Bibliografías temáticas / Cancer drug resistance, tumor metabolism / Tesis
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Tesis sobre el tema "Cancer drug resistance, tumor metabolism"

Autor: Grafiati
Publicado: 14 de marzo de 2023

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1

E, Pranzini. "Metabolic reprogramming of colorectal cancer cells resistant to 5-FU." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1095546.

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Metabolic rearrangements are essential to satisfy the different needs of cancer cells during tumorigenesis. Recent studies highlighted a role for such metabolic reprogramming in adaptation to therapies and chemo-resistance development. 5-fluorouracil (5-FU) is an antimetabolite drug widely used as a first-line treatment for colorectal cancer. Despite several advantages of 5-FU, its clinical application is still greatly limited, due to the acquisition of drug resistance. In the first part of this thesis, we illustrate the role of micro RNAs (miRNAs) in reprogramming colon cancer cells toward
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2

Shahi, Thakuri Pradip. "MODELING ANTI-CANCER DRUG RESISTANCE USING TUMOR SPHEROIDS." University of Akron / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=akron1574725861735168.

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3

Kala, Shashwati. "Role of ginsenoside Rb1 and its metabolite compound K in attenuating chemoresistance and tumour-initiating properties of ovarian cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207178.

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4

Chau, Wing-ka, and 周穎嘉. "Characterization of ovarian tumor-initiating cells and mechanisms of chemoresistance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197834.

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Chemoresistance remains a major clinical obstacle to effective management of ovarian cancer. Cancer stem cells (or tumor-initiating cells, TICs) have been discovered recently, and have played a pivotal role in changing the view of cancer development; however, the molecular mechanisms by which these cells escape conventional therapies remain elusive. In this study, TICs were isolated from ovarian cancer cells as tumor spheres with specific stem properties under TIC-selective conditions. Unlike non-TICs, TICs strongly express stem cell factor (SCF) and c-Kit. Blocking SCF-c-Kit by SCF neutralizi
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5

Kim, Gloria J. "Cancer nanotechnology engineering multifunctional nanostructures for targeting tumor cells and vasculatures /." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/22610.

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Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2007.<br>Committee Chair: Nie, Shuming; Committee Member: Lyon, L. Andrew; Committee Member: McIntire, Larry V.; Committee Member: Murthy, Niren; Committee Member: Prausnitz, Mark R.
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6

Rajabi, Fatemeh. "Role of the xenoreceptor PXR (NR1I2) in colon cancer stem cells drug resistance and tumor relapse." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT027.

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La récidive tumorale est l'un des principaux obstacles à surmonter à l'avenir pour améliorer la survie globale des patients atteints de cancer du côlon (CCR). Les échecs thérapeutiques observés chez les patients sont compatibles avec une accumulation de cellules souches cancéreuses (CSCs) résistantes aux médicaments. Dans cette étude, nous démontrons que le récepteur nucléaire PXR (NR1I2) agit comme un régulateur important de la chimiorésistance des CSCs coliques et de leur capacité à initier la rechute tumorale après traitement. Nous avons d'abord montré que l'expression de PXR augmente avec
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7

Iliopoulos, Dimitrios. "The role of the WWOX tumor suppressor in breast and lung cancer." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1155142398.

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8

IPPOLITO, LUIGI. "OXPHOS - a metabolic switch driven by tumor microenvironment and resistance to therapy in prostate carcinoma." Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1006820.

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Tumor cells exhibit metabolic reprogramming according to microenvironmental scenarios (i.e. stroma composition and/or anticancer drugs burden) to meet their demands for energy, rapid proliferation, metastasis and progression. In our experimental model, a vicious metabolic synergy between CAFs and prostate cancer (PCa) cells has been described as a pivotal engine allowing cancer cells to achieve aggressive features and evolve their malignancy. Such metabolic crosstalk is mainly based on the OXPHOS rewiring of PCa cells induced by highly glycolytic CAFs through the establishment of tumor:
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9

Wang, Xuan. "Internalization of Extracellular ATP by Cancer Cells and its Functional Roles in Cancer Drug Resistance." Ohio University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1505834714683835.

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10

Balcells, Nadal Cristina. "The supramolecular organization of cancer metabolism: From macromolecular crowding to metabolic reprogramming underlying cancer metastasis and drug resistance." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668321.

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Metastasis and drug resistance represent the two main causes of therapeutic failure in oncology. In the present dissertation, the interplay between them has been interrogated using metabolomics, systems biology and biophysical approaches, in an attempt to find common phenotypic adaptations and metabolic vulnerabilities of metastatic and resistant cancer cells, potentially exploitable in novel combination therapies. The obtained results unveil that highly metastatic e-CSC phenotypes of CRPC present particular metabolic vulnerabilities that can potentially lead to establishing putative biomark
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11

Tabassum, Doris Priscilla. "Exploring Intra-tumor Cooperation in Metastasis and Drug Resistance using Heterogeneous Xenograft Models of Breast Cancer." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493472.

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Breast cancer is a highly heterogeneous disease, having not only several intrinsic sub-types but also significant sub-clonal heterogeneity within tumors. Intra-tumor heterogeneity can have profound impact on tumor evolution, disease progression and response to therapy. Furthermore, these phenomena can also be influenced by interactions of cancer cells with those of the microenvironment, thereby adding an extra layer of complexity to the study of tumor biology. To investigate the impact of sub-clonal heterogeneity on tumor phenotypes, we developed a heterogeneous mouse xenograft model of brea
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12

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.

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Cancer cells have been known for some time to have very different metabolismas compared to that of normal non proliferating cells. As metabolism is involvedin almost every aspect of cell function, there has been a recent resurgence ofinterest in inhibiting cancer metabolism as a therapeutic strategy. Inhibitors thatspecifically target altered metabolic components in cancer cells are being developedas antiproliferative agents. However, many such inhibitors have not progressedinto the clinic due to limited efficacy either in vitro or in vivo. In this study weexplore the hypothesis that this is o
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13

Kim, Byoungjin. "Intracellular metabolism of cancer cells and drug delivery using gold nanoparticles in an in vitro 3D tumor model." Amherst, Mass. : University of Massachusetts Amherst, 2009. http://scholarworks.umass.edu/dissertations/AAI3359901/.

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14

Wong, Ka Yeung Mark. "Drug clearance mechanisms and chemotherapy response." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28094.

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Cytotoxic chemotherapeutic agents have a major role in the treatment of cancers. However, many cytotoxic agents have a narrow therapeutic window with best treatment response achieved only within a small range of drug concentrations.
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15

LORI, GIULIA. "A novel view on LMW-PTP involvement in tumorigenesis: from apoptosis resistance to metabolic reprogramming." Doctoral thesis, Università di Siena, 2016. http://hdl.handle.net/11365/1007190.

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Protein tyrosine phosphorylation in eukaryotes is a key mechanism for cellular control, since it is involved in several processes, such as cellular metabolism, proliferation, differentiation and oncogenic transformation. A fine balancing of cellular protein tyrosine phosphorylation levels is determined by regulating the activities of protein-tyrosine kinases and/or protein-tyrosine phosphatases (PTPs) (Alonso et al., 2004). The PTP superfamily comprises almost 70 enzymes that, despite very limited sequence similarity, share a common CX5R active-site motif and an identical catalytic mechanism.
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16

Aljohani, Hashim M. "Targeting Tyrosine Kinase Drug Resistance Mechanisms and Metastatic Pathways in Brain Tumors." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846160285645.

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17

Barbato, Simona <1986&gt. "Modulation of Tumor Cell Metabolism by the ATP Synthase Inhibitor Protein (IF1) and Role of the MiRNAs as Drivers of Drug Resistance." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2016. http://amsdottorato.unibo.it/7572/1/Barbato_Simona_Tesi.pdf.

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Metabolic reprogramming in cancer cells has recently been connected to IF1, a key regulator of ATP synthase activity, which is found to be overexpressed in many human carcinomas. Considering the pivotal role of mitochondria inside the cells, mitochondrial alteration is crucial for tumors to grow and IF1 may help tumor progression by conserving cellular ATP in hypoxic conditions. Although the inhibitor has being deeply investigated, its role in tumorigenesis and/or cancer progression is still debated. Therefore, we prepared stable IF1-silenced clones from the human osteosarcoma 143B cell line a
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18

Pridham, Kevin James. "Investigating Novel Targets to Inhibit Cancer Cell Survival." Diss., Virginia Tech, 2004. http://hdl.handle.net/10919/82855.

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Cancer remains the second leading cause of death in the United States and the world, despite years of research and the development of different treatments. One reason for this is cancer cells are able to survive through adaptation to their environment and aberrantly activated growth signaling. As such, developing new therapies that overcome these hurdles are necessary to combat cancer. Previous work in our laboratory using RNA interference screening identified genes that regulate the survival of glioblastoma (GBM) or autophagy in chronic myelogenous leukemia (CML) cancer cells. One screen iden
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19

Pridham, Kevin J. "Investigating Novel Targets to Inhibit Cancer Cell Survival." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82855.

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Cancer remains the second leading cause of death in the United States and the world, despite years of research and the development of different treatments. One reason for this is cancer cells are able to survive through adaptation to their environment and aberrantly activated growth signaling. As such, developing new therapies that overcome these hurdles are necessary to combat cancer. Previous work in our laboratory using RNA interference screening identified genes that regulate the survival of glioblastoma (GBM) or autophagy in chronic myelogenous leukemia (CML) cancer cells. One screen iden
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20

Landmann, Hannes [Verfasser], Matthias [Akademischer Betreuer] Dobbelstein, and Heidi [Akademischer Betreuer] Hahn. "Drug Metabolism Determines Resistance of Colorectal Cancer to Resorcinol-Based HSP90 Inhibitors / Hannes Landmann. Gutachter: Matthias Dobbelstein ; Heidi Hahn. Betreuer: Matthias Dobbelstein." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2014. http://d-nb.info/1060543109/34.

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21

Marfia, G. "ACQUIRED ALTERATIONS OF SPHINGOSINE-1-PHOSPHATE METABOLISM CONFER STEMNESS AND DRUG RESISTANCE PROPERTIES ON GLIOBLASTOMA MULTIFORME: A NEW POTENTIAL TARGET FOR A COMBINED APPROACH TO TREAT BRAIN CANCER." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/333056.

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The eradication of glioblastoma multiforme (GBM) (WHO grade 4) remains a tremendous clinical challenge in human oncology. Indeed, this tumor accounts for the most common, aggressive and lethal primary brain cancer in adults, exhibiting a dismal prognosis, despite extensive surgical resection and adjuvant radio- and chemo-therapy. The finding that GBM contains functional subsets of cells with stem-like properties named glioblastoma stem cells (GSCs) has opened up novel opportunities and promises for the development of new therapies for this devastating cancer. GSCs are self-renewing, multipoten
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22

RIZZUTI, ILARIA FRANCESCA. "STRENGTHEN OF DPNS FEATURES FOR THERANOSTIC APPLICATIONS AND MECHANICAL-CONTROL OF CHEMOTHERAPEUTIC EFFICACY THROUGH MODULATION OF CELL PROLIFERATION." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/1000310.

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Solid tumors are complex biological structures which are composed of cellular and matrix components, everything being perfused by blood vessels. During tumor development, modifications of both biochemical and mechanical parameters are observed and can feedback on one another. Cancer cells constantly interact with their mechanical environment and the whole tissue is mostly confined by its surrounding. Compressive mechanical stress develops in part from cell proliferation and could eventually result in the clamping of blood vessels leading to increased interstitial fluid pressure (hydrostatic pr
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23

Schmidt, Anja. "Das humane Y-Box-Protein YB-1 und seine Bedeutung für die Prognose und den Therapieerfolg bei Mammakarzinom." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2003. http://dx.doi.org/10.18452/14995.

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Einer der Gründe für das Scheitern derzeitiger Behandlungsmethoden beim Brustkrebs ist die Resistenz gegenüber der angewandten Chemotherapie. Eine große Rolle bei der Entstehung der Multiplen Medikamentenresistenz spielt das MDR1-Gen und sein Genprodukt, das P-Glykoprotein. Das Y-Box-Protein YB-1 reguliert die Expression des MDR1-Gens; eine Überexpression und nukleäre Lokalisation von YB-1 geht im Brustkrebs mit einer gesteigerten P-Glykoprotein Expression einher. In dieser Arbeit wurden Gewebeproben von 83 Brustkrebspatientinnen auf eine YB-1 Überexpression im Tumor und im peritumoralen Epit
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24

Valente, Diana Maria Tavares. "The influence of cancer cell metabolism and microenvironment on tumour progression and drug resistance." Doctoral thesis, 2018. http://hdl.handle.net/1822/60065.

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Tese de Doutoramento em Ciências da Saúde<br>In the last years a new revival interest has been demonstrated in the reprogrammed metabolism of cancer cells. Described by Otto Warburg, the altered metabolism characterized mainly by a high dependence on lactic acid fermentation, even in the presence of oxygen, is an emergent hallmark of cancer cells. The increase of the glycolytic flux induces a high acidity of the extracellular space, maintained by overexpression of different pH regulators at the plasma membrane, and enhances the more aggressive characteristics of tumour cells, such as incr
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25

Travica, S., Klaus Pors, Paul M. Loadman, et al. "Colon cancer-specific cytochrome P450 2W1 converts duocarmycin analogues into potent tumor cytotoxins." 2013. http://hdl.handle.net/10454/6217.

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PURPOSE: Cytochrome P450 2W1 (CYP2W1) is a monooxygenase detected in 30% of colon cancers, whereas its expression in nontransformed adult tissues is absent, rendering it a tumor-specific drug target for development of novel colon cancer chemotherapy. Previously, we have identified duocarmycin synthetic derivatives as CYP2W1 substrates. In this study, we investigated whether two of these compounds, ICT2705 and ICT2706, could be activated by CYP2W1 into potent antitumor agents. EXPERIMENTAL DESIGN: The cytotoxic activity of ICT2705 and ICT2706 in vitro was tested in colon cancer cell lines expre
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26

Clendening, James William. "Molecular Rationale and Determinants of Sensitivity for Statin-Induced Apoptosis of Human Tumour Cells." Thesis, 2010. http://hdl.handle.net/1807/26452.

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The statin family of hydroxymethylglutaryl coenzyme A reductase (HMGCR) inhibitors, used to control hypercholesterolemia, triggers apoptosis of various human tumour cells. HMGCR is the rate-limiting enzyme of the mevalonate (MVA) pathway, a fundamental metabolic pathway required for the generation of a number of biochemical end-products including cholesterol and isoprenoids, but the contribution of the MVA pathway to human cancer remains largely unexplored. Furthermore, as only a subset of tumour cells has been shown to be highly responsive to statins, the identification of appropriate subse
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27

Landmann, Hannes. "Drug Metabolism Determines Resistance of Colorectal Cancer to Resorcinol-Based HSP90 Inhibitors." Doctoral thesis, 2014. http://hdl.handle.net/11858/00-1735-0000-0023-9928-4.

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28

Wang, Pei-chen, and 王珮甄. "Overexpression of VCAM-1 promotes tumor progression and drug resistance in breast cancer." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/18512813420133744170.

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碩士<br>國立中山大學<br>生物醫學研究所<br>98<br>VCAM-1 (CD106) is a transmembrane glycoprotein and involved in many pathological inflammatory processes. VCAM-1 plays an important role in leukocyte adhesion, leukocyte transendothelial migration and cell activation by binding to integrin VLA-1 (α4β1). In our preliminary data, we observed 2-3 fold increase in the expression of VCAM-1 in the side population of ovarian cancer, which exhibits stem cell-like properties in ovarian cancer. In addition, we have also found VCAM-1 is upregulated in many breast cancer epithelial cells and directly correlated with breast
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29

Sahoo, Subhransu Sekhar. "Role of microenvironment in endometrial cancer progression, metastasis, and drug resistance." Thesis, 2018. http://hdl.handle.net/1959.13/1386299.

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30

HUANG, WEI-LUN, and 黃偉倫. "The mechanism and biological role of autocrine IL-6 in cancer cells: focusing on tumor drug resistance." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/09383593357862264912.

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博士<br>國立成功大學<br>基礎醫學研究所<br>97<br>Spontaneous IL-6 production has been observed in various tumors and has been implicated in cancer pathogenesis, progression, and drug resistance. Most studies emphasized the importance of NF-κB and AP-1 on IL-6 regulation. Others pointed out the potential roles of HIF-1α and p53. However, the molecular mechanism of IL-6 autocrine in tumor cells and the impact of IL-6 on drug resistance are not well defined yet. The previous study in our laboratory has demonstrated high IL-6 levels in malignant pleural effusions of patients with lung adenocarcinoma than those of
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31

Giacomini, Isabella. "IDENTIFICATION OF NEW PHARMACOLOGICAL TARGETS IN CHEMOTHERAPY RESISTANCE: FOCUS ON METABOLIC REPROGRAMMING." Doctoral thesis, 2023. https://hdl.handle.net/11577/3469409.

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La chemioterapia è uno degli standard di cura per diversi tipi di tumori solidi. Sebbene i benefici dell’impiego clinico dei chemioterapici siano stati ampiamente riconosciuti, la loro efficacia terapeutica è limitata dall'insorgenza della resistenza farmacologica, che causa la recidiva del tumore, il fallimento dei trattamenti successivi e l'eventuale morte dei pazienti. La farmacoresistenza è un fenomeno multifattoriale, i cui meccanismi molecolari non sono stati ancora completamente compresi. Negli ultimi decenni, l’alterazione del metabolismo energetico cellulare è stata introdotta come se
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32

Masetto. "Novel potential treatments in the challenging scenario of drug resistance in pancreatic ductal adenocarcinoma." Doctoral thesis, 2022. http://hdl.handle.net/11562/1069886.

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According to the prediction of the Global Cancer Observatory (GCO), an interactive web platform that presents global cancer statistics, pancreatic ductal adenocarcinoma (PDAC) will be second cause of death in Western societies within the next decade. To date, the overall survival of patients at 5 years after diagnosis is only 6%, and 25% in patients undergoing surgical resection, but these represent only 15% of total cases. These data emphasize the need to find new effective drug treatments. Indeed, current therapeutic approaches have great limitations such as chemoresistance, both innate and
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33

Chia-SingLu and 盧佳杏. "Study on the role of chemotherapeutics-induced Octamer-binding transcription factor 4 (Oct4) expression in drug resistance and tumor recurrence in bladder cancer." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/g5wuy3.

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博士<br>國立成功大學<br>基礎醫學研究所<br>104<br>Acquisition of drug resistance to conventional chemotherapy is a challenge in treating recurrent cancer. Bladder cancer has the highest recurrence rate of any malignancy. Although primary tumors can be eliminated by surgery, chemotherapy, and radiotherapy, the tumors recur frequently and progress to muscle-invasive disease. Here we investigated whether anticancer drugs induced Oct4 expression and ultimately results in tumor recurrence in bladder cancer. We identified a positive correlation of the expression levels of Oct4 with the rate of tumor recurrence in 1
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34

Shakibaei, M., A. Mobasheri, C. Lueders, F. Busch, P. Shayan, and A. Goel. "Curcumin enhances the effect of chemotherapy against colorectal cancer cells by inhibition of NF-kappaB and Src protein kinase signaling pathways." 2013. http://hdl.handle.net/10454/6183.

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OBJECTIVE: Development of treatment resistance and adverse toxicity associated with classical chemotherapeutic agents highlights the need for safer and effective therapeutic approaches. Herein, we examined the effectiveness of a combination treatment regimen of 5-fluorouracil (5-FU) and curcumin in colorectal cancer (CRC) cells. METHODS: Wild type HCT116 cells and HCT116+ch3 cells (complemented with chromosome 3) were treated with curcumin and 5-FU in a time- and dose-dependent manner and evaluated by cell proliferation assays, DAPI staining, transmission electron microscopy, cell cycle analys
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35

Armstrong, Catherine. "Characterizing the Expression of Cytochrome P450s in Breast Cancer Cells." Thèse, 2011. http://hdl.handle.net/1866/9017.

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Une résistance aux agents anticancéreux utilisés dans le traitement du cancer du sein est souvent associée à un échec de traitement. Des variations dans le devenir des agents anticancéreux dans l’organisme, sont des facteurs pouvant expliquer des phénomènes de résistance. Notre but était d’évaluer l’impact des isoenzymes du CYP450s, dans le métabolisme local des agents anticancéreux. Notre premier objectif était de valider un gène rapporteur pour nos analyses de PCR en temps réel. Pour ce faire, nous avons criblé l’expression de 6 gènes rapporteurs dans 23 lignées cellulaires. NUP-214 a été dé
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Qiao, B., M. Kerr, B. Groselj, et al. "Imatinib radiosensitizes bladder cancer by targeting homologous recombination." 2013. http://hdl.handle.net/10454/6140.

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Radiotherapy is a major treatment modality used to treat muscle-invasive bladder cancer, with patient outcomes similar to surgery. However, radioresistance is a significant factor in treatment failure. Cell-free extracts of muscle-invasive bladder tumors are defective in nonhomologous end-joining (NHEJ), and this phenotype may be used clinically by combining radiotherapy with a radiosensitizing drug that targets homologous recombination, thereby sparing normal tissues with intact NHEJ. The response of the homologous recombination protein RAD51 to radiation is inhibited by the small-molecule ty
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