Relevant bibliographies by topics / Cancer epigenetics

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cancer epigenetics'

Author: Grafiati
Published: 8 March 2025

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Journal articles on the topic "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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Dissertations / Theses on the topic "Cancer epigenetics"

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Donovan, Micah Gerard, and Micah Gerard Donovan. "Breast Cancer Epigenetics: Modification by Genistein." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624144.

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Breast cancer it is the most common type of cancer and leading cause of cancer mortality among women worldwide. Women who inherit mutations in the breast cancer 1 susceptibility gene (BRCA1) are five times more likely to develop breast cancer than women who do not. However, only ~5-10% of breast cancer cases are due to germline mutations in tumor suppressor genes. There are currently no targeted therapies available triple negative breast cancers (TNBC), which often lack BRCA1 expression. BRCA1 is epigenetically silenced by the activated aryl-hydrocarbon receptor (AhR), suggesting that dietary antagonists of the AhR may inhibit BRCA1 silencing. Genistein is an isoflavone abundant in soy foods and its high consumption levels is thought to underlie the lower prevalence of breast cancer in Asian countries compared to Western countries. The hypothesis of this work is that genistein antagonizes AhR-dependent epigenetic silencing of BRCA1. To test this hypothesis we first determined the capacity of genistein to prevent AhR-dependent silencing of BRCA1 in estrogen receptor-alpha (ERα) expressing cells, with wild-type BRCA1 and inducible AhR (MCF-7). We also determined the effectiveness of genistein in reversing silencing of BRCA1 in ERα-negative cells with hypermethylated BRCA1 and constitutively active AhR (UACC-3199). The effect of genistein on BRCA1 promoter methylation and markers of cell proliferation was also determined in both cell lines.
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Giger, O. T. "Epigenetics in regulation of oesophageal cancer stromal myofibroblasts." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3007985/.

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Cancer is the 2nd most common cause of death in our society and is associated with high morbidity and costs. The word ‘cancer’ amalgamates the complex interplay between cells which have acquired genetic alterations leading to uncontrolled proliferation, i.e. the malignant cells, and genetically ‘normal’ host cells, i.e. stromal cells, vascular cells and inflammatory cells which all acquire modified biological phenotypes in the presence of malignant cells. This community of cells and their secreted proteins defines the tumour microenvironment. Stromal cells in the tumour microenvironment display characteristic biological changes which promote cancer growth. Little is known on the underlying regulatory mechanisms defining this phenotype. Epigenetics describes inheritable changes not encoded by the nucleic acid sequence. Epigenetic regulation has been described to occur in stromal cells in the tumour microenvironment, but little is known about its role on myofibroblasts. In this work I describe how oesophageal cancer derived stromal cells, i.e. cancer associated myofibroblasts (CAMs) accelerate tumour growth in vivo. I observed that CAMs not only affect the local tumour microenvironment but might also accelerate tumour growth at a distant site. I also show how myofibroblasts play an important role in early tumour niche formation in xenograft models and describe their disappearance and replacement by murine stromal cells during tumour progression. Oesophageal CAMs were shown to be epigenetically distinct from matched adjacent tissue myofibroblasts (ATMs). They exhibited a global DNA hypo- methylation compared to ATMs. We identified distinct DNA methylation signatures between oesophageal cancer CAMs and ATMs with the use of the Illumina 450k bead chip methylation array. The methylation array data showed altered methylation signatures of genes implicated Wnt/β-catenin signalling pathway. The transcription factor paired like homeodomain (PITX) 2 and the regulatory protein secreted frizzled like protein (SFRP) 2 both showed altered methylation signatures and expression patterns between oesophageal cancer CAMs and ATMs. I found that upregulation of SFRP2 in myofibroblasts induces angiogenesis and I hypothesise that epigenetic modification regulates myofibroblasts-derived SFRP2 expression which may play an important role in tumour neovascularisation. Based on these findings I conclude that ATMs and CAMs are epigenetically distinct and altered protein expression is at least partially regulated by altered DNA methylation. This work also presents a model for epigenetic modification of tumour stroma cells: exposure of myofibroblasts to the DNA methyl transferase inhibitor 5’Aza-3’deoxycytosine (DAC) lead to a mild decrease of global DNA methylation and induced persistent biological changes in myofibroblasts. These epigenetically modified myofibroblasts induced an accelerated xenograft growth when injected together with oesophageal cancer cells. Based on these experiments I conclude that DAC epigenetically modifies myofibroblasts which induces an activation of normally silenced genes leading to a biologically more active cell.
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Tufegdžić-Vidaković, Ana. "Epigenetic determinants of context specificity in breast cancer." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708671.

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Simpson, Louise. "Epigenetics and breast cancer : a candidate gene association study." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=225333.

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Cooper, Matthew L. "Selenium and the Genetics and Epigenetics of Prostate Cancer." Thesis, University of Surrey, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499409.

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Muñoz-Rodríguez, José Luis. "Postpartum Breast Cancer in Hispanic Women: Epigenetics and microRNAs." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/603490.

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The risk of breast cancer transiently increases immediately following pregnancy. Hispanic women have one of the highest rates of postpartum breast cancers of all racial/ethnic minority groups in the US. The biology that underlies this risk window and the effect on the natural history of the disease is unknown. MicroRNAs (miRNAs) are small non-coding RNAs that have been shown to be dysregulated in breast cancer. In this study, we measured the miRNA expression of 56 tumors from a case series of multiparous Hispanic women and assessed the pattern of expression by time since last full-term pregnancy. A data-driven splitting analysis on the pattern of 355 miRNAs separated the case series into two groups: a) an early group representing women diagnosed with breast cancer ≤ 5.2 years postpartum (n=12), and b) a late group representing women diagnosed with breast cancer ≥ 5.3 years postpartum (n=44). We identified 15 miRNAs that are differentially expressed between the early and late postpartum groups; 60% of these miRNAs are encoded on the X chromosome. Ten miRNAs had a two-fold or higher difference in expression; miR-138, miR-660, miR-31, miR-135b, miR-17, miR-454, and miR-934 were overexpressed in the early versus the late group; while miR-892a, miR-199a-5p, and miR-542-5p were under expressed in the early versus the late postpartum group. The DNA methylation of three out of five tested miRNAs (miR-31, miR-135b, and miR-138) was lower in the early versus late postpartum group, and negatively correlated with miRNA expression. Taken together, the results of this study show that miRNAs are differentially expressed and differentially methylated between tumors of the early versus late postpartum, suggesting that potential differences in epigenetic dysfunction may be operative in postpartum breast cancers.
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Hinshelwood, Rebecca Garvan Institute of Medical Research UNSW. "Epigenetic changes in breast cancer." Publisher:University of New South Wales. Garvan Institute of Medical Research, 2009. http://handle.unsw.edu.au/1959.4/43633.

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Changes in the epigenetic landscape are widespread in neoplasia, with de novo methylation and histone repressive marks commonly occurring in association with gene silencing. However, understanding the dynamics of epigenetic changes is often hindered due to the absence of adequate in vitro model systems that accurately reflect events occurring in vivo. Human mammary epithelial cells (HMECs) grown under standard culture conditions enter a growth arrest termed selection, but a subpopulation is able to escape from arrest and continue to proliferate. These cells, called post-selection cells, have many of the hallmarks seen in the earliest lesions of breast cancer, including transcriptional silencing and hypermethylation of the p16INK4A tumour suppressor gene. The overall aim of my thesis was to use post-selection HMECs as model system to identify and dissect the mechanism involved in early epigenetic aberrations. Firstly, using a microarray approach, I found that multiple members of the TGF-β signalling pathway were concordantly suppressed in post-selection cells, and this was associated with functional disruption of the TGF-β pathway. Interestingly, concordant gene suppression was not associated with aberrant DNA methylation, but with repressive chromatin remodelling. Secondly, to further understand the mechanism underpinning epigenetic silencing, I demonstrated using laser capture technology, that p16INK4A silencing is a precursor to DNA methylation and histone remodelling. Thirdly, I found that individual post-selection HMEC strains during the early passages shared a common 'wave' pattern of regional-specific methylation within the p16INK4A CpG island. Interestingly, the 'wave' pattern of early de novo methylation correlated with the apparent footprint of nucleosomes within the p16INK4A CpG island. Lastly, to further characterise the properties of the HMEC culture system, I demonstrated that post-selection cells do not possess a natural tumour-inducing property when transplanted into the mammary fat pad of immunocompromised mice. However, post-selection HMECs were associated with high expression of a variety of stem/progenitor markers, as well as stem/progenitor associated polycomb genes, thus demonstrating that these cells share some common features of stem/progenitor cells. The research presented in this thesis demonstrate that epigenetic changes occur early in the growth of post-selection HMECs and many of these changes are common in breast cancer.
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Custodio, Rojo Joaquín. "Epigenetic mechanisms in colorectal cancer." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/287891.

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Mitjançant tècniques d’anàlisi de tot el genoma hem sigut capaços d'identificar regions diferencialment metilades entre teixit de colon normal i tumoral provinents del mateix pacient. Un dels gens més importants és AKR1B1, l'illa CpG associada al promotor d’aquest gen esdevé hipermetilada en un 90% dels càncers colorectals estudiats (més de 200), aquesta troballa ha estat confirmada en dos sets de mostres independents. Sorprenentment, la hipermetilació no està acompanyada per una clara baixada de l’expressió d’AKR1B1, de fet vam observar que aquesta hipermetilació estava associada amb el silenciament dels gens AKR1B10 i AKR1B15 (tots ells membres de la mateixa família d’aldo-keto reductases), localitzats a 60 Kbs de l'illa CpG. Utilitzant tècniques per esbrinar l'estructura de la cromatina dins del nucli vam observar que l'illa CpG es troba en contacte amb el promotor de AKR1B10, el que indica una possible funció d’enhancer per a l'illa CpG. Aquesta funció enhancer va ser corroborada mitjançant assajos de luciferasa i demostrada in situ mitjançant l’alteració de la regió enhancer, utilitzant la tècnica d’edició genòmica CRISPR. A més a més, l’acció enhancer va ser recuperada en models cel·lulars gràcies a l’acció de diverses drogues epigenètiques, que produïen l’activació de l’enhancer (observable per la reaparició de la marca H3K27ac) i la reactivació de l’expressió d’AKR1B10 i AKR1B15. En aquest treball també s’avalua l’impacte de la hipermetilació en la via de l’àcid retinoic, a la qual pertanyen els enzims de la família AKR1B. Observem que la via està fortament hipermetilada i, en conseqüència, silenciada. El fet més remarcable a nivell clínic és que aquestes alteracions poden servir com a marcador de pronòstic de la malaltia i com a marcador de diagnòstic no invasiu.
By applying a genome-wide approach to detect differential methylation between colorectal tumors and their paired normal tissue we identified a number of genes that suffer hypermethylation in colorectal cancer. One of the most interesting genes was AKR1B1, which promoter CpG island became hypermethylated in about 90% of all the colorectal cancers samples analyzed. Unexpectedly, this hypermethylation was not accompanied by a clear downregulation of the AKR1B1 transcript. After extending the analysis to the neighboring genes, we realized that this hypermethylation was actually associated with silencing of AKR1B10 and AKR1B15 genes (all of them members of the same aldo-keto reductase gene family), located 60 Kb upstream of the methylated CpG island. Using techniques to elucidate the chromatin structure within the nucleus, we realized that the CpG island was in close contact with the AKR1B10 promoter, what indicates a putative enhancer role for the CpG island. This enhancer function was checked using luciferase assays and was demonstrated in situ through the alteration of the enhancer region, using the genome editing technique CRISPR. Moreover, the enhancer activity was recovered using cellular models through the treatments with different epigenetic drugs, which produced the activation of the enhancer (with the characteristic H3K27ac mark) and the reexpression of AKR1B10 and AKR1B15 genes. In this work we also evaluated the impact of the hypermethylation in the retinoic acid pathway, where AKR1B enzymes belong to. We observed a strong hypermethylation of the retinoic acid pathway and, as a consequence, silencing. The most remarkable finding is that those alterations can be used to predict the outcome of the disease and also as a non-invasive diagnostic marker.
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Kutanzi, Kristy, and University of Lethbridge Faculty of Arts and Science. "The role of epigenetics in the rat mammary gland." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, c2010, 2010. http://hdl.handle.net/10133/2492.

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Epigenetics plays an important role in carcinogenesis with heritable changes in DNA methylation and histone modifications intricately linked to the initiation, promotion, and progression of cancer. Evidence shows that a number of chemical and physical agents can induce epigenetic changes during carcinogenesis. Two such agents, estrogen and ionizing radiation, are generally recognized as being carcinogenic. Yet the epigenetic repercussions of these carcinogens remain relatively unknown. More importantly, the combined effect of these carcinogens has never been addressed in vivo from an epigenetic standpoint. Therefore, we focused on the effect of estrogen and ionizing radiation applied separately or in conjunction. We have found that the exposure to estrogen, either alone or in combination with radiation, induced pronounced morphological alterations, which was paralleled by modifications to the epigenomic landscape in the mammary gland. The results obtained from these rodent models can potentially be extrapolated to humans.
xiv, 190 leaves : ill. (chiefly col.) ; 29 cm
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Wu, Jiejun. "Genome-wide analysis of epigenetics and alternative promoters in cancer cells." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187019769.

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Books on the topic "Cancer epigenetics"

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Dumitrescu, Ramona G., and Mukesh Verma, eds. Cancer Epigenetics. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-612-8.

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Verma, Mukesh, ed. Cancer Epigenetics. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1804-1.

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Giordano, Antonio, and Marcella Macaluso, eds. Cancer Epigenetics. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.

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O, Tollefsbol Trygve, ed. Cancer epigenetics. Boca Raton: CRC Press/Taylor & Francis Group, 2009.

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Kalkan, Rasime, ed. Cancer Epigenetics. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-42365-9.

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Sarkar, Fazlul H., ed. Epigenetics and Cancer. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6612-9.

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Mehdipour, Parvin, ed. Epigenetics Territory and Cancer. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9639-2.

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Antonio, Giordano. Cancer epigenetics: Biomolecular therapeutics in human cancer. Hoboken, N.J: Wiley-Blackwell, 2011.

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Berger, Nathan A., ed. Epigenetics, Energy Balance, and Cancer. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41610-6.

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Dumitrescu, Ramona G., and Mukesh Verma, eds. Cancer Epigenetics for Precision Medicine. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8751-1.

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Book chapters on the topic "Cancer epigenetics"

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Carlberg, Carsten, and Ferdinand Molnár. "Cancer Epigenetics." In Human Epigenetics: How Science Works, 89–99. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22907-8_8.

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Demircan, Berna, and Kevin Brown. "Cancer Epigenetics." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_807-2.

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Demircan, Berna, and Kevin Brown. "Cancer Epigenetics." In Encyclopedia of Cancer, 755–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_807.

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Schulz, Wolfgang A. "Cancer Epigenetics." In Molecular Biology of Human Cancers, 177–204. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-16286-2_8.

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Carlberg, Carsten. "Cancer Epigenetics." In Gene Regulation and Epigenetics, 213–29. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-68730-3_15.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Epigenetics and Cancer." In Introduction to Epigenetics, 151–77. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_8.

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AbstractAlterations in chromatin function and epigenetic mechanisms are a hallmark of cancer. The disruption of epigenetic processes has been linked to altered gene expression and to cancer initiation and progression. Recent cancer genome sequencing projects revealed that numerous epigenetic regulators are frequently mutated in various cancers. This information has not only started to be utilized as prognostic and predictive markers to guide treatment decisions but also provided important information for the understanding of the molecular mechanisms of epigenetic regulation in both physiological and pathological conditions. Furthermore, the reversible nature of epigenetic aberrations has led to the emergence of the promising field of epigenetic therapy that has already provided new therapeutic options for patients with malignancies characterized by epigenetic alterations, laying the basis for new and personalized medicine.
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Montanari, Micaela, Antonio Giordano, Marcella Cintorino, and Marcella Macaluso. "Epigenetic Modulation of Cell Cycle: An Overview." In Cancer Epigenetics, 1–14. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch1.

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Fratta, Elisabetta, Luca Sigalotti, Alessia Covre, Giulia Parisi, Riccardo Danielli, Hugues Jean Marie Nicolay, Sandra Coral, and Michele Maio. "Epigenetic Mechanisms in Cancer Formation and Progression." In Cancer Epigenetics, 253–98. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch10.

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Romano, Gaetano. "Recent Advances in the Field of Stem Cell Research: Toward the Definition of the Epigenetic and Genetic Codes of Pluripotency." In Cancer Epigenetics, 299–313. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch11.

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Otvos, Laszlo. "Potential of Heat Shock Protein Targeting for Human Therapy." In Cancer Epigenetics, 315–35. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch12.

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Conference papers on the topic "Cancer epigenetics"

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Andrade, Gustavo Moreira, Antonio Márcio Teodoro Cordeiro Silva, Amanda Hasan Figueiredo, Ana Luiza Gomes Monteiro, Leonardo Chaves de Oliveira Moraes, and Giovanna Silva Quirino. "The use of epigenetics in the treatment of triplenegative breast cancer, focusing on IncRNA." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1032.

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Objective: In triple-negative breast cancer (CMTN), the standard therapeutic procedure is usually not very effective due to the aggressiveness of the disease. Therefore, it is important to identify and characterize new forms of treatment for this neoplasm. In this context, the study of the genetic material of diseases has gained notoriety among alternative forms of therapy, as long non-coding RNAs (IncRNAs) have been identified in neoplastic cells. Therefore, the aim of this study was to evaluate the use of epigenetics in the treatment of CMTN, with emphasis on lncRNAs. Methodology: A systematic review of the specialized scientific literature was carried out, in the PubMed database, with the descriptors: “breast cancer,” “epigenetic,” and “treatment”; the Boolean operator: “AND”; and the filters: “free full text,” “adults: 19+ years,” and publication date from 2021 to 2023. A total of 32 articles were identified, with 3 included Results: Epigenetics influences the treatment of breast cancer; as the lncRNA was found in neoplastic cells, it was possible to monitor the prognosis of the disease. The lncRNA Uc003xsl.1 was associated with a poor prognosis, as it was related to advanced stages of CMTN, increasing the transcriptional activity of NFkB, which promotes tumor progression. On the contrary, the lncRNA LINC00472 proved to be a marker of good prognosis, as it inhibited the proliferation, invasion, and migration of neoplastic cells in the CMTN. Furthermore, with regard to breast cancer, lncRNA IGF-2AS proved to be an important biomarker, as it slows tumor growth in vivo, repressing malignancy and tumor progression. Therefore, IncRNAs have gained notoriety in treatment as regulators of breast cancer tumorigenesis. Conclusion: Thus, the use of epigenetics in the treatment of CMTN has proven to be essential to curbing neoplastic cells, as it interferes with tumor proliferation in different ways, either by influencing transcription or by slowing down growth.
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Marques, Flavia Araújo Marques, and Matheus Moreira. "EPIGENETICS IN COLORECTAL CANCER." In Congresso Online de Atualização em Oncologia. Congresse.me, 2023. http://dx.doi.org/10.54265/mobq8354.

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Raj, Utkarsh, Saurav Kumar Mishra, Chakshu Bhatia, Pritish Kumar Varadwaj, and Gaurav Harit. "A Comprehensive Knowledgebase on Cancer Epigenetics." In 2018 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2018. http://dx.doi.org/10.1109/bsb.2018.8770626.

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Jones, Peter A. "Abstract IA01: The epigenetics of cancer." In Abstracts: AACR Special Conference on Bladder Cancer: Transforming the Field; May 18-21, 2019; Denver, CO. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.bladder19-ia01.

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Miyamoto, K., and T. Ushijima. "MicroRNAs and epigenetics in human breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4051.

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Waterland, Robert A. "Abstract PL02-01: Nutrition, epigenetics, and cancer." In Abstracts: Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; September 27 - October 1, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1940-6215.prev-14-pl02-01.

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Zhao, Xinyue. "Review of Role of Epigenetics in Cancer Research." In ICBET '21: 2021 11th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3460238.3460263.

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Brown, Myles. "Abstract IA15: Epigenetics of hormone dependence." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia15.

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Riggins, Karen, Benjamin Musher, Michael Scheurer, Li Yang, Patricia Castro, Neda Zarrin-Khameh, and Lanlan Shen. "Abstract 1251: Epigenetics in early onset colorectal cancer (EOCRC)." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1251.

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Thakkar, Kaushik N., Shiming Jiang, Sabrina Stratton, and Michelle Barton. "Abstract B17: TRIM24 links epigenetics and metabolism in cancer." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-b17.

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Reports on the topic "Cancer epigenetics"

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Wang, Ying yuan, Zechang Chen, Luxin Zhang, Shuangyi Chen, Zhuomiao Ye, Tingting Xu, and Yingying Zhang c. A systematic review and network meta-analysis: Role of SNPs in predicting breast carcinoma risk. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2022. http://dx.doi.org/10.37766/inplasy2022.2.0092.

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Review question / Objective: P: Breast cancer patient; I: Single nucleotide polymorphisms associated with breast cancer risk; C: Healthy person; O: By comparing the proportion of SNP mutations in the tumor group and the control group, the effect of BREAST cancer risk-related SNP was investigated; S: Case-control study. Condition being studied: Breast cancer (BC) is one of the most common cancers among women, and its morbidity and mortality have continued to increase worldwide in recent years, reflecting the strong invasiveness and metastasis characteristics of this cancer. BC is a complex disease that involves a sequence of genetic, epigenetic, and phenotypic changes. Polymorphisms of genes involved in multiple biological pathways have been identified as potential risks of BC. These genetic polymorphisms further lead to differences in disease susceptibility and severity among individuals. The development of accurate molecular diagnoses and biological indicators of prognosis are crucial for individualized and precise treatment of BC patients.
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Murphy, Susan K. Epigenetic Characterization of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada452440.

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Murphy, Susan K. Epigenetic Characterization of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada509791.

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Margueron, Raphael F. An Epigenetic Link to Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada484222.

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Reich, Norbert R. An Epigenetic Approach to Breast Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada429260.

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Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada581650.

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Euhus, David. Epigenetic Testing for Breast Cancer Risk Stratification. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada582383.

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Williams, Kristin P. Epigenetic Control of Tamoxifen-Resistant Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada601260.

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Liao, Jianhua, Jingting Liu, Baoqing Liu, Chunyan Meng, and Peiwen Yuan. Effect of OIP5-AS1 on clinicopathological characteristics and prognosis of cancer patients: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0118.

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Review question / Objective: According to recent studies, long non-coding RNA (lncRNAs) i.e., OPA-interacting protein 5 antisense RNA 1 (OIP5-AS1) has an important role in various carcinomas. However, its role in the cancer is contradictory. Therefore, we aimed to evaluate the link between OIP5-AS1 and cancer patients' clinicopathological characteristics and prognosis to better understand OIP5-AS1's role in cancer. Condition being studied: Reported studies have revealed that long non-coding RNA (lncRNAs) are considerably involved in crucial physiological events in several carcinomas, it can inhibit or promote the occurrence and development of tumors by changing the sequence and spatial structure, modulating epigenetic, regulating the expression level and interacting with binding proteins. However, the mechanism of cancer regulation via lncRNAs was incompletely understood. Hence, clarifying the application value of lncRNAs in preclinical and clinical disease diagnosis and treatment was therefore the prime objective in the field of cancer research at the time.
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Simon, Jeffrey A., and Carol A. Lange. Histone Methylation and Epigenetic Silencing in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada491094.

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