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Dissertations / Theses on the topic 'Mutants de p53'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Ang, H. C. "Biophysical characterisation and rescue of p53 cancer mutants." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596120.

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The aim of this thesis was to use biophysical methods to characterise the stabilities and DNA binding properties of monomeric and tetrameric p53 cancer mutants, and to study various approaches aimed at rescuing structural mutants of p53. A detailed study of the destabilising effects of p53 mutations was performed using differential scanning calorimetry and urea denaturation, while equilibrium binding of p53 mutants to a specific promoter sequence, <i>gadd45</i>, was studied using fluorescence anisotropy and analytical ultracentrifugation. This thesis will also discuss how p53 structural mutant

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2

Estevan, Barber Anna. "Influence of genotoxic drug-induced post-translational modifications on mutant p53 stability and oncogenic activities." Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/1ec28205-8590-4044-91b0-0c5f68206c2c.

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The tumour suppressor p53 is often disrupted by missense mutations that can result in p53 protein accumulation and acquisition of novel oncogenic activities. Various studies have demonstrated that DNA-damaging drugs currently used in the clinic aimed at activating wild type p53, can also stabilise and activate mutant p53 oncogenic functions and thereby paradoxically enhance tumour progression, resulting in poor response to the treatment. In this study we aimed to investigate whether, like in wt p53, post-translational modifications (PTMs) drive such drug-induced mutant p53 accumulation and act

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3

Souza, Felipe da Costa. "Geração e caracterização de linhagens isogênicas portadoras de mutantes de p53: modelo para avaliar a estratégia de reparação dos genes p53 e p16 INK4A na presença dos mutantes p53R175H e p53R248Q." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-26072012-102241/.

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A destruição funcional das vias de controle do ciclo celular constituem um evento comuns em todos os tumores humanos. Muitos estudos associam mutações em p53 com mau prognostico no tratamento do câncer. Nesse trabalho, visamos a geração e caracterização de linhagens isogênicas portando diferentes mutantes de p53 como modelo de estudo para remediação simultânea de p53 e p16 na presença de mutantes hotspots específicos. Os mutantes R175H e R248Q não geraram alterações na cinética de proliferação da linhagem H358, mas levaram a um aumento de 27,5% na eficiência de plaqueamento e, no caso de R248Q

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4

Roger, Lauréline. "Etude des mécanismes de la régulation de l'EMT par le suppresseur de tumeur p53 dans un modèle de cellules de carcinome du colon." Montpellier 2, 2007. http://www.theses.fr/2007MON20182.

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Le suppresseur de tumeur p53 est un facteur de transcription impliqué dans la progression du cycle cellulaire et dans l'apoptose. Outre ses fonctions majeures, p53 régule également la migration et l'adhérence cellulaire qui sont deux évènements impliqués dans le processus métastatique. L'évolution maligne d'un carcinome peut aussi impliquer la répression transcriptionnelle de CDH1, qui code pour la E-cadhérine, protéine constitutive des jonctions adhérentes. Nous avons recherché si et comment p53 régule certains évènements moléculaires qui contrôle le processus métastatique. Nous montrons que

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5

Li, Lianjie. "Mutations in tumor suppressor p53 and deregulation of cellular metabolism." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19513.

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Mutation des p53 Gen ist die häufigste genetische Veränderung in allen humanen Tumoren. Weit verbreitete p53 misssense-Mutationen heben die Tumor suppressive Funktion auf und führen zu gain-of-function Eigenschaften, die Tumorproliferation, Chemoresistenz, Angiogenese, Migration, Invasion und Metastasen fördern. In dieser Arbeit haben ich für drei solche Hotspot-Mutationen, p53R245Q, p53R246S und p53R270H, eine höhere Sensitivität gegenüber Behandlung mit Piperlongumine in p53-defizienten MEFs und Eµ-myc Lymphomzellen im Vergleich zur Kontrolle und den anderen drei Hotspot-Mutationen, p53R172

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6

Toppaldoddi, Katte Rao. "Role of rare calreticulin mutants and of the endoplasmic reticulum stress in the pathogenesis of myeloproliferative neoplasms." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC322/document.

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Après la découverte des mutations de la calréticuline dans les néoplasmes classiques myéloproliferatifs négatifs pour le Ph1, les travaux se sont focalisés sur les deux mutations les plus fréquentes, c'est-à-dire la calréticuline del52 et l’ins5, mais il existe environ 20% de mutants rares de la calréticuline (une cinquantaine), qui ont été classés en type-1 « like » et type-2 « like », classification basée sur leur structure. Cependant il reste à déterminer si cette classification est pertinente du point de vue fonctionnel, ce qui pourrait avoir des conséquences pour la prise en charge des pa

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7

Osadchuk, Olha. "Optimalizace izolace mutantního proteinu p53 a jeho DNA vazebné vlastnosti." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2020. http://www.nusl.cz/ntk/nusl-413550.

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Protein p53 je jednou z nejdůležitějších molekul v lidském těle. P53 reguluje celou řadu procesů v buňce, jako je například oprava DNA, buněčný cyklus nebo indukce apoptózy. Protein p53 je známý i jako „strážce genomu“. DNA vazebné schopnosti proteinu p53 jsou důležité pro normální vývoj a růst buňky. Mutace genu pro p53 mohou vést ke ztrátě jeho DNA vazebných vlastností a funkce nádorového supresoru, což muže způsobit rozvoj rakoviny. Teoretická část této diplomové práce je zaměřena na popis vlastností, funkce a mechanismus aktivace proteinu p53 a popis lokálních sekundárních struktur DNA. Hl

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8

Pellerano, Morgan. "Développement d'un biosenseur fluorescent d'un mutant de p53 sujet à l'agrégation dans les cancers." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT053.

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P53 est un suppresseur de tumeur qui joue un rôle clé dans la régulation de la transcription, la réparation de l'ADN, l'instabilité génétique, la sénescence, la régulation du cycle cellulaire et l'apoptose. Cette protéine, normalement nucléaire, se lie à l’ADN et régule la transactivation. Cependant, elle est souvent mutée dans les tumeurs humaines, entraînant une inactivation fonctionnelle et une prédisposition au cancer. Les mutants p53 se peuvent-être de deux catégories des mutants de « contact » ou « conformationnel ». Ces derniers entraînant des changements de conformation pouvant induire

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9

Saundh, Harpal. "Targeting mutant p53 in cSCCs." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/29e37f0d-5ed7-483c-9a92-87212934d72b.

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Cutaneous squamous cell carcinoma (cSCC) is a type of non-melanoma skin cancer that is the 4th most common cancer registration in Scotland after BCC, lung and breast cancer. Over 30,000 cSCC incidences are reported each year in the United Kingdom. In addition, around 1 in 4 skin cancer deaths in the UK are due to cSCCs. Amongst those highly prone to developing cSCCs include organ transplant recipient, immunosuppressed, recessive dystrophic epidermolysis bullosa (RDEB) and Xeroderma Pigmentosum (XP) patients. cSCC patients that display regional metastasis have a 5-year survival rate of 25-50%,

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10

Marini, Wanda. "Comparing mutant p53 and a wild-type p53 isoform, p47 : rationale for the selection of mutant p53 in tumours." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116033.

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One of the major unresolved questions in cancer biology is why the majority of tumour cells express mutant p53 proteins. p53 is considered the prototype tumour suppressor protein, whose inactivation is the most frequent single genetic event in human cancer (Bourdon et al., 2005). Genetically-engineered p53-null knockout mice acquire multiple tumours very early on in life and human Li-Fraumeni families who carry germline mutations in p53 are highly cancer-prone (reviewed in Vousden and Lane, 2007). p53 mutant proteins have been found to acquire novel functions that promote cancer cell prolifera

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11

Zache, Nicole. "Studies of mutant p53-targeting small molecules /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-322-1/.

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12

Field, Brittany. "MUTANT P53 REGULATION OF CXC-CHEMOKINE EXPRESSION IN HEAD AND NECK SQUAMOUS CELL CARCINOMA." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/442.

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Head and neck squamous cell carcinoma (HNSCC) is the 6th most common type of cancer in the western hemisphere with a five-year survival rate of only 50% for patients with a localized tumor, which decreases significantly to as low as 5% for those patients with tumors that have metastasized to distant sites of the body. It has been found that both mutant p53 and epidermal growth factor receptor (EGFR) signaling pathways function to increase the expression of CXCL5, which has been identified as a key mediator in the process of tumor metastasis. Previous data from our lab suggested that the p53 ho

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13

Johnson, Thomas M. "p53 transactivation domain mutant knock-in mice provide novel insight into p53 tumor suppressor function /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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14

Vaughan, Catherine. "Investigation of Gain-of-Function Induced by Mutant p53." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3965.

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p53 is mutated in 50% of all human cancers, and up to 70% of lung cancer. Mutant p53 is usually expressed at elevated levels in cancer cells and has been correlated with a poor prognosis. Cancer cells that express mutant p53 show an increase in oncogenic phenotypes including an increase in growth rate, resistance to chemotherapeutic drugs, and an increase in motility and tumorigenicity to name a few. We have identified several genes involved in cell growth and survival that are upregulated by expression of common p53 mutants: NFκB2, Axl, and epidermal growth factor receptor (EGFR). The aim

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15

Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.

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Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and

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16

Turrell, Frances Kathryn. "Gain-of-function and dominant-negative effects of distinct p53 mutations in lung tumours." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271848.

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Lung cancer is the most common cause of cancer-related mortality worldwide with current treatments providing limited therapeutic benefit in most cases. TP53 (Trp53, p53) mutations occur in approximately 50% of lung adenocarcinoma cases and are associated with poor prognosis and so novel therapies that target these p53 mutant lung tumours are urgently needed. Despite the high frequency of p53 mutations in lung tumours, the impact these mutations have on response to therapy remains unclear in this cancer type. The aim of my project is to characterise the gain-of-function and dominant-negative ef

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17

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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18

Khokhar, Shama Khan. "Differential effects of mutant TAp63γ on transactivation of p53 and/or p63 responsive genes and their effects on global gene expression". Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1197497418.

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19

Chandrachud, Uma. "Differential interaction of wild type and mutant p53 to promoter sequences and analysis of interacting proteins." Diss., Online access via UMI:, 2009.

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20

Olive, Kenneth P. "The germline- and tissue-specific effects of endogenous point-mutant p53." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/31186.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2005.<br>Vita.<br>Includes bibliographical references.<br>p53 is frequently altered in human tumors through missense mutations that result in accumulation of mutant p53 protein. These mutations may confer dominant-negative or gain-of- function properties to p53. To ascertain the physiological effects of tumor-associated point- mutations in p53, the structural mutant p53R172H and the contact mutant p53R270H (codons 175 and 273 in humans) were engineered into the endogenous p53 locus in mice. p53R270H/+ and p53R172H/+ mice

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21

Masood, Rubana. "The Effects of Gain of Function Mutant p53 and p63 on EPS8 and CXCL5 Expression in Head and Neck Squamous Cell Carcinoma." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/530.

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Head and neck squamous cell carcinoma (HNSCC) is one of the ten most common cancers worldwide, with a survival rate of less than 50%. A class of mutant p53, known as gain of function (GOF) mutant p53, has been found to be expressed in tumors in these patients. GOF mutant p53 not only loses the wild type tumor suppressor functions, but also gains aberrant functions that have been linked to tumorigenesis. In this current study, we utilized a model system consisting of cells derived from HNSCC tumors in order to investigate our hypothesis that GOF mutant p53 enhances, and p63 inhibits, EPS8 and

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22

Jones, Rhiannon N. "Towards the design and synthesis of a p53 mutant Y220C rescue drug." Thesis, University of Sussex, 2018. http://sro.sussex.ac.uk/id/eprint/74884/.

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The DNA damage response is an important barrier to tumorigenesis. Impairment of p53 function is crucial to tumorigenesis by allowing evasion of p53 dependent responses. The mechanisms involve either (i) missense mutations, (ii) partial abrogation of signaling pathways or effector molecules that regulate p53, (iii) epigenetic deregulation. The tyrosine to cysteine mutation, Y220C, in p53 is found in around 100,000 new cancer cases per annum. This mutation destabilizes the core domain by 4 kcal mol-1 and destabilizes p53 under physiological conditions. The large to small mutation results in the

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23

Ruddell, Carolyn Jennifer. "Antisense oligonucleotide-mediated inhibition of mutant P53 expression in cultured human cells." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367250.

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24

Woods, Nicholas Taylor. "Regulation of bax activation and apoptosis by src and acetylated mutant p53." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002641.

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David, Karine. "Analyse der Expression von Mutanten p53 in normalen und Tumorzellen." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=963606085.

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Hill, Natasha Tremayne. "Vitamin D receptor and 1alpha, 25-dihydroxyvitamin D3 mediated regulation of DeltaNp63alpha." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1450456950.

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27

Klimovich, Boris [Verfasser], and Oleg [Akademischer Betreuer] Timofeev. "Exploring mutant p53 targeting strategies for cancer therapy / Boris Klimovich ; Betreuer: Oleg Timofeev." Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/1204199825/34.

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28

Gadepalli, Venkat Sundar. "ISOLATION AND CHARACTERIZATION OF MULTIPOTENT LUNG STEM CELLS FROM p53 MUTANT MICE MODELS." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3644.

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Recent advances in understanding lung biology have shown evidence for the existence of resident lung stem cells. Independent studies in identifying and characterizing these somatic lung stem cells have shown the potential role of these cells in lung repair and regeneration. Understanding the functional characteristics of these tissue resident stem/progenitor cells has gained much importance with increasing evidence of cancer stem cells, cells in a tumor tissue with stem cell characteristics. Lung cancer is most commonly characterized by loss of p53 function which results in uncontrolled cell d

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29

Kuzniar, Beata. "Human lymphoblastoid cell lines expressing mutant p53 exhibit decreased sensitivity to cisplatin-induced cytotoxicity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ34061.pdf.

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30

Heath, Nikki. "An investigation into the role of microvesicles in mutant p53 invasive gain-of-function." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6895/.

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p53 is a transcription factor with tumour suppressive attributes which is known to be mutated in over half of human cancers. As well as compromising the ability of p53 to function as a transcription factor, mutations in p53 often result in a gain-of-function phenotype which is characterised by increased ability of cancer cells to migrate and invade. This is mediated by the ability of mutant p53 to increase recycling of α5β1 integrin and receptor tyrosine kinases (RTK) from endosomes to the plasma membrane; a process which is dependent on the Rab11 effector, Rab Coupling Protein (RCP) and the p

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Agarwal, Stuti. "Pemetrexed, A Modulator of AMP-activated Kinase Signaling and an Inhibitor of Wild type and Mutant p53." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/4003.

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New drug discoveries and new approaches towards diagnosis and treatment have improved cancer therapeutics remarkably. One of the most influential and effective discoveries in the field of cancer therapeutics was antimetabolites, such as the antifolates. The interest in antifolates increased as some of the antifolates showed responses in cancers, such as mesothelioma, leukemia, and breast cancers. When pemetrexed (PTX) was discovered, our laboratory had established that the primary mechanism of action of pemetrexed is to inhibit thymidylate 22 synthase (TS) (E. Taylor et al., 1992). Preclinical

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Najem, Ahmad. "Drug combination strategies to abrogate resistance in NRAS mutant melanoma." Doctoral thesis, Universite Libre de Bruxelles, 2017. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/258096.

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Melanoma is the deadliest form of skin cancer and one of the most difficult cancers to treat. Gene alterations identified in melanoma pointed to distinct molecular subsets of tumors with direct implications in therapeutic strategies. Activating mutations in NRAS, found in 20-30% of melanomas have been associated with aggressive clinical behavior and a poor prognosis. Nevertheless, there is lack of effective targeted therapies for NRAS mutant melanoma.Out of the few MEK inhibitors, pimasertib, a potent inhibitor of both MEK1 and MEK2 has showed promising results in NRAS mutant advanced melanoma

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Takeda, Haruna. "Accelerated onsets of gastric hamartomas and hepatic adenomas/carcinomas in Lkb1[+/-]p53[-/-] compound mutant mice." Kyoto University, 2007. http://hdl.handle.net/2433/135681.

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34

Shi, Hong. "Propriétés fonctionnelles et modulation pharmacologique de p53ser249, un mutant de la p53 spécifiquement exprimé dans les Carcinomes hépatocellulaires." Lyon 1, 2007. http://www.theses.fr/2007LYO10334.

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Le gène TP53 code pour un suppresseur de tumeurs, la protéine p53, qui est inactivée par mutation ou perte d'allèles dans plus de 50% des cancers. Une mutation particulière, R249S, qui consiste en une substitution au codon 249 (AGG vers AGT, arginine vers sérine), est très souvent détectée dans les carcinomes hépatocellulaire (CHC) dans un contexte étiologique d'exposition à l'aflatoxine. Dans ce contexte, il est rare d'observer des mutations sur d'autres codons, même ceux qui sont des cibles pour la formation d'adduits par des métabolites de l'aflatoxine in vitro. Pour explorer ce paradox, no

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Greene, Shaquita T., and Ying Zhang. "HIV-1 PR P51 Mutant Complex Formation with Inhibitors." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/biology_hontheses/4.

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Human Immunodeficiency Virus (HIV) has become a global pandemic with at least 25 million deaths and no cure. One of the most important targets to inhibit this virus is HIV-1 protease (PR), which is required to cleave the viral proteins needed for maturation of the virus after it invades and replicates in the host cell. There are nine protease inhibitors that are used in AIDS treatment. The virus loses susceptibility to these inhibitors by drug resistance due to mutations. The goal of the project is to examine the highly drug resistant HIV PR P51 in its complex with inhibitors. In this experi

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Scian, Mariano J. "MODULATION OF GENE EXPRESSION BY TUMOR-DERIVED MUTANT p53. ROLE OF TRANSACTIVATION IN GAIN-OF-FUNCTION." VCU Scholars Compass, 2005. https://scholarscompass.vcu.edu/etd/5518.

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It was hypothesized that the C-terminal sequences for mutant p53 would be required for oligomerization. and oligomerization may be critical for gain-of-function. An N-terminal deletion mutant of p53 that deletes amino acids 1-293 was used as a tool to perform hetero-oligomerization studies. This mutant retains the entire oligomerization domain but dispenses off the transactivation domain and a large portion of the sequence- speciﬁc DNA-binding domain. Co-transfection experiments show that p53 del. 1-293 forms hetero-oligomeric complexes with p53-D281G. Also. co-expression of p53 del. 1- 293 wi

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Meneghetti, Bruna Valandro. "Efeitos de proteínas p53 mutantes associadas à síndrome de Li-Fraumeni na viabilidade celular em condições basais e sob estresse genotóxico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/163707.

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A síndrome de Li-Fraumeni (SLF) é uma síndrome rara de predisposição a câncer associada a mutações germinativas no gene supressor tumoral TP53. As vias de sinalização da proteína p53 estão envolvidas na regulação da apoptose, das paradas do ciclo celular, da senescência e do reparo de danos no DNA. As mutações em p53 mais comumente encontradas em tumores estão distribuídas ao longo do domínio de ligação ao DNA, incluindo a mutação G245S associada à SLF. No entanto, a mutação mais frequentemente associada à SLF nas regiões Sul e Sudeste do Brasil é a mutação R337H, que afeta o domínio de oligom

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Westrop, Gareth D. "The genetic basis for the attenuation of the Sabin type 3 poliomyelitis vaccine, P3/Leon/12a₁b." Thesis, University of Leicester, 1986. http://hdl.handle.net/2381/35427.

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Complete nucleotide sequences have been derived for the Sabin type 3 vaccine, P3/Leon/l2a1b, and its neurovirulent progenitor, P3/Leon/37 (Stanway et al., 1983, 1984). These studies revealed 10 base substitution mutations which must account for the attenuated and temperature sensitive phenotypes of the vaccine. Complete DNA copies of the genomes of P3/Leon/12a1b and P3/Leon/37 were constructed, each within the prokaryote vector, pAT 153. The full-length cDNA clones were shown to be infectious following transfection of human epithelial cells. Virus rescued from the cDNA clone of P3/Leon/12a1b c

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Wülfing, Verena [Verfasser], and Jochen [Akademischer Betreuer] Dahm-Daphi. "Stimulation of Homologous Recombination by P53 gain-of-function mutant M237I / Verena Wülfing. Betreuer: Jochen Dahm-Daphi." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1027574041/34.

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Jethwa, Alexander [Verfasser], and Philipp [Akademischer Betreuer] Beckhove. "Identification of regulators of mutant p53 accumulation in lymphoma using RNA interference / Alexander Jethwa ; Betreuer: Philipp Beckhove." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1177148951/34.

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Chung, Maureen. "Expression of the c-fos proto-oncogene, mutant p53 anti-oncogene and statin in colorectal carcinoma and adjacent mucosa." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56961.

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The purpose of this study was to provide evidence for a field defect around colorectal carcinomas using c-fos, mutant p53 and statin markers. Tissue from ten colorectal carcinomas and mucosa at 1, 5 and 10 cm from the primary lesion was obtained from surgical specimens and frozen in liquid nitrogen. Detergent-extracted protein was separated by electrophoresis through polyacrylamide gells and western blots performed using monoclonal antibodies against c-fos, mutant p53 and statin. Expression of c-fos within the carcinoma was increased relative to its expression at 1 cm, which was increased rela

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Gouas, Doriane. "Association entre le mutant p.R249S de p53 et la protéine HBx du virus de l’hépatite B dans les carcinomes hépatocellulaires." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10280.

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La mutation R249S (mutant p.R249S) du gène TP53, caractéristique de l'exposition à l'aflatoxine B1 (AFB1), est la plus fréquente dans les carcinomes hépatocellulaires (CHC) et est dans la plupart des cas associée à une infection chronique par le virus de l'hépatite B (VHB). En effet, il existe une synergie entre ces deux facteurs de risque, augmentant ainsi le risque de développer un CHC. Dans une première partie, nous avons étudié les mécanismes moléculaires de cette synergie dans différents modèles cellulaires puis dans une deuxième partie nous avons utilisé une approche épidémiologique pour

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Bug, Monika [Verfasser], Matthias [Akademischer Betreuer] Dobbelstein, Frauke [Akademischer Betreuer] Melchior, and Silvio [Akademischer Betreuer] Rizzoli. "The accumulation of mutant p53 in human cancer cells / Monika Bug. Gutachter: Matthias Dobbelstein ; Frauke Melchior ; Silvio Rizzoli. Betreuer: Matthias Dobbelstein." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1042346119/34.

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Levy, Claudia Bustamante. "Análise de mutações no gene TP53 em casos de câncer de mama e estudo da proteína p53 mutante: aspectos fisiopatológicos do tumor." Universidade do Estado do Rio de Janeiro, 2010. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=1772.

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O câncer de mama é o tipo mais frequente de neoplasia maligna entre as mulheres, com a incidência de mais de um milhão de novos casos no mundo, por ano. O gene TP53 é responsável por regular o destino da célula em resposta a estresses genotóxicos e não genotóxicos. Mutações somáticas neste gene são encontradas em, aproximadamente, 50% dos carcinomas humanos. No câncer de mama, a frequência das mutações no TP53 é em torno de 20 a 50%, sendo a alteração mais encontrada. Estas mutações podem alterar a conformação da proteína, prejudicando sua função de ativadora da transcrição de genes alvo e, po

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Zheng, Changyu. "Transfection of cells of low grade lymphoproliferative disorders (chronic lymphocyte leukemia and follicular lymphoma) with myc and/or ras and mutant p53." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23960.pdf.

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Chollat-Namy, Marie. "Effet de l’inactivation du gène suppresseur de tumeur p53 et de sa réactivation pharmacologique sur la réponse cytotoxique anti-tumorale The Pharmalogical Reactivation of p53 Function Improves Breast Tumor Cell Lysis by Granzyme B and NK Cells Through Induction of Autophagy Mutant P53 Gain of Function Stimulates PD-L1 Expression." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL032.

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Le système immunitaire joue un rôle important dans le contrôle et l'éradication du cancer. Des acteurs majeurs de la réponse immune antitumorale sont les cellules tueuses naturelles (ou cellules NK) et les lymphocytes T cytotoxiques (ou CTL), capable de reconnaitre et détruire des cellules tumorales par l’exocytose de perforine et de granzymes contenus dans leur granule cytotoxique. Il a été montré au sein du laboratoire l’implication de la protéine suppresseur de tumeur p53 dans cette voie apoptotique. Or, plus de 50% des tumeurs humaines présentent des mutations inactivatrices de p53 ce qui

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Stojanović, Nataša [Verfasser], Günter [Akademischer Betreuer] Schneider, Klaus-Peter [Akademischer Betreuer] Janssen, and Dieter [Akademischer Betreuer] Saur. "Development of novel models to investigate mutant p53 functions in pancreatic cancer and determinants of deregulated expression / Nataša Stojanović. Gutachter: Klaus-Peter Janssen ; Dieter Saur. Betreuer: Günter Schneider." München : Universitätsbibliothek der TU München, 2014. http://d-nb.info/1068908297/34.

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Pinezi, Juliana Castro Dourado. "Efeitos colaterais tardios na bexiga após radioterapia por câncer de colo de útero: avaliação da associação com polimorfismos de TP53, ATM e MDM2." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5151/tde-09012015-163553/.

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Introdução: Na prática clínica se observa que há diferenças na incidência de efeitos colaterais entre pacientes submetidos ao mesmo esquema terapêutico de radioterapia. Tais diferenças podem ser entendidas como uma radiossensibilidade individual determinada geneticamente. Objetivos: Este estudo teve como objetivo avaliar os efeitos tardios na bexiga em pacientes com câncer do colo uterino tratadas com radioterapia, com ou sem cirurgia, e o valor prognóstico de três polimorfismos genéticos de base única com relação ao desenvolvimento de cistite actínica. Material e métodos: Foi realizada uma an

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Nadal, Serrano Mercedes. "Efectos de los Estrógenos, la Genisteína y la Leptina sobre el Estrés Oxidativo en el Cáncer de Mama. Importancia de la UCP2." Doctoral thesis, Universitat de les Illes Balears, 2014. http://hdl.handle.net/10803/284237.

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El estrés oxidativo es un desequilibrio entre la producción de radicales libres y los sistemas antioxidantes encargados de su neutralización. El resultado de este desequilibrio es la acumulación de daños en diversas estructuras celulares incluyendo el DNA. El cáncer se acompaña de un mayor estrés oxidativo a nivel celular, por este motivo, muchos de los tratamientos terapéuticos van dirigidos a aumentar los niveles citotóxicos de ROS, conduciendo a la célula tumoral a la apoptosis. Sin embargo, durante la tumorigénesis las células van adquiriendo una serie de características que permiten mante

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Chiao, Ming-Tsang, and 矯明昌. "Characterization of p53 Mutants Identified from Lung Carcinoma in Taiwan." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/71030562517077944067.

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碩士<br>中山醫學院<br>毒理學研究所<br>88<br>p53 is a critical tumor suppressor gene, which can respond to multiple signals of cellular gatekeeper for growth and division. MDM2 gene is one of the downstream target genes for transcriptional activation by the product of p53 tumor suppressor gene. Transactivation of MDM2 gene expression is represented by the presence of a functional p53 protein. To understand the biological function of the mutant p53 that may play the role in tumorigenesis, we construct a number of p53 mutants by site directed mutagenesis (H179Y, P67C/L194R, S240R, R249S, A276D, E286Q, G361R),

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