Journal articles: 'Cancer epigenetics'

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Youness, Eman. "Overview on Epigenetics and Cancer." Clinical Medical Reviews and Reports 2, no. 3 (June 22, 2020): 01–06. http://dx.doi.org/10.31579/2690-8794/015.

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Epigenetics is considered as the science of hereditary phenotype which does not encompass amendment in the DNA. This occurs through chemical processes that modify the phenotype, without altering the genotype. A large number of studies showed that metabolic diseases are highly associated with epigenetic alterations suggesting that epigenetic factors may play a central role in cancer. Recent advancements in the rapidly evolving field of cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer including DNA methylation, histone modifications, nucleosome positioning and non-coding RNAs, specifically microRNA expression. Studies of the mechanism(s) of epigenetic regulation and its reversibility have resulted in the identification of novel targets that may be useful in developing new strategies for the prevention and treatment of cancer.

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Li, Jiaqiu, Hongchuan Jin, and Xian Wang. "Epigenetic Biomarkers: Potential Applications in Gastrointestinal Cancers." ISRN Gastroenterology 2014 (March 6, 2014): 1–10. http://dx.doi.org/10.1155/2014/464015.

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Genetics and epigenetics coregulate the cancer initiation and progression. Epigenetic mechanisms include DNA methylation, histone modification, chromatin remodeling, and noncoding RNAs. Aberrant epigenetic modifications play a fundamental role in the formation of gastrointestinal cancers. Advances in epigenetics offer a better understanding of the carcinogenesis and provide new insights into the discovery of biomarkers for diagnosis, and prognosis prediction of human cancers. This review aims to overview the epigenetic aberrance and the clinical applications as biomarkers in gastrointestinal cancers mainly gastric cancer and colorectal cancer.

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Pathak, Ayush, Sarthak Tomar, and Sujata Pathak. "Epigenetics and Cancer: A Comprehensive Review." Asian Pacific Journal of Cancer Biology 8, no. 1 (March 16, 2023): 75–89. http://dx.doi.org/10.31557/apjcb.2023.8.1.75-89.

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Cancer is a disease with extraordinary clinical significance, with much of medical research being devoted to it. Innumerable factors are relevant in fully understanding cancer but the epigenetic aspect stands out. Epigenetics is the study of changes, often germ-line, to the genome affecting the gene expression by silencing certain genes and modifying the gene expression. The three primary mechanisms for epigenetic changes are DNA methylation, histone modification and non-coding RNA (ncRNA) associated gene silencing. While epigenetics is a pivotal mechanism for the regular maintenance of a myriad of processes- including in cell differentiation and adaptability- aberrant epigenetic changes can lead to depreciated/altered gene function which may ultimately culminate in cancer. Consequently, the connection between epigenetics and cancer has been intensely studied over the past two decades and has generated substantial clinical data attesting to the efficacy of epigenetics as a viable approach to understand cancer progression or therapy. In this review, we look at the fundamental epigenetic principles, the changes in the epigenome which can often be a precursor to cancer, analyse the increasingly important role of epigenetics in decoding carcinogenesis, explore the latest advancements in use of epigenetics in cancer therapy and how the reversible nature of these epigenetic changes have changed the way we approach cancer therapy.

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Rahman, Md, HM Jamil, Naznin Akhtar, Rashedul Islam, Md Rana, SM AbdulAwal, and SM Asaduzzaman. "Cancer epigenetics and epigenetical therapy." Journal of Experimental and Integrative Medicine 6, no. 3 (2016): 143. http://dx.doi.org/10.5455/jeim.270616.rw.016.

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Chou, PoChung Jordan, Rebecca Mary Peter, Ahmad Shannar, Yuxin Pan, Parv Dushyant Dave, Jiawei Xu, Md Shahid Sarwar, and Ah-Ng Kong. "Epigenetics of Dietary Phytochemicals in Cancer Prevention." Cancer Journal 30, no. 5 (September 2024): 320–28. http://dx.doi.org/10.1097/ppo.0000000000000742.

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Abstract Cancer development takes 10 to 50 years, and epigenetics plays an important role. Recent evidence suggests that ~80% of human cancers are linked to environmental factors impinging upon genetics/epigenetics. Because advanced metastasized cancers are resistant to radiation/chemotherapeutic drugs, cancer prevention by relatively nontoxic “epigenetic modifiers” will be logical. Many dietary phytochemicals possess powerful antioxidant and anti-inflammatory properties that are hallmarks of cancer prevention. Dietary phytochemicals can regulate gene expression of the cellular genome via epigenetic mechanisms. In this review, we will summarize preclinical studies that demonstrate epigenetic mechanisms of dietary phytochemicals in skin, colorectal, and prostate cancer prevention. Key examples of the importance of epigenetic regulation in carcinogenesis include hypermethylation of the NRF2 promoter region in cancer cells, resulting in inhibition of NRF2-ARE signaling. Many dietary phytochemicals demethylate NRF2 promoter region and restore NRF2 signaling. Phytochemicals can also inhibit inflammatory responses via hypermethylation of inflammation-relevant genes to block gene expression. Altogether, dietary phytochemicals are excellent candidates for cancer prevention due to their low toxicity, potent antioxidant and anti-inflammatory properties, and powerful epigenetic effects in reversing procarcinogenic events.

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Maio, Michele. "Introduction: Cancer Epigenetics and Epigenetic Treatment of Cancer." Seminars in Oncology 32, no. 5 (October 2005): 435–36. http://dx.doi.org/10.1053/j.seminoncol.2005.08.001.

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Hatzimichael, Eleftheria, and Tim Crook. "Cancer Epigenetics: New Therapies and New Challenges." Journal of Drug Delivery 2013 (February 26, 2013): 1–9. http://dx.doi.org/10.1155/2013/529312.

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Cancer is nowadays considered to be both a genetic and an epigenetic disease. The most well studied epigenetic modification in humans is DNA methylation; however it becomes increasingly acknowledged that DNA methylation does not work alone, but rather is linked to other modifications, such as histone modifications. Epigenetic abnormalities are reversible and as a result novel therapies that work by reversing epigenetic effects are being increasingly explored. The biggest clinical impact of epigenetic modifying agents in neoplastic disorders thus far has been in haematological malignancies, and the efficacy of DNMT inhibitors and HDAC inhibitors in blood cancers clearly attests to the principle that therapeutic modification of the cancer cell epigenome can produce clinical benefit. This paper will discuss the most well studied epigenetic modifications and how these are linked to cancer, will give a brief overview of the clinical use of epigenetics as biomarkers, and will focus in more detail on epigenetic drugs and their use in solid and blood cancers.

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Kanwal, Rajnee, and Sanjay Gupta. "Epigenetics and cancer." Journal of Applied Physiology 109, no. 2 (August 2010): 598–605. http://dx.doi.org/10.1152/japplphysiol.00066.2010.

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Epigenetic modifications are central to many human diseases, including cancer. Traditionally, cancer has been viewed as a genetic disease, and it is now becoming apparent that the onset of cancer is preceded by epigenetic abnormalities. Investigators in the rapidly expanding field of epigenetics have documented extensive genomic reprogramming in cancer cells, including methylation of DNA, chemical modification of the histone proteins, and RNA-dependent regulation. Recognizing that carcinogenesis involves both genetic and epigenetic alterations has led to a better understanding of the molecular pathways that govern the development of cancer and to improvements in diagnosing and predicting the outcome of various types of cancer. Studies of the mechanism(s) of epigenetic regulation and its reversibility have resulted in the identification of novel targets that may be useful in developing new strategies for the prevention and treatment of cancer.

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van Engeland, Manon, Sarah Derks, Kim M. Smits, Gerrit A. Meijer, and James G. Herman. "Colorectal Cancer Epigenetics: Complex Simplicity." Journal of Clinical Oncology 29, no. 10 (April 1, 2011): 1382–91. http://dx.doi.org/10.1200/jco.2010.28.2319.

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Colorectal cancer (CRC) has predominantly been considered a genetic disease, characterized by sequential accumulation of genetic alterations. Growing evidence indicates that epigenetic alterations add an additional layer of complexity to the pathogenesis of CRC, and characterize a subgroup of colorectal cancers with a distinct etiology and prognosis. Epigenetic dysregulation in colorectal cancer is organized at multiple levels, involving DNA methylation, histone modifications, nucleosomal occupancy and remodeling, chromatin looping, and noncoding RNAs. Interactions between these processes and complex associations with genetic alterations have recently been unraveled. It appears that CRC epigenetics will be the paradigm for multistep carcinogenesis, as CRC genetics has been for the past three decades. This review integrates recent data on epigenetic regulation of gene expression in CRC and describes how the understanding of these processes will alter the management of CRC.

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Mir, Snober Shabnam, Uzma Afaq, Adria Hasan, Suroor Fatima Rizvi, and Sana Parveen. "Novel Insights into Epigenetic Control of Autophagy in Cancer." OBM Genetics 06, no. 04 (November 8, 2022): 1–45. http://dx.doi.org/10.21926/obm.genet.2204170.

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The autophagy mechanism recycles the damaged and long-standing macromolecular substrates and thus maintains cellular homeostatic and proteostatic conditions. Autophagy can be an unavoidable target in cancer therapy because its deregulation leads to cancer formation and progression. Cancer can be controlled by regulating autophagy at different genetic, epigenetic, and post-translational levels. Epigenetics refers to the heritable phenotypic changes that affect gene activity without changing the sequence. Modern biology employs epigenetic alterations as molecular tools to detect and treat a wide range of disorders, including cancer. However, modulating autophagy at the epigenetic level may inhibit cancer growth and progression. Epigenetics-targeting drugs involved in preclinical and clinical trials may trigger antitumor immunity. Here, we have reviewed some experimental evidence in which epigenetics have been used to control deregulated autophagy in cancerous diseases. Furthermore, we also reviewed some current clinical trials of epigenetic therapy against cancer. We hope that this information can be utilized in the near future to treat and overcome cancer.

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Katu, Amina H. "The Role of Epigenetics in Disease Development." RESEARCH INVENTION JOURNAL OF PUBLIC HEALTH AND PHARMACY 3, no. 2 (September 1, 2024): 41–44. http://dx.doi.org/10.59298/rijpp/2024/3234144.

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Epigenetics, the study of heritable changes in gene expression without alterations to the DNA sequence, plays a critical role in the development of various diseases. These epigenetic mechanisms, which include DNA methylation, histone modifications, and non-coding RNA-mediated gene silencing, regulate essential cellular processes such as differentiation, development, and tissue-specific gene expression. Environmental factors and lifestyle choices influence these epigenetic changes, often leading to disease by modifying transcriptional profiles. This paper discusses the role of epigenetics in the onset and progression of diseases like cancer and cardiovascular disorders, highlighting the potential of epigenetic biomarkers for early diagnosis and the promise of epigenetic therapies. Understanding the intricate relationship between epigenetics and disease mechanisms can open new avenues for personalized treatment strategies. Keywords: Epigenetics, DNA methylation, histone modification, disease development, cancer, cardiovascular diseases

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Zhang, Xiaolin, Zhen Dong, and Hongjuan Cui. "Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer." Biomolecules 11, no. 10 (September 25, 2021): 1406. http://dx.doi.org/10.3390/biom11101406.

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Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy.

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Liu, Yu’e, Chao Chen, Xinye Wang, Yihong Sun, Jin Zhang, Juxiang Chen, and Yufeng Shi. "An Epigenetic Role of Mitochondria in Cancer." Cells 11, no. 16 (August 13, 2022): 2518. http://dx.doi.org/10.3390/cells11162518.

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Mitochondria are not only the main energy supplier but are also the cell metabolic center regulating multiple key metaborates that play pivotal roles in epigenetics regulation. These metabolites include acetyl-CoA, α-ketoglutarate (α-KG), S-adenosyl methionine (SAM), NAD+, and O-linked beta-N-acetylglucosamine (O-GlcNAc), which are the main substrates for DNA methylation and histone post-translation modifications, essential for gene transcriptional regulation and cell fate determination. Tumorigenesis is attributed to many factors, including gene mutations and tumor microenvironment. Mitochondria and epigenetics play essential roles in tumor initiation, evolution, metastasis, and recurrence. Targeting mitochondrial metabolism and epigenetics are promising therapeutic strategies for tumor treatment. In this review, we summarize the roles of mitochondria in key metabolites required for epigenetics modification and in cell fate regulation and discuss the current strategy in cancer therapies via targeting epigenetic modifiers and related enzymes in metabolic regulation. This review is an important contribution to the understanding of the current metabolic-epigenetic-tumorigenesis concept.

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Taby, Rodolphe, and Jean-Pierre J. Issa. "Cancer Epigenetics." CA: A Cancer Journal for Clinicians 60, no. 6 (October 20, 2010): 376–92. http://dx.doi.org/10.3322/caac.20085.

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Momparler, Richard L. "Cancer epigenetics." Oncogene 22, no. 42 (September 2003): 6479–83. http://dx.doi.org/10.1038/sj.onc.1206774.

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Laird, Peter W. "Cancer epigenetics." Human Molecular Genetics 14, suppl_1 (April 15, 2005): R65—R76. http://dx.doi.org/10.1093/hmg/ddi113.

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Ahmed, Hafiz Ghulam Muhu-Din, Aziz Ullah, Abdul Malik, and Babar Islam. "Review; Role of epigenetics in cancer." World Journal of Biology and Biotechnology 5, no. 2 (July 12, 2020): 51. http://dx.doi.org/10.33865/wjb.005.02.0304.

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The epigenetic alterations are central to numerous human diseases, counting cancer. Typically, cancer has been seen as a hereditary infection, and it is presently getting to be clear that the onset of cancer is gone before by epigenetic anomalies. Examiners within the quickly growing field of epigenetics have recorded broad genomic reconstructing in cancer cells, counting methylation of deoxyribonucleic acid (DNA), chemical alteration of the histone proteins, and RNA-dependent control. Recognizing that carcinogenesis includes both hereditary and epigenetic alterations have driven to distant better an understanding of the molecular pathways that oversee the advancement of cancer and to changes in diagnosing and foreseeing the result of different sorts of cancer. Thinks about of the mechanism (s) of epigenetic control and its reversibility have brought about within the recognizable proof of novel targets which will be valuable in creating unused methodologies for the avoidance and treatment of cancer. Cancer is the appearance of both hereditary and epigenetic adjustments. In spite of the fact that cancer start and movement is overwhelmingly driven by procured hereditary modifications, it is getting to be clear that microenvironment mediated epigenetic annoyances play critical parts in neoplastic advancement. Epigenetics is characterized as heritable changes in quality expression, movement and expression that happen without change in DNA arrangements but which are adequately capable to control the flow of quality expression. The key forms that are mindful for epigenetic control are DNA methylation, adjustments in chromatin (covalent adjustment of center histones), nucleosome situating (physical modification), and post-transcriptional quality direction by noncoding RNA (micro-RNAs). A number of well characterized epigenetic adjustments are connected to distorted quality capacities and modified designs of quality expression that play basic parts within the patho-biology of cancer

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Sachdev, Sanpreet Singh, and Sonali Kohli. "Epigenetics: Unraveling the molecular threads of aging and dermal cancer." IP Indian Journal of Clinical and Experimental Dermatology 10, no. 1 (March 15, 2024): 103–6. http://dx.doi.org/10.18231/j.ijced.2024.020.

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Epigenetics, the study of heritable alterations in gene expression without changes to the DNA sequence, plays a pivotal role in understanding the complex processes of aging and cancer. This manuscript delves into the intricate world of epigenetics, exploring how it influences the pathophysiology of aging and aging-related diseases, with a particular focus on cancer. We discuss the mechanisms of epigenetic regulation, the interplay between genetic and epigenetic alterations, and the potential implications for diagnosis and drug discovery.

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Sengupta, Deepanwita. "Epigenetic Drugs - The Future of Cancer Therapy." Annals of Experimental and Molecular Biology 2, no. 1 (2019): 1–2. http://dx.doi.org/10.23880/aemb-16000106.

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Epigenetics refers to any alteration in gene expression that occurs without affecting the underlying DNA sequence. Epigenetic mechanisms regulate the accessibility of chromatin to transcription factors by promoting nucleosomal rearrangement via the addition or removal of acetyl or/and methyl groups to histones. Nucleosomes are basic units of chromosomes comprising of 147 base pairs of DNA wrapped around an octamer of histone proteins

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Bassal, Mahmoud Adel. "The Interplay between Dysregulated Metabolism and Epigenetics in Cancer." Biomolecules 13, no. 6 (June 5, 2023): 944. http://dx.doi.org/10.3390/biom13060944.

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Cellular metabolism (or energetics) and epigenetics are tightly coupled cellular processes. It is arguable that of all the described cancer hallmarks, dysregulated cellular energetics and epigenetics are the most tightly coregulated. Cellular metabolic states regulate and drive epigenetic changes while also being capable of influencing, if not driving, epigenetic reprogramming. Conversely, epigenetic changes can drive altered and compensatory metabolic states. Cancer cells meticulously modify and control each of these two linked cellular processes in order to maintain their tumorigenic potential and capacity. This review aims to explore the interplay between these two processes and discuss how each affects the other, driving and enhancing tumorigenic states in certain contexts.

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Pardo, Juan C., Vicenç Ruiz de Porras, Joan Gil, Albert Font, Manel Puig-Domingo, and Mireia Jordà. "Lipid Metabolism and Epigenetics Crosstalk in Prostate Cancer." Nutrients 14, no. 4 (February 18, 2022): 851. http://dx.doi.org/10.3390/nu14040851.

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Prostate cancer (PCa) is the most commonly diagnosed malignant neoplasm in men in the Western world. Localized low-risk PCa has an excellent prognosis thanks to effective local treatments; however, despite the incorporation of new therapeutic strategies, metastatic PCa remains incurable mainly due to disease heterogeneity and the development of resistance to therapy. The mechanisms underlying PCa progression and therapy resistance are multiple and include metabolic reprogramming, especially in relation to lipid metabolism, as well as epigenetic remodelling, both of which enable cancer cells to adapt to dynamic changes in the tumour. Interestingly, metabolism and epigenetics are interconnected. Metabolism can regulate epigenetics through the direct influence of metabolites on epigenetic processes, while epigenetics can control metabolism by directly or indirectly regulating the expression of metabolic genes. Moreover, epidemiological studies suggest an association between a high-fat diet, which can alter the availability of metabolites, and PCa progression. Here, we review the alterations of lipid metabolism and epigenetics in PCa, before focusing on the mechanisms that connect them. We also discuss the influence of diet in this scenario. This information may help to identify prognostic and predictive biomarkers as well as targetable vulnerabilities.

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Albany, Costantine, Ajjai S. Alva, Ana M. Aparicio, Rakesh Singal, Sarvari Yellapragada, Guru Sonpavde, and Noah M. Hahn. "Epigenetics in Prostate Cancer." Prostate Cancer 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/580318.

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Prostate cancer (PC) is the most commonly diagnosed nonskin malignancy and the second most common cause of cancer death among men in the United States. Epigenetics is the study of heritable changes in gene expression caused by mechanisms other than changes in the underlying DNA sequences. Two common epigenetic mechanisms, DNA methylation and histone modification, have demonstrated critical roles in prostate cancer growth and metastasis. DNA hypermethylation of cytosine-guanine (CpG) rich sequence islands within gene promoter regions is widespread during neoplastic transformation of prostate cells, suggesting that treatment-induced restoration of a “normal” epigenome could be clinically beneficial. Histone modification leads to altered tumor gene function by changing chromosome structure and the level of gene transcription. The reversibility of epigenetic aberrations and restoration of tumor suppression gene function have made them attractive targets for prostate cancer treatment with modulators that demethylate DNA and inhibit histone deacetylases.

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Lee, Dong Yeul, Talha Salahuddin, and Jabed Iqbal. "Lysine-Specific Demethylase 1 (LSD1)-Mediated Epigenetic Modification of Immunogenicity and Immunomodulatory Effects in Breast Cancers." Current Oncology 30, no. 2 (February 9, 2023): 2127–43. http://dx.doi.org/10.3390/curroncol30020164.

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Tumor evolution to evade immune surveillance is a hallmark of carcinogenesis, and the modulation of tumor immunogenicity has been a challenge to present therapeutic responses in immunotherapies alone for numerous cancers. By altering the cell phenotype and reshaping the tumor microenvironment, epigenetic modifications enable tumor cells to overcome immune surveillance as a mechanism of cancer progression and immunotherapy resistance. Demethylase enzymatic activity of lysine-specific demethylase 1 (LSD1), a histone demethylase first identified in 2004, plays a pivotal role in the vast cellular processes of cancer. While FDA-approved indications for epigenetic therapies are limited to hematological malignancies, it is imperative to understand how epigenetic machinery can be targeted to prime immunotherapy responses in breast cancers. In this review, we discuss the potential roles of epigenetics and demethylating agent LSD1 as a potent new cancer management strategy to combat the current challenges of breast cancers, which have presented modest efficacy to immune checkpoint inhibitors till date. Additionally, we describe the combined use of LSD1-specific inhibitors and immune checkpoint inhibitors in existing breast cancer preclinical and clinical trials that elicits a robust immune response and benefit. Overall, the promising results observed in LSD1-targeting therapies signify the central role of epigenetics as a potential novel strategy to overcome resistance commonly seen in immunotherapies.

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MacLennan, Signe A., and Marco A. Marra. "Oncogenic Viruses and the Epigenome: How Viruses Hijack Epigenetic Mechanisms to Drive Cancer." International Journal of Molecular Sciences 24, no. 11 (May 31, 2023): 9543. http://dx.doi.org/10.3390/ijms24119543.

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Globally, viral infections substantially contribute to cancer development. Oncogenic viruses are taxonomically heterogeneous and drive cancers using diverse strategies, including epigenomic dysregulation. Here, we discuss how oncogenic viruses disrupt epigenetic homeostasis to drive cancer and focus on how virally mediated dysregulation of host and viral epigenomes impacts the hallmarks of cancer. To illustrate the relationship between epigenetics and viral life cycles, we describe how epigenetic changes facilitate the human papillomavirus (HPV) life cycle and how changes to this process can spur malignancy. We also highlight the clinical impact of virally mediated epigenetic changes on cancer diagnosis, prognosis, and treatment.

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Li, Yinglu, Zhiming Li, and Wei-Guo Zhu. "Molecular Mechanisms of Epigenetic Regulators as Activatable Targets in Cancer Theranostics." Current Medicinal Chemistry 26, no. 8 (May 16, 2019): 1328–50. http://dx.doi.org/10.2174/0929867324666170921101947.

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Epigenetics is defined as somatically inheritable changes that are not accompanied by alterations in DNA sequence. Epigenetics encompasses DNA methylation, covalent histone modifications, non-coding RNA as well as nucleosome remodeling. Notably, abnormal epigenetic changes play a critical role in cancer development including malignant transformation, metastasis, prognosis, drug resistance and tumor recurrence, which can provide effective targets for cancer prognosis, diagnosis and therapy. Understanding these changes provide effective means for cancer diagnosis and druggable targets for better clinical applications. Histone modifications and related enzymes have been found to correlate well with cancer incidence and prognosis in recent years. Dysregulated expression or mutation of histone modification enzymes and histone modification status abnormalities have been considered to play essential roles in tumorigenesis and clinical outcomes of cancer treatment. Some of the histone modification inhibitors have been extensively employed in clinical practice and many others are still under laboratory research or pre-clinical assessment. Here we summarize the important roles of epigenetics, especially histone modifications in cancer diagnostics and therapeutics, and also discuss the developmental implications of activatable epigenetic targets in cancer theranostics.

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Hoque, Majedul, Kazi Emon, Kazi Emon Md Aktaruzzaman, Md Nahid Hasan, Arafath Jubayer, and Mohammad Sabbir Hossain. "A Mini Review on Cancer Epigenetics." Middle East Research Journal of Medical Sciences 3, no. 02 (October 23, 2023): 28–38. http://dx.doi.org/10.36348/merjms.2023.v03i02.002.

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Cancer epigenetics is the study of epigenetic changes to cancer cells' DNA that don't involve a change in the nucleotide sequence but instead affect how the genetic code is expressed. The complicated disease of cancer is brought on by genetic and epigenetic changes in the regulation of cell division. Our knowledge of the molecular etiology of cancer has substantially advanced and also the discoveries in the fields of cancer genomics and epigenomics, which have improved our comprehension of the development and evolution of tumorigenic processes. The interaction between genetic and epigenetic mutations and their interaction with environmental factors, including our microbiome, that influences cellular metabolism and proliferation rates, must therefore be taken into account in any modern perspective on cancer research. Future genetic and epigenetic therapeutics as well as diagnostics and prognosis will all benefit from the integration and increased understanding of these processes. Here, we tried to give a general summary of the disrupted epigenetic processes in cancer and how they affect the beginning and development of the illness. In conclusion, we talked about how advanced experimental methods and computational tools, such as fresh methods for utilizing enormous data sets, could help us better understand and cure cancer.

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Tarashi, Samira, Sara Ahmadi Badi, Arfa Moshiri, Nayereh Ebrahimzadeh, Abolfazl Fateh, Farzam Vaziri, Hossein Aazami, Seyed Davar Siadat, and Andrea Fuso. "The inter-talk between Mycobacterium tuberculosis and the epigenetic mechanisms." Epigenomics 12, no. 5 (March 2020): 455–69. http://dx.doi.org/10.2217/epi-2019-0187.

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Epigenetics regulate gene function without any alteration in the DNA sequence. The epigenetics represent one of the most important regulators in different cellular processes and have initially been developed in microorganisms as a protective strategy. The evaluation of the epigenetic mechanisms is also important in achieving an efficient control strategy in tuberculosis (TB). TB is one of the most significant epidemiological concerns in human history. Despite several in vivo and in vitro studies that have evaluated different epigenetic modifications in TB, many aspects of the association between epigenetics and TB are not fully understood. The current paper is aimed at reviewing our knowledge on histone modifications and DNA methylation modifications, as well as miRNAs regulation in TB.

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Vinokurova, Svetlana. "Epigenetics of Virus-Induced Tumors: Perspectives for Therapeutic Targeting." Current Pharmaceutical Design 23, no. 32 (December 21, 2017): 4842–61. http://dx.doi.org/10.2174/1381612823666170822100627.

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About 15–20% of human cancers worldwide have viral etiology. Seven human DNA and RNA viruses are accepted to be oncogenic viruses or oncoviruses and contribute to the development of various cancer types. Human oncoviruses have developed multiple molecular mechanisms to interfere with specific cellular pathways to promote viral replication and viral life cycle maintenance in the host. Despite the diversity of oncogenic viruses, they use similar strategies for cancer development. Viral oncoproteins and viral non-coding RNAs are the key factors that can affect multiple cellular processes on both genetic and epigenetic levels. Epigenetics research allows better understanding of the complex interplay between oncoviruses and the host cells. This review highlights the importance of epigenetic reprogramming for virus-induced carcinogenesis. Recent progress in the development of pharmacological tools for targeting epigenetic mechanisms opens new perspectives for modulation of virus/host interaction and intervention of virus-induced cancer. Several clinical trials have been carried out or are on-going involving epigenetic drugs not only as single therapeutic but also in combination with other targeted agents against various virus-induced cancers.

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Liu, Na, Rongtong Zhao, Yue Ma, Dongyuan Wang, Chen Yan, Dongxian Zhou, Feng Yin, and Zigang Li. "The Development of Epigenetics and Related Inhibitors for Targeted Drug Design in Cancer Therapy." Current Topics in Medicinal Chemistry 18, no. 28 (February 12, 2019): 2380–94. http://dx.doi.org/10.2174/1568026618666181115092623.

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Epigenetics process is the heritable change in gene function that does not involve changes in the DNA sequence. Until now, several types of epigenetic mechanisms have been characterized, including DNA methylation, histone modification (acetylation, methylation, etc.), nucleosome remodeling, and noncoding RNAs. With the biological investigations of these modifiers, some of them are identified as promoters in the process of various diseases, such as cancer, cardiovascular disease and virus infection. Epigenetic changes may serve as potential “first hits” for tumorigenesis. Hence, targeting epigenetic modifiers is being considered as a promising way for disease treatment. To date, six agents in two epigenetic target classes (DNMT and HDAC) have been approved by the US Food and Drug Administration (FDA). Most of these drugs are applied in leukemia, lymphoma therapy, or are combined with other drugs for the treatment of solid tumor. Due to the rapid development of epigenetics and epigenetics targeted drugs, it is becoming an emerging area in targeted drug design.

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Roalsø, Marcus T. T., Øyvind H. Hald, Marina Alexeeva, and Kjetil Søreide. "Emerging Role of Epigenetic Alterations as Biomarkers and Novel Targets for Treatments in Pancreatic Ductal Adenocarcinoma." Cancers 14, no. 3 (January 21, 2022): 546. http://dx.doi.org/10.3390/cancers14030546.

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Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited treatment options. Emerging evidence shows that epigenetic alterations are present in PDAC. The changes are potentially reversible and therefore promising therapeutic targets. Epigenetic aberrations also influence the tumor microenvironment with the potential to modulate and possibly enhance immune-based treatments. Epigenetic marks can also serve as diagnostic screening tools, as epigenetic changes occur at early stages of the disease. Further, epigenetics can be used in prognostication. The field is evolving, and this review seeks to provide an updated overview of the emerging role of epigenetics in the diagnosis, treatment, and prognostication of PDAC.

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Esteller, Manel. "Epigenetics in Cancer." New England Journal of Medicine 358, no. 11 (March 13, 2008): 1148–59. http://dx.doi.org/10.1056/nejmra072067.

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Ahmad, Aamir. "Editorial: Cancer Epigenetics." Current Cancer Drug Targets 18, no. 1 (December 8, 2017): 3–4. http://dx.doi.org/10.2174/156800961801171208144307.

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Lund, A. H. "Epigenetics and cancer." Genes & Development 18, no. 19 (September 15, 2004): 2315–35. http://dx.doi.org/10.1101/gad.1232504.

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Verma, Mukesh, Padma Maruvada, and Sudhir Srivastava. "Epigenetics and Cancer." Critical Reviews in Clinical Laboratory Sciences 41, no. 5-6 (January 2004): 585–607. http://dx.doi.org/10.1080/10408360490516922.

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Esteller, M. "Cancer pharmaco-epigenetics." Clinica Chimica Acta 493 (June 2019): S761—S762. http://dx.doi.org/10.1016/j.cca.2019.03.1353.

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Bae, Jae‐Bum, and Young‐Joon Kim. "Cancer and epigenetics." Animal Cells and Systems 12, no. 3 (January 2008): 117–25. http://dx.doi.org/10.1080/19768354.2008.9647164.

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Sharma, S., T. K. Kelly, and P. A. Jones. "Epigenetics in cancer." Carcinogenesis 31, no. 1 (September 13, 2009): 27–36. http://dx.doi.org/10.1093/carcin/bgp220.

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Aydin, Cansu, and Rasime Kalkan. "Cancer Treatment: An Epigenetic View." Global Medical Genetics 07, no. 01 (June 2020): 003–7. http://dx.doi.org/10.1055/s-0040-1713610.

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AbstractCancer can be identified as an uncontrolled growth and reproduction of cell. Accumulation of genetic aberrations (mutations of oncogenes and tumor-suppressor genes and epigenetic modifications) is one of the characteristics of cancer cell. Increasing number of studies highlighted importance of the epigenetic alterations in cancer treatment and prognosis. Now, cancer epigenetics have a huge importance for developing novel biomarkers and therapeutic target for cancer. In this review, we will provide a summary of the major epigenetic changes involved in cancer and preclinical results of epigenetic therapeutics.

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Słowikowski, Bartosz, Wojciech Owecki, Jan Jeske, Michał Jezierski, Michał Draguła, Ulyana Goutor, Paweł P. Jagodziński, Wojciech Kozubski, and Jolanta Dorszewska. "Epigenetics and the neurodegenerative process." Epigenomics 16, no. 7 (April 2024): 473–91. http://dx.doi.org/10.2217/epi-2023-0416.

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Neurological diseases are multifactorial, genetic and environmental. Environmental factors such as diet, physical activity and emotional state are epigenetic factors. Environmental markers are responsible for epigenetic modifications. The effect of epigenetic changes is increased inflammation of the nervous system and neuronal damage. In recent years, it has been shown that epigenetic changes may cause an increased risk of neurological disorders but, currently, the relationship between epigenetic modifications and neurodegeneration remains unclear. This review summarizes current knowledge about neurological disorders caused by epigenetic changes in diseases such as Alzheimer's disease, Parkinson's disease, stroke and epilepsy. Advances in epigenetic techniques may be key to understanding the epigenetics of central changes in neurological diseases.

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Bhattacharjee, Dipanjan, Smita Shenoy, and Kurady Laxminarayana Bairy. "DNA Methylation and Chromatin Remodeling: The Blueprint of Cancer Epigenetics." Scientifica 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/6072357.

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Epigenetics deals with the interactions between genes and the immediate cellular environment. These interactions go a long way in shaping up each and every person’s individuality. Further, reversibility of epigenetic interactions may offer a dynamic control over the expression of various critical genes. Thus, tweaking the epigenetic machinery may help cause or cure diseases, especially cancer. Therefore, cancer epigenetics, especially at a molecular level, needs to be scrutinised closely, as it could potentially serve as the future pharmaceutical goldmine against neoplastic diseases. However, in view of its rapidly enlarging scope of application, it has become difficult to keep abreast of scientific information coming out of various epigenetic studies directed against cancer. Using this review, we have attempted to shed light on two of the most important mechanisms implicated in cancer, that is, DNA (deoxyribonucleic acid) methylation and histone modifications, and their place in cancer pathogenesis. Further, we have attempted to take stock of the new epigenetic drugs that have emerged onto the market as well as those in the pipeline that offer hope in mankind’s fight against cancer.

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Papakonstantinou, Eleni, Konstantina Dragoumani, George P. Chrousos, and Dimitrios Vlachakis. "Exosomal Epigenetics." EMBnet.journal 29 (May 22, 2024): e1049. http://dx.doi.org/10.14806/ej.29.0.1049.

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Epigenetics is the study of heritable changes in gene expression that occur without changes to the underlying DNA sequence. Epigenetic modifications can include DNA methylation, histone modifications, and non-coding RNAs, among others. These modifications can influence the expression of genes by altering the way DNA is packaged and accessed by transcriptional machinery, thereby affecting cellular function and behavior. Epigenetic modifications can be influenced by a variety of factors, including environmental exposures, lifestyle factors, and aging, whilst abnormal epigenetic modifications have been implicated in a range of diseases, including cancer, neurodegenerative disorders, and cardiovascular disease. The study of epigenetics has the potential to provide new insights into the mechanisms of disease and could lead to the development of new diagnostic and therapeutic strategies. Exosomes can transfer epigenetic information to recipient cells, thereby influencing various physiological and pathological processes, and the identification of specific epigenetic modifications that are associated with a particular disease could lead to the development of targeted therapies that restore normal gene expression patterns. In recent years, the emerging role of exosomal epigenetics in human breast milk, highlighting its significance in infant nutrition and immune development. Milk exosomes are shown to carry epigenetic regulators, including miRNAs and long non-coding RNAs, which can modulate gene expression in recipient cells. These epigenetic modifications mediated by milk exosomal RNAs have implications for the development of the gastrointestinal tract, immune system, and metabolic processes in infants.

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LaBarge, Mark A., E. Lorena Mora-Blanco, Susan Samson, and Masaru Miyano. "Breast Cancer beyond the Age of Mutation." Gerontology 62, no. 4 (November 6, 2015): 434–42. http://dx.doi.org/10.1159/000441030.

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Age is the greatest risk factor for breast cancer, but the reasons underlying this association are unclear. While there is undeniably a genetic component to all cancers, the accumulation of mutations with age is insufficient to explain the age-dependent increase in breast cancer incidence. In this viewpoint, we propose a multilevel framework to better understand the respective roles played by somatic mutation, microenvironment, and epigenetics making women more susceptible to breast cancer with age. The process of aging is associated with gradual breast tissue changes that not only corrupt the tumor-suppressive activity of normal tissue but also impose age-specific epigenetic changes that alter gene expression, thus reinforcing cellular phenotypes that are associated with a continuum of age-related tissue microenvironments. The evidence discussed here suggests that while the riddle of whether epigenetics drives microenvironmental changes, or whether changes in the microenvironment alter heritable cellular memory has not been solved, a path has been cleared enabling functional analysis leading to the prediction of key nodes in the network that link the microenvironment with the epigenome. The hypothesis that the accumulation of somatic mutations with age drives the age-related increase in breast cancer incidence, if correct, has a somewhat nihilistic conclusion, namely that cancers will be impossible to avoid. Alternatively, if microenvironment-driven epigenetic changes are the key to explaining susceptibility to age-related breast cancers, then there is hope that primary prevention is possible because epigenomes are relatively malleable.

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Pandkar, Madhura R., and Sanjeev Shukla. "Epigenetics and alternative splicing in cancer: old enemies, new perspectives." Biochemical Journal 481, no. 21 (October 18, 2024): 1497–518. http://dx.doi.org/10.1042/bcj20240221.

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In recent years, significant strides in both conceptual understanding and technological capabilities have bolstered our comprehension of the factors underpinning cancer initiation and progression. While substantial insights have unraveled the molecular mechanisms driving carcinogenesis, there has been an overshadowing of the critical contribution made by epigenetic pathways, which works in concert with genetics. Mounting evidence demonstrates cancer as a complex interplay between genetics and epigenetics. Notably, epigenetic elements play a pivotal role in governing alternative pre-mRNA splicing, a primary contributor to protein diversity. In this review, we have provided detailed insights into the bidirectional communication between epigenetic modifiers and alternative splicing, providing examples of specific genes and isoforms affected. Notably, succinct discussion on targeting epigenetic regulators and the potential of the emerging field of epigenome editing to modulate splicing patterns is also presented. In summary, this review offers valuable insights into the intricate interplay between epigenetics and alternative splicing in cancer, paving the way for novel approaches to understanding and targeting this critical process.

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Tan, Wan Ying, Snigdha Nagabhyrava, Olivia Ang-Olson, Paromita Das, Luisa Ladel, Bethsebie Sailo, Linda He, Anup Sharma, and Nita Ahuja. "Translation of Epigenetics in Cell-Free DNA Liquid Biopsy Technology and Precision Oncology." Current Issues in Molecular Biology 46, no. 7 (June 27, 2024): 6533–65. http://dx.doi.org/10.3390/cimb46070390.

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Technological advancements in cell-free DNA (cfDNA) liquid biopsy have triggered exponential growth in numerous clinical applications. While cfDNA-based liquid biopsy has made significant strides in personalizing cancer treatment, the exploration and translation of epigenetics in liquid biopsy to clinical practice is still nascent. This comprehensive review seeks to provide a broad yet in-depth narrative of the present status of epigenetics in cfDNA liquid biopsy and its associated challenges. It highlights the potential of epigenetics in cfDNA liquid biopsy technologies with the hopes of enhancing its clinical translation. The momentum of cfDNA liquid biopsy technologies in recent years has propelled epigenetics to the forefront of molecular biology. We have only begun to reveal the true potential of epigenetics in both our understanding of disease and leveraging epigenetics in the diagnostic and therapeutic domains. Recent clinical applications of epigenetics-based cfDNA liquid biopsy revolve around DNA methylation in screening and early cancer detection, leading to the development of multi-cancer early detection tests and the capability to pinpoint tissues of origin. The clinical application of epigenetics in cfDNA liquid biopsy in minimal residual disease, monitoring, and surveillance are at their initial stages. A notable advancement in fragmentation patterns analysis has created a new avenue for epigenetic biomarkers. However, the widespread application of cfDNA liquid biopsy has many challenges, including biomarker sensitivity, specificity, logistics including infrastructure and personnel, data processing, handling, results interpretation, accessibility, and cost effectiveness. Exploring and translating epigenetics in cfDNA liquid biopsy technology can transform our understanding and perception of cancer prevention and management. cfDNA liquid biopsy has great potential in precision oncology to revolutionize conventional ways of early cancer detection, monitoring residual disease, treatment response, surveillance, and drug development. Adapting the implementation of liquid biopsy workflow to the local policy worldwide and developing point-of-care testing holds great potential to overcome global cancer disparity and improve cancer outcomes.

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Agarwal, Avarna, and Prasanta Padhan. "Understanding epigenetics in health and human diseases – An overview." Journal of Integrative Medicine and Research 2, no. 4 (October 2024): 215–18. http://dx.doi.org/10.4103/jimr.jimr_54_24.

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Abstract: Epigenetics, the study of heritable changes in gene expression without alterations to the DNA sequence, is crucial for the complex interplay of genetic and environmental factors influencing human health. This overview traces the historical evolution of epigenetics, from early conceptualizations by Valentin Haecker and Conrad Waddington to modern insights such as epigenetic editing. Key mechanisms such as DNA methylation, histone modifications, and noncoding RNAs are explored, highlighting their roles in various diseases including cancer, cardiovascular conditions, neurodegenerative disorders, autoimmune diseases, and metabolic disorders. The influence of environmental factors on epigenetic plasticity underscores the importance of lifestyle choices in health outcomes. Promising therapeutic strategies using epigenetics pave the way for personalized medicine. This comprehensive review emphasizes the need for an integrative approach to health that considers the dynamic relationship between genetics, environment, and epigenetics.

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Capparelli, Rosanna, and Domenico Iannelli. "Epigenetics and Helicobacter pylori." International Journal of Molecular Sciences 23, no. 3 (February 3, 2022): 1759. http://dx.doi.org/10.3390/ijms23031759.

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Epigenetics regulates gene expression, cell type development during differentiation, and the cell response to environmental stimuli. To survive, bacteria need to evade the host immune response. Bacteria, including Helicobacter pylori (Hp), reach this target epigenetically, altering the chromatin of the host cells, in addition to several more approaches, such as DNA mutation and recombination. This review shows that Hp prevalently silences the genes of the human gastric mucosa by DNA methylation. Epigenetics includes different mechanisms. However, DNA methylation persists after DNA replication and therefore is frequently associated with the inheritance of repressed genes. Chromatin modification can be transmitted to daughter cells leading to heritable changes in gene expression. Aberrant epigenetic alteration of the gastric mucosa DNA remains the principal cause of gastric cancer. Numerous methylated genes have been found in cancer as well as in precancerous lesions of Hp-infected patients. These methylated genes inactivate tumor-suppressor genes. It is time for us to complain about our genetic and epigenetic makeups for our diseases.

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Wolffe, Alan P., and Marjori A. Matzke. "Epigenetics: Regulation Through Repression." Science 286, no. 5439 (October 15, 1999): 481–86. http://dx.doi.org/10.1126/science.286.5439.481.

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Epigenetics is the study of heritable changes in gene expression that occur without a change in DNA sequence. Epigenetic phenomena have major economic and medical relevance, and several, such as imprinting and paramutation, violate Mendelian principles. Recent discoveries link the recognition of nucleic acid sequence homology to the targeting of DNA methylation, chromosome remodeling, and RNA turnover. Although epigenetic mechanisms help to protect cells from parasitic elements, this defense can complicate the genetic manipulation of plants and animals. Essential for normal development, epigenetic controls become misdirected in cancer cells and other human disease syndromes.

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Schulz, Wolfgang A., and Karina D. Sørensen. "Epigenetics of Urological Cancers." International Journal of Molecular Sciences 20, no. 19 (September 26, 2019): 4775. http://dx.doi.org/10.3390/ijms20194775.

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The major urological cancers comprise prostate adenocarcinoma, urinary bladder (or upper urinary tract) carcinoma, renal cell carcinoma, testicular cancer and penile carcinoma, in this order of incidence, each with various histological and molecular subtypes [...]

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Dogan, Fatma, and Nicholas R. Forsyth. "Telomerase Regulation: A Role for Epigenetics." Cancers 13, no. 6 (March 10, 2021): 1213. http://dx.doi.org/10.3390/cancers13061213.

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Telomerase was first described by Greider and Blackburn in 1984, a discovery ultimately recognized by the Nobel Prize committee in 2009. The three decades following on from its discovery have been accompanied by an increased understanding of the fundamental mechanisms of telomerase activity, and its role in telomere biology. Telomerase has a clearly defined role in telomere length maintenance and an established influence on DNA replication, differentiation, survival, development, apoptosis, tumorigenesis, and a further role in therapeutic resistance in human stem and cancer cells including those of breast and cervical origin. TERT encodes the catalytic subunit and rate-limiting factor for telomerase enzyme activity. The mechanisms of activation or silencing of TERT remain open to debate across somatic, cancer, and stem cells. Promoter mutations upstream of TERT may promote dysregulated telomerase activation in tumour cells but additional factors including epigenetic, transcriptional and posttranscriptional modifications also have a role to play. Previous systematic analysis indicated methylation and mutation of the TERT promoter in 53% and 31%, respectively, of TERT expressing cancer cell lines supporting the concept of a key role for epigenetic alteration associated with TERT dysregulation and cellular transformation. Epigenetic regulators including DNA methylation, histone modification, and non-coding RNAs are now emerging as drivers in the regulation of telomeres and telomerase activity. Epigenetic regulation may be responsible for reversible silencing of TERT in several biological processes including development and differentiation, and increased TERT expression in cancers. Understanding the epigenetic mechanisms behind telomerase regulation holds important prospects for cancer treatment, diagnosis and prognosis. This review will focus on the role of epigenetics in telomerase regulation.

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Lumpp, Tatjana, Sandra Stößer, Franziska Fischer, Andrea Hartwig, and Beate Köberle. "Role of Epigenetics for the Efficacy of Cisplatin." International Journal of Molecular Sciences 25, no. 2 (January 17, 2024): 1130. http://dx.doi.org/10.3390/ijms25021130.

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The clinical utility of the chemotherapeutic agent cisplatin is restricted by cancer drug resistance, which is either intrinsic to the tumor or acquired during therapy. Epigenetics is increasingly recognized as a factor contributing to cisplatin resistance and hence influences drug efficacy and clinical outcomes. In particular, epigenetics regulates gene expression without changing the DNA sequence. Common types of epigenetic modifications linked to chemoresistance are DNA methylation, histone modification, and non-coding RNAs. This review provides an overview of the current findings of various epigenetic modifications related to cisplatin efficacy in cell lines in vitro and in clinical tumor samples. Furthermore, it discusses whether epigenetic alterations might be used as predictors of the platinum agent response in order to prevent avoidable side effects in patients with resistant malignancies. In addition, epigenetic targeting therapies are described as a possible strategy to render cancer cells more susceptible to platinum drugs.

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Journal articles on the topic 'Cancer epigenetics'

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