Relevant bibliographies by topics / Cancer epigenetics / Dissertations / Theses
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Dissertations / Theses on the topic 'Cancer epigenetics'

Author: Grafiati
Published: 8 March 2025
Last updated: 26 July 2025

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1

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
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2

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 displa
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3

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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4

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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5

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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6

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 pregnan
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7

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, hav
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8

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 silen
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9

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 epigeneti
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10

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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11

Wu, Jiejun. "Genone-wide analysis of epigenetics and alternative promoters in cancer cells." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1187019769.

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12

Wozniak, Ryan Joseph. "Mechanisms Underlying the Pharmacologic Reversal of Genetic and Epigenetic Components of Tumor Suppressor Gene Silencing in Human Breast Cancer." Diss., Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1660%5F1%5Fm.pdf&type=application/pdf.

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13

Roberts, Kirsty Anne. "Analysis of 14-3-3σ methylation and associated changes in gene expression and function in colorectal carcinoma". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4821.

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The aims of the work presented in this thesis were: to investigate the role of methylation of 14-3-3σ (a key regulator of p53-mediated G2/M arrest and of translational control during mitosis) in colorectal cancer using colorectal cancer cell lines and fresh colorectal tumours; to investigate any relationship between 14-3-3σ methylation status and gene expression; to determine whether aberrant methylation is associated with cell cycle defects and other factors known to contribute to colorectal carcinogenesis. PCR bisulphite sequencing showed that 78% (7/9) of colorectal cancer cell lines were u
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14

TOSCANI, CECILIA. "UNCOVERING EPIGENETIC VULNERABILITIES IN INTESTINAL CANCER DEVELOPMENT." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/697052.

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Colorectal cancer (CRC) arises from a multi-step process leading to the progressive accumulation of genetic and epigenetic mutations, thus causing deregulation in homeostasis followed by neoplastic transformation.Epigenetic and genetic alterations are able to induce a constitutive activation of the WNT signaling pathway, whose aberrant activity converges into deregulation of proliferation, differentiation and cell death pathways. The most common causes of WNT pathway hyper-activation are APC loss of function, or b-catenin constitutive activation mutations. Despite this knowledge of aberrant WN
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15

Lin, Yiwei. "THE LINKAGE BETWEEN TRANSCRIPTION CONTROL AND EPIGENETIC REGULATION: THE SNAIL STORY AND BEYOND." UKnowledge, 2012. http://uknowledge.uky.edu/pharmacol_etds/2.

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Epigenetic deregulation contributes significantly to the development of multiple human diseases, including cancer. While great effort has been made to elucidate the underlying mechanism, our knowledge on epigenetic regulation is still fragmentary, an important gap being how the diverse epigenetic events coordinate to control gene transcription. In the first part of our study, we demonstrated an important link between Snail-mediated transcriptional control and epigenetic regulation during cancer development. Specifically, we found that the highly conserved SNAG domain of Snail sequentially and
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16

Carpenter, Brittany L. "INTEGRIN α6β4 PROMOTES PANCREATIC CANCER INVASION BY ALTERING DNA REPAIR-MEDIATED EPIGENETICS". UKnowledge, 2016. http://uknowledge.uky.edu/biochem_etds/27.

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Integrin α6β4 is upregulated in pancreatic carcinoma, where signaling promotes metastatic properties, in part by altering the transcriptome. Such alterations can be accomplished through DNA demethylation of specific promoters, as seen with the pro-metastatic gene S100A4. I found that signaling from integrin α6β4 dramatically upregulates expression of amphiregulin (AREG) and epiregulin (EREG), ligands for the epidermal growth factor receptor (EGFR), and that these ligands promote pancreatic carcinoma invasion. To determine if AREG and EREG are regulated by DNA methylation, pancreatic cancer cel
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17

Deatherage, Daniel E. "TGFΒ/SMAD4 Signaling and Altered Epigenetics Contribute to Increased Ovarian Cancer Severity". The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306860253.

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18

Skerry, Benjamin James Oliver. "Investigating epigenetic mechanisms of acquired endocrine resistance in an in vitro model of breast cancer." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8106.

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I have investigated epigenetic mechanisms of acquired endocrine-resistance in breast cancer using an in vitro model system based on estrogen-dependent MCF7 cells and their derivatives, LCC1 and LCC9. LCC1 cells, derived from MCF7 after passage in ovariectomised mice and routinely cultured in vitro in the absence of estrogen, exhibit estrogen-independent growth. They retain sensitivity to tamoxifen and fulvestrant. LCC9 cells, derived from LCC1 cells by growing them in increasing concentrations of fulvestrant, are completely estrogen-independent and are resistant to fulvestrant and cross-resist
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19

Cole, Alexander John. "The role of p53 and histone H2B monoubiquitination in high-grade serous ovarian carcinoma." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17639.

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Ovarian cancer is the eleventh most frequently diagnosed cancer in women and the fifth most common cause of cancer-related deaths. Epithelial ovarian cancer accounts for ~90% of cases. Serous epithelial ovarian cancer (SEOC) is the most common and aggressive histological subtype. Clinically, SEOC can be divided into type I and II tumours. Type II tumours (high grade serous ovarian carcinoma (HGSOC)), are generally diagnosed at later stages, grow aggressively and possess a mutation in the TP53 gene, which codes for the tumour suppressor protein p53. Mortality rates of HGSOC have remained largel
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20

Deliard, Sandra. "THE ROLE OF SPLICING FACTOR SF3B1 IN TRANSCRIPTIONAL AND EPIGENETIC REGULATION." Diss., Temple University Libraries, 2019. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/583882.

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Biomedical Sciences<br>Ph.D.<br>Epigenetic silencing is often altered in cancer and is a target for drug discovery. Unbiased screens in live cells are performed to identify potential novel targets of epigenetic therapy, and these screens have identified drugs that were not previously recognized to be involved in epigenetic reactivation of gene silencing such as cardiac glycosides and a CDK9 inhibitor. Recently, our lab performed a whole genome siRNA screen in combination with DNMT inhibition. One of the top targets revealed in this screen was the splicing factor SF3B1. SF3B1 is a well-known cr
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21

Good, Charly Ryan. "The role of TET1 and TET1ALT in cancer." Diss., Temple University Libraries, 2017. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/471341.

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Biomedical Sciences<br>Ph.D.<br>DNA hypermethylation is known to contribute to the formation of cancer and this process has been widely studied. However, DNA hypomethylation has received far less attention and the factors controlling the balance between hypo and hypermethylation and its impact on tumorigenesis remains unclear. TET1 is a DNA demethylase that regulates DNA methylation, hydroxymethylation and gene expression. Full length TET1 (TET1FL) has a CXXC domain that binds to un-methylated CG islands (CGIs). This CXXC domain allows TET1 to protect CGIs from aberrant methylation but it also
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22

Liao, Peter Lee Ming Liao. "Bioinformatics approaches to cancer biomarker discovery and characterization." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1525694252170957.

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23

Rosselló, Tortella Margalida. "Epigenetic Regulation of tRNA Biology in Cancer." Doctoral thesis, Universitat de Barcelona, 2021. http://hdl.handle.net/10803/673026.

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Transfer RNAs (tRNAs) are essential molecules that allow the translation of the genetic code into amino acids. Extensive research during the last 50 years have revealed that, despite their apparently simple structure and function, tRNAs are more than simple adaptors in protein synthesis –they are of high importance in normal cell functions. Reinforcing this, tRNA levels are tightly regulated to match the codon usage patterns of a given cell type or cellular status to meet the cellular specific needs and adapt to stress. Moreover, tRNA nucleoside modifications are critical for their function at
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24

Hung, Stevephen. "Genetic Determinants of Enhancer Activation in Human Colon Cancer Epigenomes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1567786267717899.

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25

Akhtar-Zaidi, Batool. "DISCOVERY OF NOVEL EPIGENETIC MECHANISMS OF CARCINOGENESIS BY GENOME-WIDE PROFILING OF NON-CODING REGULATORY ELEMENTS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1347020396.

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26

Rush, Laura J. "Global and Gene-Specific DNA Methylation Analysis in Human Leukemia." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1046352386.

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27

Cohen, Andrea. "Characterization of Altered Enhancer Usage Across the Human Colorectal Cancer Epigenome." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1491332948235594.

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28

Akulenko, Ruslan [Verfasser], and Volkhard [Akademischer Betreuer] Helms. "Data mining techniques for improving and enriching cancer epigenetics / Ruslan Akulenko. Betreuer: Volkhard Helms." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1097263231/34.

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Akulenko, Ruslan Verfasser], and Volkhard [Akademischer Betreuer] [Helms. "Data mining techniques for improving and enriching cancer epigenetics / Ruslan Akulenko. Betreuer: Volkhard Helms." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:291-scidok-64547.

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30

Nordor, Akpéli. "Toward the identification of cancer/placenta epigenetic switches." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB097.

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Les cellules placentaires portent un génome différent du génome maternel, puisque 50% de leurs gènes proviennent du génome paternel. Cependant, comme les cellules cancéreuses après la transformation néoplasique, elles réussissent à envahir les tissus de leur hôte, échapper à son système immunitaire et induire une angiogenèse afin d’établir la grossesse. Les cellules cancéreuses et placentaires arborent aussi une différence majeure : alors que de tels mécanismes typiques des cancers sont incontrôlés dans les cellules cancéreuses, ils sont spatialement et temporairement contrôlés dans les cell
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31

Nicol-Benoit, Floriane. "Rétroactions positives et mémoire cellulaire : exemples dans l'expression génétique et le métabolisme cellulaire." Thesis, Rennes 1, 2013. http://www.theses.fr/2013REN1S115/document.

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Au-delà de l'information génétique contenue dans la séquence de l'ADN des cellules, il existe une mémoire cellulaire, dite épigénétique comprenant l'ensemble des circuits génétiques avec rétroactions positives permettant d'amplifier ou de maintenir une réponse cellulaire dans le temps. Nous nous sommes intéressés, à travers deux exemples, aux boucles de rétrocontrôle positif comme élément de réponse à un signal, permettant de fixer, de manière à la fois dynamique et robuste, le comportement cellulaire. Dans un premier temps, nous avons identifié une boucle d'auto-amplification dans la producti
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32

Filkowski, Jody, and University of Lethbridge Faculty of Arts and Science. "The role of epigenetic changes in chemoresistant breast cancer cells." Thesis, Lethbridge, Alta. : University of Lethbridge, Dept. of Biological Sciences, 2010, 2010. http://hdl.handle.net/10133/2594.

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Cytotoxic chemotherapy is extremely important in adjuvant treatment of breast cancer. Yet, tumours frequently acquire chemoresistance that correlates with increased aggressiveness and poor prognosis. Three theories exist describing how the resistance develops: genetic, epigenetic and karyotypic theory. The epigenetic theory is the least explored. Here we analyzed the role of the epigenetic phenomena in the acquisition of drug resistance. To do so, we employed genome wide screens of microRNA and gene expression, DNA methylation and complete genome hybridization. We identified three novel microR
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33

Cramer, Samantha A. Cramer. "Decitabine-loaded Nanogel Treatment to Reverse Cancer Drug Resistance." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1463511936.

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34

Tomita(Uehiro), Natsue. "Circulating cell-free DNA-based epigenetic assay can detect early breast cancer." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225497.

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35

Ogawa, Satoshi. "SETDB1 Inhibits p53-Mediated Apoptosis and is Required for Formation of Pancreatic Ductal Adenocarcinomas in Mice." Kyoto University, 2020. http://hdl.handle.net/2433/259014.

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36

Nizialek, Emily A. "KLLN as Tumor Suppressor in Cowden Syndrome and Sporadic Breast Cancers." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1409778932.

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37

Junk, Damian Jerome. "Determining the Role of p53 Mutation in Human Breast Cancer Progression Using Recombinant Mutant/Wild-Type p53 Heterozygous Human Mammary Epithelial Cell Culture Models." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/193600.

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Breast cancer is the most frequently diagnosed form of cancer in women and the second leading cause of cancer-related deaths. Breast cancer is a heterogeneous disease consisting of many types of tissue neoplasia, and there appears to be no model of how a particular lesion develops into an aggressive, malignant, invasive carcinoma. Genetic mutation and aberrant epigenetic regulation are among the most common events that lead to neoplasia. In breast cancer, p53 mutation is the most common genetic defect related to a single gene. Therefore, this dissertation focuses on the mechanisms and cons
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38

Aboalela, Noran. "Acquired epigenetic and chromosomal changes in women treated for breast cancer." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3554.

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Improved survival for women receiving chemotherapy for breast cancer (BC) has been accompanied by the development/persistence of psychoneurological symptoms (PNS) that compromise their quality of life. The biological basis for these PNS is unknown, but could reflect the acquisition of soma-wide chromosomal/epigenetic alterations. An important first step in testing this hypothesis is to determine if somatic genetic/epigenetic changes arise and persist following treatment. To answer this question we longitudinally studied 71 women (ages 23-71) with early-stage BC and collected measures before ch
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Maeda, Masahiro. "Novel epigenetic markers for gastric cancer risk stratification in individuals after Helicobacter pylori eradication." Kyoto University, 2018. http://hdl.handle.net/2433/233838.

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40

Servant, Nicolas. "Analysis of chromosome conformation data and application to cancer." Electronic Thesis or Diss., Paris 6, 2017. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2017PA066535.pdf.

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L’organisation nucléaire de la chromatine n’est pas aléatoire. Sa structure est parfaitement contrôlée, suivant un modèle hiérarchique avec différents niveaux d’organisation et de compaction. A large échelle, chaque chromosome occupe son propre espace au sein du noyau. A plus fine résolution, un chromosome est subdivisé en compartiments actifs ou répressifs, caractérisés par un état de la chromatine plus ou moins compact. A l’échelle du méga-base, cette organisation hiérarchique peut encore être divisée en domaines topologiques (ou TADs), jusqu’à la caractérisation de boucle d’ADN facilitant l
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Servant, Nicolas. "Analysis of chromosome conformation data and application to cancer." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066535/document.

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L’organisation nucléaire de la chromatine n’est pas aléatoire. Sa structure est parfaitement contrôlée, suivant un modèle hiérarchique avec différents niveaux d’organisation et de compaction. A large échelle, chaque chromosome occupe son propre espace au sein du noyau. A plus fine résolution, un chromosome est subdivisé en compartiments actifs ou répressifs, caractérisés par un état de la chromatine plus ou moins compact. A l’échelle du méga-base, cette organisation hiérarchique peut encore être divisée en domaines topologiques (ou TADs), jusqu’à la caractérisation de boucle d’ADN facilitant l
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42

Cannito, Sara. "Modeling of cancer immune phenotype by new epigenetic drugs: a strategy to improve efficacy of immunotherapy." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1120775.

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Il mesotelioma pleurico maligno (MPM) è un tumore molto aggressivo e rapidamente progressivo che si sviluppa a livello del mesotelio che compone la pleura; questa neoplasia può assumere diversi sottotipi istologici (epitelioide, bifasico e sarcomatoide), i quali sono strettamente correlati alla prognosi. Le modificazioni epigenetiche che avvengono nelle fasi di iniziazione e progressione del MPM possono svolgere un ruolo fondamentale nel regolare negativamente il crosstalk tra tumore e sistema immunitario, contribuendo a mantenere un microambiente tumorale immunosoppressivo. Conoscere più dett
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Javed, Aqib. "UHRF1, an epigenetic target for an anti-cancer strategy." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ070.

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L'UHRF1 est une cible de médicaments pour traiter le cancer. Il est très présent dans de nombreux cancers, ce qui peut causer des problèmes de méthylation des gènes. Notre travail vise à étudier le potentiel anticancéreux des inhibiteurs de l'UHRF1-SRA (AMSA2, MPB7 et UM63), et à comprendre comment ils agissent et comment ils sont sélectifs envers les cellules cancéreuses. On a utilisé des techniques de biologie cellulaire et moléculaire. Cela a montré que ces composés ont un effet anticancéreux. Ils empêchent que le gène UHRF1 et le gène DNMT1 se retrouvent au même endroit. Ils contrôlent aus
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Zouggar, Aïcha. "G9a/EHMT2 Methyltransferase Activity Controls Stem-Like Identity and Tumor-Initiating Function in Human Colorectal Cancer." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/41821.

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Colorectal tumors are hierarchically organized and governed by populations of self-renewing cancer stem cells, representing one of the deadliest types of cancers worldwide. Emergence of a cancer stem-like phenotype depends on epigenetic reprogramming, associated with profound transcriptional changes. As described for pluripotent reprogramming, epigenetic modifiers play a key role in developing and maintaining cancer stem cells by establishing embryonic stem-like transcriptional programs, thus altering the balance between self-renewal and differentiation. Through my work, I have identified over
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45

Rheinheimer, Brenna Ann. "Alternative Transcription Of The SLIT2/Mir-218-1 Transcriptional Axis Mediates Pancreatic Cancer Invasion." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/605118.

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The development of several organ systems through modeling and shaping of the tissue structure occurs from signaling through axon guidance molecules. The Slit family of ligands has been shown to regulate branching morphogenesis in mammary gland duct development and loss of Slit gene expression during this time leads to the formation of hyperplastic, disorganized lesions suggesting a potential role for Slits in cancer formation. Characterization of human pancreatic ductal adenocarcinoma cell lines showed a loss of SLIT2 expression in cells that contain activated Kras. Loss of SLIT2 expression wa
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46

Lagan, Kevin J. "An examination of the role androgen receptor co-factors play in male fertility and prostate cancer epigenetics." Thesis, Ulster University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.674742.

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In this thesis I present an investigation of a novel steroid hormone receptor cochaperone, FKBPL, and its role in male infertility. I present evidence of proposed functional mutations in the FKBPL coding sequence within a subset of the infet1ile male population, namely, those presenting with non-obstructive azoospermia, that were not present within fertile control populations. FUl1her, I show that FKBPL exhibits a cell specific pattern of expression in human testis consistent with a role in androgen receptor signalling. I then demonstrate that increased expression of FKBPL can potentiate andro
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Daures, Marine. "Epigénétique et cancer de la prostate : Rôles de la déméthylase JMJD3 et de la méthyltransférase EZH2." Thesis, Université Clermont Auvergne‎ (2017-2020), 2018. http://www.theses.fr/2018CLFAS012.

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En France comme dans la majorité des pays développés, le cancer de la prostate est le plus fréquent chez l’homme. Il est clairement établi que les altérations génétiques et épigénétiques sont des événements communs dans les cancers de la prostate, se traduisant par l’expression aberrante de gènes critiques. La méthylation des histones participe à la régulation de l’expression des gènes dans la cellule. La marque épigénétique H3K27me3 est associée à la répression génique et se trouve dérégulée dans les cancers de la prostate. Ses niveaux sont déterminés par l’équilibre entre les activités de la
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48

Göndör, Anita. "Epigenetic Regulation of Higher Order Chromatin Conformations and Gene Transcription." Doctoral thesis, Uppsala universitet, Zoologisk utvecklingsbiologi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8296.

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Epigenetic states constitute heritable features of the chromatin to regulate when, where and how genes are expressed in the developing conceptus. A special case of epigenetic regulation, genomic imprinting, is defined as parent of origin-dependent monoallelic expression. The Igf2-H19 locus is considered as paradigm of genomic imprinting with a growth-promoting gene, Igf2, expressed paternally and a growth antagonist, H19 encoding a non-coding transcript, expressed only from the maternal allele. The monoallelic expression patterns are regulated by the epigenetic status at an imprinting control
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Pérez, Salvia Montserrat. "Epigenetic regulation of lysine acetylation: targeting writers, readers and erasers in cancer." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/667923.

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Cancer is considered nowadays a genetic and epigenetic disease. Aberrancies in epigenetic marks in DNA and histone tails together with alterations in epigenetic regulators responsible of catalyzing these marks have been shown to be crucial in tumorigenesis. These epigenetic regulators are commonly known as writers, readers and erasers. The plasticity of the epigenetic landscape compared to the unchangeable nature of genetic alterations has led to an increasing interest in the last years in finding specific drugs able to modulate and correct the epigenetic aberrancies present in tumors. At pre
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50

Klingbeil, Olaf. "Impact of BET bromodomain inhibition on KRAS-mutated non-small cell lung cancer." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17665.

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Nicht-kleinzelliger Lungenkrebs (NSCLC) hat bis heute einen hohen medizinischen Bedarf an effektiveren Therapien. Inhibitoren der Bromodomain and extra-terminal domain (BET) Familie wie JQ1 wirken in verschiedenen Krebsarten, einschließlich Lungenkrebs. Während ihre Aktivität auf die Expression von Onkogenen wie c-Myc in vielen Studien untersucht wurde, bleibt der Effekt von BET-Inhibition auf den Apoptose Signalweg weitgehend unbekannt. In dieser Arbeit wurde die Aktivität von BET-Inhibitoren auf den Zellzyklus und auf Komponenten der Apoptose-Antwort der Zelle untersucht. Genomweite Transkri
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