Дисертації з теми "111201 Cancer Cell Biology"
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Bair, Elisabeth Laurine. "Cell-cell and cell-matrix interactions involved in cancer invasion." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280673.
Повний текст джерелаKrubasik, Davia Regina Editla. "The role of Metalloproteinases in cancer cell biology." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612722.
Повний текст джерелаNg, Sheng Rong. "CRISPR-mediated interrogation of small cell lung cancer." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117782.
Повний текст джерелаThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged student-submitted from PDF version of thesis. Vita.
Includes bibliographical references.
Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine lung carcinoma that remains among the most lethal of solid tumor malignancies. Despite decades of research, treatment outcomes for SCLC remain very poor, highlighting the need for novel approaches to target the disease. Recent genomic sequencing studies have identified multiple recurrently altered genes in human SCLC tumors, many of which remain to be functionally validated. Genetically engineered mouse models (GEMMs) of SCLC have been developed that recapitulate many key features of human SCLC. These models have been used extensively to investigate various aspects of SCLC biology, including tumor initiation, progression and metastasis. The development of the CRISPR-Cas9 system has greatly facilitated genome editing in mammalian cells, leading to its widespread adoption for various applications in cancer biology. We have utilized this system in two complementary ways to investigate the molecular mechanisms involved in SCLC initiation, progression and maintenance. Firstly, we have adapted the CRISPR-Cas9 system for use in GEMMs of SCLC, to enable rapid modeling and functional validation of candidate tumor suppressor genes in vivo. Using this system, we have demonstrated that p107, a member of the retinoblastoma family that is mutated in a significant fraction of human SCLC tumors, is a functional tumor suppressor in SCLC. Notably, loss of p107 in SCLC tumors resulted in significant phenotypic differences compared with loss of its close relative, p130. We also demonstrated that CRISPR-induced mutations can be used to infer lineage relationships between primary and metastatic tumors in the same animal. Secondly, we have performed a CRISPR-based genetic screen, utilizing a custom sgRNA library targeting the druggable genome, to identify novel SCLC-specific genetic vulnerabilities. We found that SCLC cells displayed enhanced sensitivity towards disruption of several key metabolic pathways, including the de novo pyrimidine biosynthesis pathway. Pharmacological inhibition of Dhodh, a key enzyme in this pathway, reduced the viability of SCLC cells in vitro and strongly suppressed SCLC tumor growth in vivo, validating this pathway as a promising therapeutic target in SCLC. Taken together, the work presented here demonstrates the utility of the CRISPR-Cas9 system for performing functional interrogation of SCLC.
by Sheng Rong Ng.
Ph. D.
Kay, Sophie Kate. "Cell fate mechanisms in colorectal cancer." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:f19bf73d-0c0e-4fff-9589-bf43f9ff12f0.
Повний текст джерелаNeal, Corey Lekeil. "Snail mediates epithelial mesenchymal transition and cell adhesion in human prostate cancer cell lines." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2011. http://digitalcommons.auctr.edu/dissertations/233.
Повний текст джерелаMcNae, Fiona. "The cell biology of non-genotoxic hepatocarcinogens." Thesis, University of Surrey, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260350.
Повний текст джерелаWeitzel, Douglas H. "Modulation of cell cycle checkpoints by anti-cancer agents /." The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu148820531851081.
Повний текст джерелаHorlock, Nigel. "The cell biology of basal cell carcinoma : relationship to histology and clinical outcome." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391606.
Повний текст джерелаPoluri, Raghavendra Tejo Karthik. "Using bioinformatic analyses to understand prostate cancer cell biology." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66803.
Повний текст джерелаProstate Cancer (PCa) affects 1 in 7 men in their lifetime and is the number one diagnosed cancer in men. It is the 4th most common cancer in Canada. PCa is a hormone-dependent disease diagnosed in men. Androgens play a vital role in the disease progression. The standard of care to treat PCa, following surgery or radiation therapy, is the androgen deprivation therapy (ADT). In spite of initial positive response to androgen inhibition, the progression of the disease to castration-resistant prostate cancer (CRPC) is almost inevitable. Across the various stages of PCa, the androgen receptor (AR) plays a major role. This thesis portrays the methods developed and used to understand PCa biology. The work demonstrated in this thesis majorly consists of bioinformatic analyses performed on publicly available data sets and a pipeline built to analyse RNA-Seq data. An RNA-Seq pipeline has been developed to understand the impact of androgens and the genes regulated upon androgen treatment in PCa cell models. This bioinformatic pipeline consists of various tools which have been described below in chapter 1. The major goal of this project was to develop a pipeline to analyse the RNA-Seq data which helps to understand and define the metabolic pathways and genes regulated by androgens which play an important role in PCa disease progression. The experimental workflow consisted of two androgen receptor positive cell lines LNCaP and LAPC4. All the data used in this project has been made publicly available for the research community to perform various other comparative studies and analyses to understand the functions of androgens in a much deeper sense to develop novel therapies to treat PCa. In another project described in chapter 2, bioinformatic analyses have been performed on publicly available data to understand the loss and genomic alteration frequency of the gene PTEN occurring at 10q23. These analyses highlighted that the genomic alteration frequency of PTEN is much higher in CRPC than in localised PCa, and also helped in identifying other genes which are lost along with PTEN. The lost genes have not been studied much in literature, but few studies demonstrated that they might possess tumor suppressor characteristics. These results might be a good start for further deeper analyses regarding the lost of genes. Understanding the functions of AR and the deletion of PTEN will help for the development of novel strategies and approaches to diagnose and treat PCa. Integration of bioinformatic analyses with clinical research open up a new perspective in the PCa research domain.
Popovic, Predrag. "Cisplatin resistance in nonsmall cell lung cancer: Role of platinum accumulation and cell membranes." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/9662.
Повний текст джерелаDassie, Justin Patrick. "Selective targeting of cancer cells with RNA aptamers." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/1310.
Повний текст джерела凌明達 and Ming-tat Patrick Ling. "A study of molecular and cell biology of prostate tumorigenesis in cell culture." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223102.
Повний текст джерелаDremann, David Michael. "Pluronic Activity in Hyperthermia-induced Cancer Cell Death." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1247425426.
Повний текст джерелаBrauneis, Alison Dooley. "Investigating the initiation and progression of small cell lung cancer." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/63063.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references.
Small cell lung cancer (SCLC) comprises 18% of all lung cancer cases and is an aggressive disease with a five-year survival rate of less than 5%, mainly due to the advanced nature of the disease at the time of diagnosis. Despite the need to better understand this disease, the genetic lesions that contribute to SCLC remain poorly characterized. To investigate the genetic aberrations that occur in SCLC, we analyzed the copy number alterations in tumors and metastases arising in a mouse model of SCLC (mSCLC), driven by conditional inactivation alleles of two tumor suppressor genes, Trp53 and Rbl. We identified frequent, high-level amplification of a novel, protooncogenic transcription factor Nuclear Factor I/B (Nfib in mouse, NFIB in human), which frequently occurred coincident with amplification of a previously characterized oncogene, L-myc (Mycl). Functional studies revealed cooperation between Nfib and Lmyc in cellular transformation. Comparative genomics identified NFIB amplifications in human SCLC and uncovered a role for NFIB in regulating cell viability and proliferation. We also examined the effect of lung injury on SCLC initiation and progression utilizing naphthalene, a chemical that ablates the cells that line the bronchioles of the lung. The pulmonary neuroendocrine cells, the putative cell of origin of SCLC, are refractory to naphthalene-mediated injury. We demonstrated that naphthalene-mediated injury prior to tumor initiation in the mouse model of SCLC induced more advanced mSCLC lesions and decreased tumor latency. Throughout the course of this thesis work, we successfully utilized a mouse model of SCLC to interrogate the initiation of SCLC as well as to define the genetic alterations that occur in SCLC tumors and metastases. This work has led to the identification of candidate genes that promote tumor progression and to a better understanding of the process of tumor initiation. We anticipate that these findings will not only enhance our understanding of SCLC, but may lead to the development of therapeutics used to treat this aggressive disease.
by Alison L. Dooley.
Ph.D.
Valenciaga, Anisley. "Cell cycle regulators and transcriptional targeting in Medullary Thyroid Cancer." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523891651533415.
Повний текст джерелаLiu, Yunpeng Ph D. Massachusetts Institute of Technology. "Integrative multi-omics dissection of cancer cell states and susceptibility." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/130818.
Повний текст джерелаCataloged from the official PDF of thesis. "February 2021."
Includes bibliographical references (pages 217-239).
Cancer cells are characterized by a broad spectrum of unique genetic, epigenetic and transcriptional states, which are often concomitant with high degrees of plasticity in cell identity. These cell states and the fluidity therein are a major source of resistance to both chemotherapy and targeted therapy. Combinatorial efforts in experimental assays and computational modeling are pivotal for understanding the origins of cancer cell plasticity and exposing cell state-specific vulnerabilities. In this thesis, I will first present my studies on two clinically challenging types of hematopoietic malignancies and discuss key genes that sustain cell identity and survival programs revealed through multi-omics approaches.
In the first study, a combination expression, chromatin binding and chromatin accessibility analyses revealed the plant homeodomain finger-like family protein PHF6's novel functions as a lineage identity regulator in a mouse model of BCR-ABL-driven B cell acute lymphoblastic leukemia. In the second case, single cell transcriptomic profiling, computational inference of cell cycle trajectories and unbiased functional genomics jointly identified RAD51B as a uniquely essential gene in near-haploid leukemia. Finally, to systematically model heterogeneous cell states and generate readily testable predictions of susceptibilities in cancer, I proposed a novel computational pipeline that integrates multiple data types to construct a quantitative model of transcription regulation, which can in turn be used to infer changes in gene expression in response to transcription factor perturbation.
The pipeline then uses these gene expression responses to perturbations to estimate changes in protein activity and finds a combination of protein activity score changes that best predicts changes cell fitness. Applying the pipeline to glioblastoma multiforme - a cancer type that lacks effective targeted therapy, I prioritized a small set of genes including MYBL2 as subtype-specific candidate targets. My thesis work demonstrates the power of integrative, multi-omics approaches for effective discovery of susceptibilities in cancer and highlights an emerging paradigm for understanding the information flow in the cellular circuitry.
by Yunpeng Liu.
Ph. D.
Ph.D. Massachusetts Institute of Technology, Department of Biology
Zeid, Rhamy. "Characterization and Disruption of Cis Regulatory Elements in Cancer." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493536.
Повний текст джерелаMedical Sciences
Wright, Muelas Marina. "A systems biology approach to cancer metabolism." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/a-systems-biology-approach-to-cancer-metabolism(27286c8a-0281-4256-b749-2ec9bd36370f).html.
Повний текст джерелаThor, Straten Per. "T-cell response against human malignant melanoma." Thesis, Open University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264405.
Повний текст джерелаDowling, Ryan. "The role of mTOR signalling in translational control and cancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66869.
Повний текст джерелаRésumémTOR est une sérine/thréonine kinase qui joue un rôle primordial dans lecontrôle de plusieurs fonctions cellulaires, incluant la prolifération, la croissance, ladifférentiation, l'autophagie et la réorganisation du cytosquelette. Les cellulesmammifères possèdent deux complexes protéiques contenant mTOR, soit mTORC1 andmTORC2. mTORC1 exerce son action en contrôlant l'initiation de la traduction desARN messagers via la phosphorylation de ses principaux effecteurs : les 4E-BP et lesS6K. Dans le but de mieux comprendre les fonctions spécifiques des 4E-BP et des S6Ken aval de la signalisation cellulaire initiée par mTORC1, nous avons utilisé de nouveauxinhibiteurs spécifiques au site actif de mTOR, ainsi que des cellules n'exprimant pas les4E-BP ou les S6K. Nous avons découvert que les 4E-BP et les S6K jouent des rôlesdistinct en aval de mTORC1, les 4E-BP étant principalement impliquées dans laprolifération cellulaire, alors que les S6K jouent un rôle dans le contrôle de la croissancecellulaire. Les effets des inhibiteurs spécifiques au site actif de mTOR sur la proliférationcellulaire, la progression à travers le cycle cellulaire et la synthèse protéique sontfortement atténués dans les cellules nulles pour les 4E-BP, alors qu'ils sont inhibés demanière importante dans les cellules de type sauvage. Cependant, la croissance descellules 4E-BP nulles, en présence des inhibiteurs spécifiques au site actif de mTOR, estla même que celle observée pour les cellules de type sauvage. À l'opposé, la croissancedes cellules S6K nulles n'est pas affectée par ces inhibiteurs, tandis que les inhibiteursconservent leurs effets négatifs sur la prolifération et la progression au travers du cyclecellulaire dans ces mêmes cellules. Ces résultats sont en accord avec un modèle danslequel la signalisation en aval de mTORC1, pour promouvoir la prolifération et lacroissance cellulair
Mireuta, Matei. "Aspects of insulin-like growth factor binding proteins in cancer." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114128.
Повний текст джерелаL'ensemble du système de facteurs de croissance insulinomimétique (IGF) est composé de deux ligands (IGF-1 et IGF-2), de deux récepteurs (IGF- 1R et IGF-2R) et de six protéines de liaison (IGFBP-1 à 6). Les IGFs sont des hormones endocrines, paracrines et autocrines qui stimulent la croissance cellulaire, la prolifération et le métabolisme. Il existe un grand nombre d'études utilisant des approches épidémiologiques ou des modèles in vivo et in vitro qui démontrent l'importance des IGFs dans le contexte du cancer. Le IGF-1R est le récepteur physiologique des deux ligands et son activation mène à d'importants changements cellulaires tels que l'activation des voies de signalisation PI3K/AKT/mTOR et Ras/Raf/MAPK. Étant donné son rôle dans la promotion et dans la progression du cancer, le système des IGFs représente une cible potentielle pour le traitement du cancer. De façon classique, les protéines de liaison IGFBP ont été décrites comme de simples porteurs d'IGFs dans le sang et autres fluides. Les IGFBPs peuvent modifier la biodisponibilité des IGFs de façon positive en augmentant leur demi-vie ou de façon négative due à leur compétition avec le IGF-1R pour la liaison. En plus de leur rôle classique, il est de plus en plus évident que ces protéines peuvent agir de manière indépendante, mais les mécanismes impliqués restent flous. Également, il existe des études épidémiologiques qui ont corrélé la surexpression de IGFBPs, en particulier IGFBP-2, avec un pronostic défavorable dans plusieurs formes de cancer. Bien que le rôle des IGFBPs ait été largement étudié dans le contexte de la croissance normale et en néoplasie, la présente thèse révèle quelques nouveaux aspects de la physiologie des IGFBPs dans le contexte du cancer. En première partie, nous étudions l'effet de la voie de signalisation PI3K/AKT/mTOR sur l'expression du gène IGFBP-2 dans une lignée cellulaire de cancer du sein. Nous démontrons que l'activation de cette voie mène essentiellement à une augmentation de la transcription de ce gène de manière dépendante au facteur de transcription Sp-1. De plus, nous établissons que Sp-1 est phosphorylé par l'activation de la voie PI3K/AKT/mTOR et s'accumule dans le noyau. En deuxième partie, nous étudions les effets de la molécule 2-deoxyglucose (2-DG) sur la liaison entre IGF-1 et IGFBP-3. Un récent article avait suggéré un effet inhibitoire de cette molécule sur la formation de complexes IGF -1 :IGFBP-3. Nous démontrons par trois méthodes différentes que 2-DG ou la molécule apparentée glucose n'ont aucun effet sur la liaison entre IGF-1 et IGFBP-3. De plus, nous démontrons que les effets cellulaires de 2-DG sur l'activation de la voie PI3K/AKT/mTOR observées par les auteurs de l'article en question ne sont pas universels et sont probablement le résultat de signaux intracellulaires. Finalement, en dernière partie, nous étudions les effets d'un nouvel anticorps thérapeutique nommé BI836845 qui possède une grande affinité pour IGF-1 et IGF-2. Dans des échantillons de sérum de souris ex vivo, nous démontrons que l'ajout de BI836845 déplace IGF-1 des complexes naturels contenant les IGFBPs vers des complexes contenant l'anticorps. In vivo, nous démontrons que BI836845 lie la grande majorité d'IGF-1. Nous démontrons aussi que l'anticorps mène à une baisse de la concentration de IGFBP-3 et à une hausse de la concentration de l'hormone de croissance chez des souris C57 BL/6.
Challa, Sridevi. "Mechanisms of IKBKE Activation in Cancer." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6617.
Повний текст джерелаSubedee, Ashim. "Molecular Determinants and Transcriptional Regulators in Triple Negative Breast Cancer." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845415.
Повний текст джерелаMedical Sciences
Labonte, Laura E. "Vascular progenitor cell and extracellular matrix protein interactions in cancer." Thesis, University of Ottawa (Canada), 2010. http://hdl.handle.net/10393/28878.
Повний текст джерелаHosseini, Shirazi Seyed Farshad. "Cell cycle dependency of cisplatin cytotoxicity on ovarian cancer cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ36776.pdf.
Повний текст джерелаLeung, Yu Hing Nelly. "Carcinoembryonic antigen cell adhesion molecule 1: cancer and metabolic regulation." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18740.
Повний текст джерелаLa glycoprotéine CEACAM1 (Carcinoembryonic antigen cell adhesion molecule 1) est une molécule d'adhésion appartenant à la famille des CEA (Antigène carcinoembryonnaire). CEACAM1 se retrouve à la surface des cellules épithéliales, endothéliales, et hématopoétiques, du tube digestif, des organes reproducteurs, du foie, des poumons et des reins. CEACAM1 présente plusieurs fonctions: inhibition de la réponse immunitaire, adhésion cellulaire, clairance de l'insuline, apoptose et prolifération cellulaire, angiogénèse, et rôle de suppresseur de tumeurs. L'expression de CEACAM1 est souvent diminuée dans plusieurs cas de cancers humains dont le côlon, le foie, la prostate, et 30% des cancers du sein. Le modèle de souris Ceacam1-/- a été utilisé afin d'étudier le rôle de CEACAM1 dans la formation de tumeur. En l'absence de CEACAM1, le tissu épithélial de l'intestin grêle et du côlon subit moins d'apoptose. En contrepartie, une augmentation de la prolifération est détectée dans le côlon des souris Ceacam1-/-. L'absence de CEACAM1 n'étant pas suffisante pour induire l'apparition de tumeurs, nous avons utilisé un cancérogène chimique, l'azoxymethane. Les tumeurs observées dans le côlon des souris Ceacam1-/- s'avèrent être plus importantes que celles des souris contrôles. Le désavantage de l'utilisation de l'azoxymethane est que celui-ci provoque des mutations dans plusieurs gènes plus ou moins définis. Afin de comprendre la contribution de CEACAM1 dans le développement tumoral, la souris Ceacam1-/- a été croisée avec la souris Apc1638N/+ qui forme spontanément des tumeurs dans l'intestin grêle. Les souris Apc1638N/+: Ceacam1-/- développent plus de tumeurs présentant un phénotype tumoral plus agressif que celui formé dans les souris Apc1638N/+. Par ailleurs, les cellules épithéliales de l'intestin grêle Ceacam1-/- montrent une dérégulation de la voie de signalisation Wnt. CEACAM1 étant un facteu
Austin, Lauren Anne. "Exploring some aspects of cancer cell biology with plasmonic nanoparticles." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/54236.
Повний текст джерелаAvva, Jayant. "Complex Systems Biology of Mammalian Cell Cycle Signaling in Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1295625781.
Повний текст джерелаDive, C. "Flow cytoenzymology with special reference to cancer chemotherapy." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384585.
Повний текст джерелаCerone, Maria Antonietta. "Telomere maintenance in human cells : implications in cancer and ageing diseases." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86067.
Повний текст джерелаHere we report the isolation of an immortal human cell line that maintains short telomeres in the absence of biologically active telomerase and key features of active ALT. Our results suggest that the mechanisms of telomere maintenance in human cells may be more diverse than previously thought and have important implications for the development of anti-cancer strategies based on the inhibition of telomere maintenance.
Due to widespread distribution of telomerase in human tumors and its absence in most normal cells, telomerase is the main target of these anti-cancer strategies. However, targeting telomerase per se or in combination with anti-cancer drugs is not sufficient to trigger rapid cell death of tumor cells. On the other hand, disturbances in telomere capping do not require telomere shortening to induce growth arrest and may act more quickly. Our goal was to investigate the feasibility of a new approach based on the combination of telomere destabilization and chemotherapeutic drugs. Our results show that interfering with telomere maintenance enhances the susceptibility of human tumor cells to anti-cancer drugs independently of their telomere lengths and mechanisms to maintain them.
Finally, given the involvement of telomeres in maintaining genomic stability, we investigated the mechanism by which mutations in the telomerase RNA subunit contribute to autosomal dominant dyskeratosis congenita, a premature ageing disease associated with mutations in the telomerase holoenzyme. Our data strongly indicate that the clinical manifestations of this disease may be caused by telomere shortening due to haploinsufficiency of telomerase activity and provide a direct correlation between disturbances in telomere length maintenance and human disease.
Sarkar, Abby Joya. "Investigating the Role of Sox2 in Stomach Tissue Homeostasis and Cancer." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467240.
Повний текст джерелаMedical Sciences
Hwang, Katie Lee. "The Metabolic Role of the Hippo Pathway in Liver Development and Cancer." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467350.
Повний текст джерелаMedical Sciences
Schlueter, Daniela K. "A multiscale systems biology study of in vitro cell migration and cancer cell invasion." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/9e7f0415-f565-4a3d-ade3-f3eb540bf088.
Повний текст джерелаGerman, Natalie Janelle. "Investigating and Exploiting Metabolic Vulnerabilities in Cancer." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467175.
Повний текст джерелаMedical Sciences
Hoopes, Justin Darrel. "Mechanisms of Induced Cell Death in Bluetongue Virus Challenged Human Cell Lines." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/252.
Повний текст джерелаChinaranagari, Swathi. "Epigenetic Silencing of ID4 in Prostate Cancer: Mechanistic Insight." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2015. http://digitalcommons.auctr.edu/cauetds/13.
Повний текст джерелаEng, Jamei Raena. "Localization of anthracyclines in drug resistant human MCF-7 breast cancer cells." Thesis, University of Ottawa (Canada), 2007. http://hdl.handle.net/10393/27841.
Повний текст джерелаGerrard, Diana Lea. "Characterization Of Epigenetic Plasticity And Chromatin Dynamics In Cancer Cell Models." ScholarWorks @ UVM, 2019. https://scholarworks.uvm.edu/graddis/1060.
Повний текст джерелаHenry, Whitney Ingrid. "Investigating the Phosphoinositide 3-Kinase (PI3K) Pathway for Therapeutic Strategies for Breast Cancer." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:26718731.
Повний текст джерелаMedical Sciences
MacDonald, Patricia. "Defining functional domains within GPNMB important for breast cancer cell invasion." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96829.
Повний текст джерелаGlycoprotein non-metastatic melanoma protein B (GPNMB), aussi connu sous le nom de Ostéoactivine (OA), est une protéine transmembranaire fréquemment exprimée dans les tumeurs mammaires appartement au sous-type triple négatif. Notre groupe a mis en évidence que l'expression de GPNMB/OA est suffisante pour accroître, in vitro, les capacités migratoires et invasives associées aux cellules murines de cancer du sein faiblement métastatiques. In vivo, l'expression de GPNMB/OA est caractérisée par une augmentation de la formation des métastases osseuses et pulmonaires. Dans cette étude, nous avons cherché à caractériser le rôle pro-invasif associé à l'expression de GPNMB/OA dans les cellules humaines de cancer du sein en identifiant les domaines ou motifs de GPNMB/OA impliqués dans le phénotype invasif des cellules de cancer du sein. D'une part, nous avons entrepris l'identification de protéines interagissant avec GPNMB/OA et qui pourraient participer aux phénotypes associés à l'expression de GPNMB/OA. Pour ce faire, nous avons généré une série de mutants pour la protéine GPNMB et nous les avons exprimées dans les lignées cellulaires BT-549 et MDA-MB-453, qui n'exprime normalement pas GPNMB/OA, que nous avons par la suite soumis à des essais d'invasion in vitro. D'autre part, une étude de la littérature scientifique, associée à une analyse par spectrométrie de masse, ont été utilisées pour identifier les protéines partenaires potentielles de GPNMB/OA. Finalement, nous avons généré une lignée de souris transgénique qui exprime la forme humaine de GPNMB/OA sous le contrôle du promoteur Mouse Mammary Tumor Virus (MMTV). Ce modèle murin a été utilisé pour étudier le rôle de GPNMB/OA sur le développement de la glande mammaire et sur la tumorigenèse in vivo. Ainsi, ces travaux ont démontré que la forme humaine de GPNMB/OA est suffisante pour induire une augmentation des propriétés invasives des cellules BT549 et que ce phénotype requiert à la fois la région cytoplasmique et le motif RGD de la protéine GPNMB/OA. La caractérisation, des souris transgéniques MMTV-GPNMB/OA a révélé, pour sa part, que GPNMB/OA n'interfère pas avec le développement normal des glandes mammaires chez les femelles vierges et aucune tumeur n'a été détectée à ce jour. L'ensemble de nos données démontre que GPNMB/OA est capable d'induire les propriétés invasives associées aux cellules de cancer du sein, et que ce phénotype requiert l'interaction du motif RGD de la protéine GPNMB avec les intégrines et/ou des résidus ou motifs présents dans la partie cytoplasmique de GPNMB/OA et qui pourraient induire le recrutement de molécule de signalisation dans cette région de GPNMB/OA.
Anderson, Nicole Shree. "The Roles of Elevated Bcl-2 in Ovarian Cancer." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/6161.
Повний текст джерелаLi, Xiaodong 1966. "Characterization of the signaling pathways underlying netrin-1 receptor deleted in colorectal cancer." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84281.
Повний текст джерелаIn the first part of this thesis, we have demonstrated that the Rho GTPases are required for embryonic spinal commissural axon outgrowth induced by netrin-1. Using NIE-115 neuroblastoma cells we found that both Rac1 and Cdc42 activities are required for DCC-induced neurite outgrowth. In Swiss 3T3 fibroblasts, DCC was found to trigger actin reorganization through activation of Rac1. These results implicate the small GTPases as important signaling components in the molecular mechanisms underlying DCC.
In the second part, we found that DCC interacts constitutively with the adaptor protein Nck in commissural neurons. Moreover, dominant negative Nck-1 inhibits the ability of DCC to induce neurite outgrowth in NIE-115 cells and to activate Rac1 in fibroblasts in response to netrin-1. These studies provide evidence for an important role of Nck-1 in a novel signaling pathway from an extracellular guidance cue to changes in the actin-based cytoskeleton responsible for axonal guidance.
In the last part, we found that disruption of each of the PxxP motifs in the cytoplasmic domain of DCC is not able to block the interaction of DCC with Nck-1, suggesting that more than one PxxP motifs or non-PxxP sequences may mediate the interaction of DCC with Nck-1.
Taken together, the data in this thesis contribute to our understanding of the intracellular mechanisms mediating the response of an axon to netrin-1 during neural development.
Xia, Xianfang. "Cell Shape and Treatment Duration: How They Influence a Cancer Cell's Response to TNF." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493296.
Повний текст джерелаMedical Sciences
Gao, Chen. "Role of SPDEF in Prostate Cancer." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1343051932.
Повний текст джерелаDai, Meiou. "Regulation of TGFß signaling on tumor cell migration, invasion and stem cell activity in triple negative breast cancer." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119559.
Повний текст джерелаLe cancer du sein triple-négatif (CSTN) de type basal démontre des signes cliniques caractéristiques d'un mauvais pronostique, tels qu'une taille et un grade plus élevés des tumeurs, un risque augmenté de développer des métastases lymphatiques et distantes, ainsi qu'un plus grand risque de récurrence de la maladie. Le TGFβ est un régulateur clé des procédés cellulaires par lesquels les cellules cancéreuses du cancer du sein se détachent de la tumeur primaire pour former des métastases aux organes distants. Cependant, les mécanismes moléculaires par lesquels le TGFβ accomplit son rôle pro-métastatique restent à être élucidés. Ici, nous investiguons le rôle du TGFβ dans la régulation de la migration cellulaire, l'invasion, et la capacité des cellules souches à se renouveler, qui sont les étapes initiales et critiques à la formation de métastases dans le cancer du sein. Notre étude a tout d'abord identifié une nouvelle fonction pour le régulateur de cycle cellulaire p21 et son partenaire associé, l'acetyltransférase pCAF, comme étant des régulateurs de transcription dont la présence est critique pour la migration et l'invasion cellulaire in vitro et l'invasion tumorale in vivo médiées par le TGFβ pour le CSNT. Le p21 pouvant interagir avec différents complexes de cycline et CDK, nous avons investigué si d'autres régulateurs du cycle cellulaire sont aussi impliqués dans la progression tumorale médiée par le TGFβ. Nous avons trouvé que le TGFβ promeut l'interaction physique et la co-localisation nucléaire entre la cycline D21 et p21. La co-expression de la cycline D1 et de p21 promeut la croissance tumorale et l'invasion locale des tumeurs. De plus, nous avons trouvé que le TGFβ peut activer le complexe cycline D1/CDK4 pour promouvoir l'activité des cellules souches cancéreuses, ainsi que leur capacité de renouvèlement dans le CSNT. Ces résultats nous ont permis de définir p21, la cycline D1, et CDK4, comme des régulateurs clés en aval du TGFβ dans ses fonctions pro-métastatiques
Mercado-Matos, Jose R. "A Mechanistic Investigation of Insulin Receptor Substrate 2 Function in Breast Cancer Progression." eScholarship@UMMS, 2017. http://escholarship.umassmed.edu/gsbs_diss/918.
Повний текст джерелаCocolakis, Eftihia. "The effect of activin/TGF [beta] signaling in mammary epithelial and breast cancer cells /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103038.
Повний текст джерелаTo date, the molecular signaling mechanisms for activin/TGFbeta in mammary gland growth and differentiation have not been fully elucidated. Our data identify a novel regulatory crosstalk mechanism by which activin/TGFbeta induced Smad signaling acts to antagonize Stat5 transactivation in mammary epithelial cells. We demonstrate an inhibitory effect of activin/TGFbeta on milk protein expression, specifically betacasein. We further show that activin/TGFbeta inhibitory effect upon betacasein expression is not due to changes in either Stat5 phosphorylation, translocation to the nucleus or binding on the Stat5 response element. We finally demonstrate that the Smads are required to block Stat5 transactivation by activin/TGFbeta and show that they are important mediators in activin/TGFbeta inhibitory response upon Stat5 target gene expression, in particular betacasein and cyclin D1. Finally, we unveil the mechanism by which these two signaling cascades antagonize their effects and find that activated Smads inhibit Stat5 association with its co-activator CBP, thus blocking Stat5 transactivation of its target genes. Thus, we define a novel crosstalk mechanism between two divergent signaling pathways that are involved in regulating mammary gland growth and differentiation.
Whereas the role of TGFbeta signaling in breast cancer has been well characterized, we sought out to study the role and mechanism of action of activin in the human breast cancer T47D cells. We found that activin treatment of T47D cells leads to a potent inhibition of cell growth. We further show that activin induces the Smad, the p38-mitogen activated kinase pathways and the p38 downstream target ATF2. Finally, using specific inhibitors to block p38 MAPK, activin-mediated cell growth inhibition is completely abolished. Together, these results define a novel signaling mechanism induced by activin in breast cancer cells.
Finally in an attempt to identify genes regulated by activin in breast cancer cells, we discover the death adaptor molecule RAIDD as a novel target of activin signaling. We show that RAIDD mRNA and protein levels are potently upregulated by activin. Using antisense-oligos directed against RAIDD, we show that RAIDD expression is necessary in mediating activin inhibition in breast cancer cells. Hence, we define the involvement of a new player in activin mediated cell growth inhibition.
Collectively, these studies reveal novel mechanisms of the activin/TGFbeta signaling cascade in normal mammary epithelial cells and breast cancer cells.
Till, Kathleen June. "The biology of hairy-cell leukaemia, with particular reference to #alpha#-interferon." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386848.
Повний текст джерелаSpence, Andrew J. "The Effect of Lactic Acid on Mast Cell Function." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3629.
Повний текст джерелаWeng, Yaochung. "Measuring the effects of drugs on single cancer cell growth." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/72638.
Повний текст джерелаThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student submitted PDF version of thesis.
Includes bibliographical references.
Understanding the effectiveness of a drug therapy on halting disease progression is an essential aspect of cancer biology. Conventional assays that study cell behavior after a drug intervention report the average response of a cell population which can mask the heterogeneity and dynamics of seemingly identical cells. Recently, many single-cell techniques have been developed, but there are currently no methods that can fully characterize the long-term effects of drug treatment on cancer cell growth. To accomplish such, we developed an instrument to measure single-cell growth before and after drug treatment. In order to achieve femtogram-level mass resolution, we employed the suspended microchannel resonator (SMR), a vacuum-packaged cantilever with an embedded channel. Here, we describe three implementations that involve different technologies (optical trap, mechanical trap, and dynamic ow trapping) to capture a cell for repeated measurements and to perform drug delivery. Applying the technique we developed based on the dynamic ow trapping, we were able to monitor one or more generations of a cancer cell before and after drug treatment. We investigated the growth of mouse leukemia cells in response to drugs that inhibit the mammalian target of rapamycin (mTOR) pathway, induce apoptosis, or prevent translational activity directly at the ribosome. Our method was able to discern a particular growth signature for each drug investigated and to discover a new phenotype in cells following mTOR inhibition. Furthermore, our data demonstrates that the instantaneous growth rate changes following a drug treatment could potentially predict the long-term inhibitory effect on cellular biogenesis and mass accumulation.
by Yaochung Weng.
Ph.D.