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Dissertations / Theses on the topic 'P53 Alterations'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Reles, Angela. "Molecular genetic alterations in ovarian cancer." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/13801.

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Einleitung: Das p53 Tumorsuppressorgen spielt eine zentrale Rolle für Regulation des Zellzyklus und die Induktion der Apoptose. MDM2, das Protein des mdm2 Gens, bindet an p53, hemmt seine Funktion als Transkriptionsfaktor und bewirkt den raschen Abbau des Proteins. Methode: Gefriergewebe von 178 primären Ovarialkarzinomen wurde mittels PCR, SSCP Single Strand Conformation Polymorphism), DNA-Sequenzierung und Immunhistochemie auf p53 Mutationen (exon 2-11) und p53 Proteinüberexpression untersucht. Das mdm2-Gen wurde an 92 Ovarialkarzinomen, neun Borderline-Tumoren, sechs Cystadenomen und 2

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2

Saffroy, Raphael. "Instabilite genomique et alterations de p53 dans le carcinome hepatocellulaire." Paris 5, 2000. http://www.theses.fr/2000PA05N117.

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3

Ling, Gao. "p53 alterations in human skin : a molecular study based on morphology /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5131-4/.

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4

Gao, Ling. "p53 Alterations in Human Skin : A Molecular Study Based on Morphology." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1465.

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<p>Mutation of the p53 gene appears to be an early event in skin cancer development. The present study is based on morphology and represents a cellular and genetic investigation of p53 alterations in normal human skin and basal cell cancer.</p><p>Using double immunofluorescent labelling, we have demonstrated an increase in thymine dimers and p53 protein expression in the same keratinocytes following ultraviolet radiation. Large inter-individual differences in the kinetics of thymine dimer repair and subsequent epidermal p53 response were evident in both sunscreen-protected and non-protected s

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5

Froggatt, Nicola Jane. "Alterations to the tumour suppressor genes p53 and dcc in colorectal neplasia." Thesis, University of York, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385322.

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6

Wäster, Larsson Petra. "UVA/B induced redox alterations and apoptosis in human melanocytes." Doctoral thesis, Linköpings universitet, Dermatologi och venerologi, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-8880.

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Malignant melanoma is one of the most rapidly increasing cancers and accounts for about three-quarter of all skin cancer deaths worldwide. Despite compelling evidence that ultraviolet (UV) irradiation causes melanoma the knowledge how various wavelength spectra affect the balance between proliferation and apoptosis controlling the homeostasis of the melanocyte population is still limited. The aim of this thesis was to elucidate the regulation of UVA/B induced apoptotic signaling in human epidermal melanocytes in vitro in relation to redox alterations and antioxidant photoprotection. UVA irradi

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7

Sivertsson, Åsa. "Detection and analysis of genetic alterations in normal skin and skin tumours." Doctoral thesis, KTH, Biotechnology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-3432.

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<p>The investigation of genetic alterations in cancer-relatedgenes is useful for research, prognostic and therapeuticpurposes. However, the genetic heterogeneity that often occursduring tumour progression can make correct analysischallenging. The objective of this work has been to develop,evaluate and apply techniques that are sufficiently sensitiveand specific to detect and analyse genetic alterations in skintumours as well as in normal skin.</p><p>Initially, a method based on laser-assisted microdissectionin combination with conventional dideoxy sequencing wasdeveloped and evaluated for the

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8

Heminger, Katherine Ann. "LOSS OF HDMX LEADS TO ALTERATIONS IN GENE EXPRESSION AND INHIBITION OF CELL GROWTH IN TUMOR CELLS WITH WILD-TYPE p53." Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1175282827.

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9

Rafki, Beljebbar Naïma. "Etude des alterations du phenotype nucleaire liees a la resistance mdr dans des cellules leucemiques humaines sensibles et resistantes a la chimiotherapie." Reims, 1996. http://www.theses.fr/1996REIMP213.

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10

Tammemagi, Martin Carl. "Tobacco smoking, p53 tumour suppressor gene alterations, and clinicopathologic features and prognosis in non-small cell lung cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0013/NQ35341.pdf.

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11

Raveux, Aurélien. "In vivo exploration of the impact of ribosome biogenesis alterations on intestinal homeostasis and tumorigenesis in the adult mouse." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS517.

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La biogenèse des ribosomes est un processus cellulaire essentiel. Des altérations de ce processus induisent une forte activation de p53 et d’autres voies de surveillance encore mal connues, auxquelles les cellules tumorales semblent particulièrement sensibles in vitro. L’inhibition de la synthèse des ribosomes constitue ainsi une stratégie prometteuse pour lutter contre le cancer. L’inactivation conditionnelle du facteur de biogenèse des ribosomes Notchless (Nle) dans l’intestin de souris adulte conduit à l’élimination rapide des cellules souches et des progéniteurs intestinaux. Au cours de ma

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12

Saidj, Djamel. "Alteration of p53 and NF-kB pathways by E7 protein from cutaneous Human Papillomavirus type 38." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10237/document.

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Les infections virales sont responsables de 15 à 20 % des cancers humains. L étude des mécanismes moléculaires avec lesquels les virus oncogènes induisent la transformation cellulaire est essentielle pour la compréhension des cancers qui en résultent. Cela permettra également la découverte de nouveaux mécanismes pouvant être impliqués dans le développement de cancers, qui peuvent être ciblés par des approches thérapeutiques. Les virus du papillome humain (HPV) sont des petit virus à ADN qui futs isolés de la peau de patients souffrants de Epidermodysplasia Verruciformis (EV) qui cause un risqu

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13

Oelsner, Roselyne [Verfasser]. "p53-Alterationen in Kolonadenomen : Beziehung zu Zellproliferation und Klinik / Roselyne Oelsner." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/101077655X/34.

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14

Patel, Angana Heet. "Unravelingthe molecular mechanism behind metabolic reprogramming caused by alterations of the enzyme PI3-kinase." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-17410.

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Oncogenes and tumor suppressor genes play a key role in cancer induction and progression. They directly or indirectly regulate critical metabolic pathways, phosphatidylinositol-3 kinase pathway being frequently activated pathway in cancer. The catalytic subunit of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K), p110α, is the most frequently mutated kinase in human cancer, E542K, E545K, and H1047R mutations being the most common. Expression of hepatic E545K and H1047R p110α mutants in vivo shows marked and rapid increase in hepatic lipid and glycogen accumulation in mice with development

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15

Yamada, Atsushi. "Aberrant expression of EZH2 is associated with a poor outcome and P53 alteration in squamous cell carcinoma of the esophagus." Kyoto University, 2011. http://hdl.handle.net/2433/142063.

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16

Friderici, Steinman Elisa-Gabriele Friederike Margarethe von Verfasser], and Guido [Akademischer Betreuer] [Sauter. "Häufigkeit und prognostische Bedeutung von p53- und bcl-2-Alterationen bei menschlichen Weichgewebstumoren / Elisa-Gabriele Friederike Margarethe von Friderici Steinman. Betreuer: Guido Sauter." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2011. http://d-nb.info/1020466014/34.

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17

an, Ts'ao te, and 曹德安. "Alterations of p53 gene in human bladder cancers." Thesis, 1993. http://ndltd.ncl.edu.tw/handle/27218818845479645829.

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18

Yeager, Thomas R. "Role of p16, pRb and p53 alterations in bladder cancer pathogenesis." 1997. http://catalog.hathitrust.org/api/volumes/oclc/38851937.html.

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19

Puthenveettil, Jairaj A. "Alterations in p53 and p16/pRb pathways in human uroepithelial cell immortalization." 1998. http://catalog.hathitrust.org/api/volumes/oclc/42903283.html.

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20

Wang, Yu-Chien, and 王郁茜. "Etiological association of alterations in p53-hdm2-p14ARF pathway with lung tumorigenesis in Taiwan." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/19243168942193336071.

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碩士<br>國立臺灣師範大學<br>生物研究所<br>91<br>Lung cancer is the leading and second cause of cancer deaths among women and men in Taiwan, respectively. However, the molecular mechanisms involved in lung tumorigenesis in Taiwan remain poorly defined. There is increasing evidence that alterations in tumor suppressor genes and oncogenes are common in many forms of human cancer including lung cancer. We found that p53 gene mutation frequency was 17% in resected non-small cell lung cancers (NSCLC). However, p53 protein overexpression frequency was 48%. To further identify the molecular basis for this p53 immuno

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21

Wen-Ting, Yeh, and 葉文婷. "Analysis of gene alterations of p14ARF-p53 and p16INK4a-Rb pathways in bladder cancers." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/87649100212305782273.

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碩士<br>高雄醫學大學<br>醫學研究所<br>89<br>Bladder cancer is a significant health problem in the world. According to previously reports, alteration on chromosome 9 is the most common events in bladder cancer. The 9p21 gene cluster, harboring growth suppressive genes p14ARF and p16INK4a, play active roles in the p53 and Rb growth control pathways, respectively. p16INK4a is a cyclin- dependent kinase inhibitor functioning upstream Rb. p14ARF restrains cell growth by abrogating Mdm2 inhibition of the p53 activity and facilitates p53 mediated cell cycle arrest and apoptosis. Recent studies revealed that inact

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22

Gu, Wen-Hui, and 古文慧. "Genomic alterations in cervical carcinoma:loss of heterozygosity on chromosomes 3p, 5p and p53 gene." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/25479985478281183348.

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23

王化千. "Alterations of p53、apc、mcc and L-myc Gene in Colorectal Cancer:Relationship to Clinicopathologic Variables." Thesis, 1997. http://ndltd.ncl.edu.tw/handle/92274902762733007242.

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碩士<br>長庚大學<br>基礎醫學研究所<br>85<br>Colorectal cancer is one of the common cancers in Taiwan. According to health and vital statistics by Department of Health, Executive Yuan, the death rate of colorectal cancer was 11.62 per 100,000 population in 1995. In fact, the death rate of this cancer is gradually increasing year after year. Now, colorectal cancer is the third and highest cause of cancer death for man and woman, respectively. Epidemiological studies have indicated that dietary factors as well as genetic factors play some important role in the development of this cancer. In hu

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24

Li, Pei-Lun, and 李佩倫. "Alterations of p53 and p16 Tumor Suppressor Genes by Tobacco Smoking in Oral Squamous Cell Carcinoma." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/94477847570229272279.

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25

Sun, Yan [Verfasser]. "Genetic alterations in advanced head and neck cancer : loss of heterozygosity, microsatellite instability, p53 mutation / von Yan Sun." 2000. http://d-nb.info/961309199/34.

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26

Reles, Angela [Verfasser]. "Molecular genetic alterations in ovarian cancer : the role of the p53 tumor suppressor gene and the mdm2 oncogene / Angela Reles." 2001. http://d-nb.info/964505622/34.

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27

Chen, Ya-Wen, and 陳雅雯. "Genomic Alterations associated with Liver Carcinogenesis─Characterization of Candidate Tumor Suppressor Genes on Chromosome 16q and Analysis of Genetic Changes of p53 Gene and Wnt Signaling Pathway." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/56451866136201103114.

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博士<br>國立臺灣大學<br>分子醫學研究所<br>91<br>The frequency of loss of heterozygosity (LOH) on chromosome 16q is particularly high (30-70%) in hepatocellular carcinoma (HCC), suggesting a possible existence of tumor suppressor genes associated with tumorgenesis of HCC on chromosome 16q. To narrow down the common regions of LOH on chromosome 16q, a total of 40 microsatellite markers, distributed evenly with 1-cM interval, were used to map the LOH regions in 46 pairs of HCCs and their corresponding normal tissues. Two refined regions of common allelic loss revealed by minimum LOH overlapping were obtained. O

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28

Teh, Bee-Heong, and 鄭美香. "The molecular epidemiology study of the alteration of p53 in female breast cancer in Taiwan." Thesis, 1996. http://ndltd.ncl.edu.tw/handle/64132050651020284199.

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碩士<br>國立陽明大學<br>公共衛生學研究所<br>84<br>p53基因是目前最常被發現和癌症發生有關的抑癌基因。其在乳癌之突變率約為25-40%。台灣乳癌p53之變異是否和國外研究有所不同是值得探究的問題。本實驗利用PCR-SSCP、DNA定序實驗、PCR-M、及免疫組織化學染色法分別分析p53基因、染色體、及蛋白質層面之變異，進而探討台灣乳癌p53基因之致突變模式以及和p53蛋白失去活性有關之危險因子。本研究所偵測之p53基因突變率為27.3%(27/99)。其中有26位個案完成DNA定序實驗。DNA突變型式以CpG位置之G to A transition最為常見，佔所有突變型式之30.8%。為進一步瞭解國人乳癌p53之分子流行病學特徵，本研究對國內、外乳癌p53之突變率與突變型式之異同也作了描述性流行病學之探討。另一方面，在p53基因與染色體層面之分析，顯示p53突變與其染色體缺失有高度的相關性。然而在p53基因與蛋白層面之分層分析，p53基因突變僅和p53蛋白在細胞核內蓄積有關，而和其在細胞質內蓄積無關，顯示p53蛋白在細胞質內蓄積為受細胞環境因子干擾所致。在危險因子之分析方面，賀爾蒙替補治療和p53蛋白受細胞環境因子干擾而失去活性有非常顯著的相關性。綜合研究的結果，本研究發現:一、內源性去氨機制所主導之CpG位置之G to Atranstion走台灣女性乳癌非常重要

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29

Lee, Chin Chu, and 李金祝. "HIC1 alteration and its association with deregulation of p53/SIRT1-mediated control in lung cancer." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/67563641661992505291.

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碩士<br>國立臺灣師範大學<br>生命科學研究所<br>94<br>Purpose: We have previously reported that the chromosomal regions at 17p13.3 showed a high frequency of loss of heterozygosity in tumors from non-small cell lung cancer (NSCLC) patients. HIC1 (hypermethylated in cancer 1) is a candidate tumor suppressor gene at 17p13.3 and is epigenetically inactivated in many human cancers. A circular regulation of HIC1, SIRT1 deacetylase, and p53 is proposed for modulation of cellular responses to DNA damage in cell and animal studies. However, the etiological role of HIC1 alteration and its correlation with p53 and SIRT1 d

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