression, but some of them may be associated with particular stages of cancer development.

What are the two main ways that epigenetic changes can occur? ›

There are two main ways histones can be modified: acetylation and methylation. These are chemical processes that add either an acetyl or methyl group, respectively, to the amino acid lysine that is located in the histone.

What are 5 things that can cause epigenetic changes? ›

Several lifestyle factors have been identified that might modify epigenetic patterns, such as diet, obesity, physical activity, tobacco smoking, alcohol consumption, environmental pollutants, psychological stress, and working on night shifts.

What is the difference between epigenetics and epigenome? ›

Epigenetics focuses on processes that regulate how and when certain genes are turned on and turned off, while epigenomics pertains to analysis of epigenetic changes across many genes in a cell or entire organism.

What are the diseases caused by epigenetics? ›

Epigenetic changes are responsible for human diseases, including Fragile X syndrome, Angelman's syndrome, Prader-Willi syndrome, and various cancers.

What are the three major epigenetic mechanisms? ›

  • Epigenetic mechanisms form a layer of control within a cell that regulates gene expression and silencing. ...
  • Three different epigenetic mechanisms have been identified: DNA methylation, histone modification, and non-coding RNA (ncRNA)-associated gene silencing.
Aug 8, 2022

What is an example of epigenetics in humans? ›

Epigenetics explains how early experiences can have lifelong impacts. The genes children inherit from their biological parents provide information that guides their development. For example, how tall they could eventually become or the kind of temperament they could have.

What are the waves of epigenetic reprogramming? ›

Epigenetics of Transgenerational Inheritance of Disease

In humans and rodents, there are two waves of dynamic epigenetic reprogramming that occur between generations. The first wave is in the developing primordial germ cells, and second wave is in the postfertilization zygote [44].

What is epigenetic reprogramming of aging era? ›

The company's proprietary mRNA platform technology, ERA (Epigenetic Reprogramming of Aging) restores optimal gene expression by combatting the effects of aging in the epigenome. This restores cells' ability to prevent or treat disease and heal or regenerate tissue. It will help to fight incurable chronic diseases.

What are the 4 reprogramming factors? ›

The original set of reprogramming factors (also dubbed Yamanaka factors) are the transcription factors Oct4 (Pou5f1), Sox2, Klf4 and cMyc.

What are the four reprogramming factors? ›

The nuclear reprogramming involves the transduction of four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) —into somatic cells that led to the generation of iPSCs.

How do you reprogram yourself? ›

Six tips on how to reprogram your subconscious
  1. Adopt empowering beliefs. Limiting beliefs hold us back from what we want in life. ...
  2. Embrace the beauty of uncertainty. ...
  3. Focus on gratitude. ...
  4. Watch your environment. ...
  5. Visualize. ...
  6. Biohack your subconscious mind with binaural beats.

What causes epigenetic changes in cancer? ›

Epigenetic switching in cancer

As mentioned previously, DNA methylation and histone modifications work independently and in concert to alter gene expression during tumorigenesis. A key facet of such silencing mechanisms is the formation of a rigid repressive chromatin state that results in reduced cellular plasticity.

Is cancer genetic or epigenetic? ›

Cancers develop due to the accumulation of genetic and epigenetic alterations. Genetic alterations are induced by aging, mutagenic chemicals, ultraviolet light, and other factors; whereas, epigenetic alterations are mainly by aging and chronic inflammation.

What are the top 3 influences for epigenetics in the human? ›

The three types of epigenetic modifications explained above i.e., DNA methylation, histone modification and RNA silencing are responsible for such regulation of OCT4 gene expression.

How do you detect epigenetic changes? ›

Key Epigenetic Analysis Techniques
  1. DNA Methylation Analysis. Investigate methylation patterns quantitatively across the genome using sequencing- and array-based techniques. ...
  2. DNA–Protein Interaction Analysis. Gain insight into protein–DNA interactions. ...
  3. Chromatin Accessibility Analysis.

What was the first disease linked to epigenetics? ›

One of the first diseases to be linked to epigenetic changes was cancer. In the late 1970s Holliday and Pugh demonstrated that hypermethylation of DNA resulted in changes to normal gene regulation which led to cancer.

Can epigenetic changes be inherited? ›

This definition emphasizes that epigenetic changes are heritable, which implies that any change in cells that do not divide, such as neurons in the adult brain, are excluded.

What does epigenetics ultimately affect? ›

At the biochemical level, epigenetics affects transcription and ultimately the protein repertoire of a cell. The epigenetic mechanism serves four essential cellular roles: 1) X-chromosome inactivation; 2) differentiation; 3) imprinting; 4) medium and long-term transcriptional control.

What is controversial about epigenetics? ›

Several social scientists have criticized how epigenetic research treats the social, environmental, and temporal modulators of disease (risk and etiology). Among these critical scholars, there is a fear of novel forms of reductionism in epigenetics that are no less worrying than those attributed to genetics.

What is the most common epigenetic? ›

DNA methylation is the most common epigenetic modification in normal and cancer cells and typically involves the addition of a methyl group to a cytosine residue [6].

What is the difference between the genome and the epigenome? ›

The epigenome is a multitude of chemical compounds that can tell the genome what to do. The human genome is the complete assembly of DNA (deoxyribonucleic acid)-about 3 billion base pairs - that makes each individual unique.

Which of the following is not an example of epigenetics? ›

Answer and Explanation: Epigenetics is the study of heritable changes in DNA that do not include changes in the sequence. Therefore, (b) the inheritance of a single nucleotide mutation in the DNA would not be an example of epigenetic inheritance, as it is a change in a base pair in the DNA sequence.

Does trauma affect epigenetics? ›

Research has shown that the effects of trauma can be intergenerationally passed on through epigenetic mechanisms, such as methylation (264). Specifically, childhood trauma has been associated with alteration in methylation patterns in human sperm, which may induce intergenerational effects.

Can epigenetics affect personality? ›

There are a few neural functions where epigenetic effects on a small number of genes may be important, such as regulation of stress responsiveness and drug addiction, for example. But psychological traits like intelligence and personality are not determined by the ongoing action of a few genes.

What are the body types in epigenetics? ›

According to Epigenetics, there are six Biotype categories - The Crusader, The Diplomat, The Guardian, The Connector, The Activator and The Sensor – that represent a broad set of common genetic traits.

What is the role of epigenetic modifications? ›

Epigenetic modifications

In a multicellular organism, the epigenetic changes enable different adult cells to express specific genes that are required for the existence of each cell type and transfer of information to the daughter cells.

What is epigenetic reprogramming in trained immunity? ›

Epigenetic reprogramming. Induction of a trained immune phenotype in innate immune cells enables them to react with stronger, more rapid or qualitatively different transcriptional responses when challenged with subsequent triggers.

What are the 3 types epigenetic modifications? ›

Three classes of epigenetic regulation exist: DNA methylation, histone modification, and noncoding RNA action.

What is the role of epigenetics in human development? ›

Epigenetics explains how early experiences can have lifelong impacts. The genes children inherit from their biological parents provide information that guides their development. For example, how tall they could eventually become or the kind of temperament they could have.

What impact do epigenetic modifiers have on the immune system? ›

These epigenetic modifiers play critical roles in regulating immune responses and provide a molecular basis for understanding immune cell development and differentiation, memory, and effector functions.

What are the two types of epigenetic modifications? ›

Types of epigenetic changes include:
  • DNA Methylation. DNA methylation works by adding a chemical group to DNA. ...
  • Histone modification. DNA wraps around proteins called histones. ...
  • Non-coding RNA. Your DNA is used as instructions for making coding and non-coding RNA.

What is an example of epigenetic modification? ›

Epigenetic changes alter the physical structure of DNA. One example of an epigenetic change is DNA methylation — the addition of a methyl group, or a "chemical cap," to part of the DNA molecule, which prevents certain genes from being expressed. Another example is histone modification.

What is an example of epigenetic control? ›

Examples of epigenetic control are DNA methylation, histone deacetylation and mi-RNA expression. Methylation of several tumor suppressor gene promoters is responsible for their silencing and thus potentially sustain cancerogenesis. Similarly, histone deacetylation can lead to oncogene activation.

How can I improve my epigenetics? ›

While you should consult a health professional for advice specific to your needs, it has been shown that consuming adequate amounts of the following minerals is especially important for fueling epigenetic change: iron, zinc, magnesium, manganese, calcium, selenium, chromium and copper.

What is new limit epigenetic reprogramming? ›

NewLimit was founded to significantly extend healthy human healthspan. We are developing epigenetic reprogramming medicines to treat age-related diseases on our way to a more general use medicine to control aging itself. The core of our approach is rooted in epigenetic control of gene expression.

How do you reverse epigenetic aging? ›

Engaging in regular exercise, ideally at least 4 times per week for at least 20 minutes at a time, can improve your epigenetic age.


1. The Effects of Epigenetic Therapies on the Tumor and Host Immune System
2. Stephen Baylin, M.D. - Epigenetics
(Johns Hopkins Medicine)
3. Epigenetic Therapies Presentation
(International Journal of Clinical Practice)
4. Epigenetics in Mental Health
(Royal Talks)
5. Total Human Optimization: Optimizing Health Through Epigenetics & Lifestyle with Dr. Daniel Stickler
(Flow Research Collective)
6. 6 Successful Science Studies In Epigenetic Rejuvenation
(Reverse Aging Revolution)
Top Articles
Latest Posts
Article information

Author: Duncan Muller

Last Updated: 13/07/2023

Views: 5776

Rating: 4.9 / 5 (79 voted)

Reviews: 86% of readers found this page helpful

Author information

Name: Duncan Muller

Birthday: 1997-01-13

Address: Apt. 505 914 Phillip Crossroad, O'Konborough, NV 62411

Phone: +8555305800947

Job: Construction Agent

Hobby: Shopping, Table tennis, Snowboarding, Rafting, Motor sports, Homebrewing, Taxidermy

Introduction: My name is Duncan Muller, I am a enchanting, good, gentle, modern, tasty, nice, elegant person who loves writing and wants to share my knowledge and understanding with you.