Dissertations / Theses on the topic 'Metastasis promotion'
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1
Chen, Chen. "Investigation of the MUC1-independent action of circulating galectins in metastasis promotion." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/18533/.
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Galectins are galactoside-binding proteins that are expressed by various types of human cells. Recent studies have shown that the levels of circulating galectins are significantly higher in the bloodstream of cancer patients and promote cancer cell adhesion and aggregation by interaction with the cancer-associated mucin protein MUC1. However, previous studies have also shown that circulating galectins have MUC1-independent actions in metastasis promotion. This thesis further explores these MUC-1 independent actions. The studies reported here show that galectin-2, 3, -4 and -8, whose serum concentrations are all increased in cancer patients, induce secretion of various cytokines from endothelial cells in vitro and in vivo: (G-CSF, GM-CSF, IL-6 and sICAM-1 by galectin-3; G-CSF, IL-6 and GROα/CXCL1 by galectin-2; G-CSF, IL-6, GROα/CXCL1 and MCP-1/CCL2 by galectin-4 and -8). The secretion of these cytokines autocrinely/paracrinely enhances the endothelial expression of cell surface adhesion molecules, causing adhesion of cancer cells to the blood vascular endothelium. The galectin-induced secretion of cytokines is also shown to promote endothelial cell migration and tubule formation in angiogenesis. Intravenous introduction of a pathological galectin concentration into nude mice resulted in significant increase of circulating cytokine concentrations within 24 or 48 hours. Higher serum levels of these galectins correlated with higher serum levels of these cytokines in colon and breast cancer patients. Thus the increased circulation of galectins in the bloodstream of cancer patients promotes secretion from the blood vascular endothelium of metastasis-promoting cytokines that enhance circulating cancer cell adhesion and angiogenesis. These MUC1-independent actions of circulating galectins likely make an important contribution to the metastasis-promoting action of circulating galectins. Targeting the actions of circulating galectins in cancer patients therefore represents a promising therapeutic strategy to reduce metastasis and improve survival.
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Li, Jiarong. "Role of parathyroid hormone-related protein (PTHrP) in tumor initiation, promotion and metastasis of breast cancer." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=94925.
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In this study, we have used a well-validated breast cancer animal model to examine the malignant progression process. We have demonstrated that disruption of Pthrp dramatically delays the initial and subsequent steps of malignant conversion of the mammary epithelial cell, without affecting the mammary gland development. PTHrP acts as a promoter of oncogenesis and metastasis upstream of a number of critical checkpoints for PyVMT, such as Akt1, Akt2, factor VIII, Bcl-2 and cyclin D1, with the most interesting being CXCR4. This suggests a novel role for PTHrP as a facilitator of oncogenes and emphasizes the importance of attempting its targeting for therapeutic purposes.Dans cette étude, nous avons utilisé un modèle animal bien connu, le PyVMT, pour illustrer les effets de PTHrP sur l'initation du cancer du sein et sur sa progression métastatique. Nous avons démontré que l'ablation du gène Pthrp provoque un délai significatif des étapes initiales et des processus subséquents de la conversion maligne de la cellule épitheliale de la glande mammaire, sans affecter le développement normal de la glande mammaire. Nous démontrons que le PTHrP peut promouvoir l'oncogénèse et les phénomènes métastatiques en amont de plusieurs points de contrôle critiques chez le PyVMT, comme les Akt1, Akt2, facteur VIII, Bcl-2 et cycline D1, et le plus intéressant d'entre eux, le CXCR4. Ceci suggère un rôle nouveau pour le PTHrP comme facilitateur d'oncogènes, et renforce le concept de ciblage de l'activité de signal du PTHrP à des fins thérapeutiques.
3
Seachrist, Darcie Dawn. "Elucidation of Metastasis-promoting Mechanisms of Activin and BCL11A in Breast Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1600271384300217.
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Graham, Alastair Noel John. "An investigation into the factors promoting metastasis in non-small cell lung cancer." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326409.
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Nouhi, Zaynab. "Prolactin plays a dual role in breast cancer : promoting formation of breast tumour while inhibiting its metastasis." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97983.
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Prolactin is a key mammary gland differentiation factor. However, the contribution of prolactin (PRL) to breast carcinogenesis is less clear. Accumulating evidences indicate that in established breast carcinomas autocrine/paracrine PRL can enhance growth/viability of breast cancer cells. Still, it is not known whether the ascribed pro-oncogenic activity of PRL describes fully the role of PRL in regulating breast carcinogenesis. On the other hand a critical role for Ras-Erk1/2 and TGF-beta (Transforming Growth Factor beta) pathway in breast cancer progression has already been established. Our results indicate that blocking PRL signal leads to activation of Ras-Erk1/2 pathway and TGF-beta pathway, two key pathways contributing to breast cancer metastasis. I showed that modulation of PRL signaling in breast cancer cells alters their morphogenic program. My results highlight a critical role for PRL in regulating epithelial plasticity and implicate PRL as invasive suppressor hormone in breast cancer cells.
6
Schroeder, Krista Marie. "Disparities in Monoclonal Antibody Treatment of Elderly Metastatic Colorectal Cancer Patients." ScholarWorks, 2015. https://scholarworks.waldenu.edu/dissertations/1421.
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Multiple research studies have demonstrated racial, socioeconomic status (SES), and neighborhood disparities in first-line treatment of colorectal cancer patients, including those with metastatic colorectal cancer. However, disparities in adjunct monoclonal antibody treatment disparities have not been explored. The purpose of this study was to assess racial, SES, and neighborhood disparities in adjunct monoclonal antibody treatment of elderly metastatic colorectal cancer patients. The research was rooted in 3 theories: the fundamental cause theory, the diffusion of innovations theory, and theory of health disparities and medical technology. Data from the SEER-Medicare database and logistic regression were used to assess the relationship between the variables of interest and adjunct monoclonal antibody therapy. In this study, race (p = 0.070), SES (p = 0.881), and neighborhood characteristics (p = 0.309) did not significantly predict who would receive monoclonal antibody therapy. The results demonstrated a potential improvement in historically documented colorectal cancer treatment disparities. Specifically, historical treatment disparities may not be relevant to newer therapies prescribed to patients with severe disease. The difference could be related to improved access to care or a change in treatment paradigm due to the severity of metastatic colorectal cancer. Future studies aimed at understanding the causes of this social change (i.e., reduced treatment disparities) are warranted. Understanding the root cause of the reduced treatment disparities observed in this study could be used to reduce treatment disparities in other cancer populations.
7
Fahs, Sara [Verfasser], and Maja [Akademischer Betreuer] Köhn. "Interpreting the Activity of Metastasis-Promoting PRL-3 Through the Total Synthesis of Phosphatidylinositol Analogues / Sara Fahs ; Betreuer: Maja Köhn." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177149540/34.
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Roberts, Ryan David. "Taking Corrective Action: Efforts To Change The Malignancy-Promoting Behaviors Of Monocytes And Macrophages Elicited By Tumor Education." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1210630643.
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Li, Tianshu. "Identification of Epithelial Stromal Interaction 1 and Epidermal Growth Factor Receptor as Novel Kruppel-Like Factor 8 Targets in Promoting Breast Cancer Progression." Doctoral diss., University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/6311.
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Breast cancer is the major cause of cancer death among women worldwide. Understanding the mechanisms underlying breast cancer progression remains urgent for developing effective treatment strategies to eliminate breast cancer mortality. Our recent studies have demonstrated that Kruppel-like transcriptional factor 8 (KLF8) plays a critical role for breast cancer progression. Other studies have shown that Epithelial stromal interaction 1 (EPSTI1), a recently identified stromal fibroblast-induced gene in non-invasive breast cancer cells and epidermal growth factor receptor (EGFR) are highly overexpressed in aggressively invasive breast carcinomas including triple negative breast cancers. In this thesis project, we demonstrate high co-overexpression of KLF8 with EPSTI1 as well as EGFR in invasive breast cancer cells and patient tumors. We also show that KLF8 upregulates the expression of EPSTI1 by directly binding and activating the EPSTI1 gene promoter, and KLF8 upregulates the expression of EGFR not only by directly activating the EGFR gene promoter but also by preventing EGFR translation from microRNA141-dependent inhibition. Genetic, signaling and animal cancer model analyses indicate that downstream of KLF8, EPSTI1 promotes the tumor invasion and metastasis by activating NF-?B through binding valosin containing protein (VCP) and subsequent degradation of I?B?, whereas EGFR promotes tumor growth and metastasis via activation of ERK. Taken together, these data identify EPSTI1 and EGFR as novel KLF8 targets in breast cancer and suggest that KLF8 may be targeted for new effective treatment of breast cancer.Ph.D.
Doctorate
Molecular Biology and Microbiology
Medicine
Biomedical Sciences
10
Salazar, Montano Ylia [Verfasser]. "Microenvironmental Th9 and Th17 lymphocytes induce epithelial-mesenchymal transition in lung cancer cells thereby promoting metastatic spreading / Ylia Maria Salazar Montano." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1223461866/34.
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Salazar, Montano Ylia Maria [Verfasser]. "Microenvironmental Th9 and Th17 lymphocytes induce epithelial-mesenchymal transition in lung cancer cells thereby promoting metastatic spreading / Ylia Maria Salazar Montano." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1223461866/34.
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12
Hsu, Chung-Hsien, and 許仲賢. "Promotion of artificial lung metastasis in mice by pre-irradiation of thorax." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/86267431926086718719.
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碩士國立清華大學
原子科學系
90
The aim of this research was to establish an artificial metastatic model to study the influence of pre-irradiation (6 MV X-ray) of thorax on the process of metastasis in lung. C3H/HeN mice were injected i.v. with 1x10E5 NFsa cells/mouse, sacrificed at the 8th day after injection. The number of lung colony at lung surface was counted. For irradiated group, the mice’ thorax was irradiated 20 Gy X-ray and injected i.v. NFsa tumors cells immediately after irradiation. In 8 repeated experiments, the ratio of the number of lung colonies at surface between irradiated group and non-irradiated group was 3.18±1.26 (p = 0.02). In lung sections, the number of metastatic tumors per normal lung area and the ratio between total tumor area and total normal lung area in irradiated group were both higher than those of the non-irradiated. The ratios were similar to that we observed in the number of lung colonies at lung surface. To evaluate if pre-irradiation promote the growth rate of tumor, the lung section was stained with H&E and the distribution of the size of lung tumor was calculated. We observed that irradiated group had more potential to get bigger tumors than those of non-irradiated group. To evaluate the dose-response, we gave the grading radiation doses including 0 Gy, 6 Gy, 12 Gy and 20 Gy. The results showed that even at lower dose of 6 Gy, the formation of lung colony was still promoted by the pre-irradiation of thorax but the effect was less obvious than that at 20 Gy. To evaluate if the promotion of tumor is time-dependent, we injected NFsa tumor cells at various time after irradiation. Immediately or at the first day after irradiation of thorax, we found both can promote metastasis in lung. When the time interval between irradiation and injection of tumor cells became longer; the ability of metastasis was lower and no significant increase of lung metastasis was found if time interval was up to 1 month. Finally, we found that aspirin cannot inhibit the promotion of metastasis induced by pre-irradiation of thorax.
13
Tran, Duc-Dung, and 陳德勇. "Molecular mechanisms of promotion of apoptosis,proliferation inhibition, and metastasis suppression inHA22T human hepatocarcinoma cells byZanthoxylum avicennae extracts and Diosmin in vitroand in vivo." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/y6k4by.
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博士中國醫藥大學
中醫學系博士班
100
Hepatocellular carcinoma (HCC) is one of the five most common cancers in the world, however, diagnosis and outcomes of treatments still have shown no satisfactory results today. [Zanthoxylum avicennae (Lam.) DC (Rutaceae)] (Ying Bu Bo, YBB) is a traditional Vietnamese herbal medicine that effectively alleviates the inflammatory response in liver tissue. Inhibition of cell proliferation, metastasis and induction of liver cancer cell apoptosis by YBB remain to be determined. In this study, we investigated effects of YBB root skin ethanol extracts (YBBEs) on HA22T human hepatocellular carcinoma cells in vitro and in a mouse xenograft model. HA22T cells were treated with different concentrations of YBBEs and analyzed with MTT assay, western blot analysis, flow cytometry, TUNEL staining, JC-1 staining, wound healing, migration assay, invasion assay, gelatin zymography, RT-PCR, immunofluorescence staining assay, nuclear & cytoplasmic fractionation, siRNA transfection, and co-immunoprecipitation. From our experimental results, YBBEs showed a strong inhibition of HA22T cell viability in a dose-dependent manner and significantly reduced cell proliferation-related proteins as well as induced G2/M cell cycle arrest. YBBEs induced apoptosis, up-regulated death receptor apoptotic pathway markers as well as mitochondrial proteins, and suppressed the survival proteins in a dose-dependent manner. Further it was found that pro-survival Bcl-2 family proteins were attenuated and the pro-apoptotic ones were increased. Further results demonstrated that YBBEs effectively inhibits HA22T cell migration. YBBEs showed 54.5 to 96.6% cancer cell inhibition of HA22T cell invasion at concentrations of 50 to 250 μg/ml, respectively, compared to control. Moreover, ECM degradation-associated pathway including uPA and tPA and their downstream targets MMP-2/-9, were effectively suppressed. The endogenous inhibitors, including TIMP-1/-2 and PAI-1, were enhanced in HA22T cells by YBBEs treatments. Expression and activity of MMP-2/-9 and TIMP-1/-2 was assessed using RT-PCR and gelatin zymography, respectively. mRNA levels and enzymatic activities of MMP-2/-9 were down-regulated by YBBEs treatment in a dose-dependent manner, while TIMP-1/-2 levels conversely markedly increased. On the other hand, there was a strong increasing trend in PP2A-Cα, GSK-3β, APC and β-TrCP/HOS caused by YBBEs. However, expression of β-catenin, p-GSK-3β, TBX 3 and IL8 showed a decreasing mode. Therefore YBBEs inhibited HA22T cell metastasis. It was also found that YBBEs was able to significantly downregulate nuclear and cytosolic of β-catenin. Meanwhile, YBBEs was able to reduce the amount of β-catenin by facilitating its degradation by MG123 proteasome. In addition, protein-protein interactions between GSK-3β, β-TrCP, APC, PP2A and β-catenin were observed by co-immunoprecipitation. In addition, protein phosphatase 2A (PP2A) siRNA or PP2A inhibitor totally blocked effects of YBBEs on cell proliferation, metastasis inhibition and induction of HA22T apoptosis. Finally, further, in the nude mice xenografted animal experiments, results which were similar to ones in the in vitro system were demonstrated. In conclusion, both in vitro and in vivo models clearly demonstrated that YBBEs inhibits cell proliferation and metastasis, promotes HA22T apoptosis and reduces tumor sizes in xenograft nude mice via PP2A in a dose-dependent manner, which may be a powerful candidate for developing an alternative therapy for liver cancer.
14
LAN, YI-MING, and 藍翊銘. "Piceatannol inhibits M2 macrophage promoting colon metastasis and underlying molecular mechisms." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/sd9ph7.
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碩士國立臺灣大學
食品科技研究所
107
In the world, colorectal cancer is the third most commonly diagnosed cancer worldwide today. According to the World Health Organization survey, the global prevalence rate of colorectal cancer has increased in the past 30 years, and the incidence rate in Taiwan is the highest in the world. At present, the cure rate of colorectal cancer is low and the recurrence rate is high. The tumor microenvironment is known to be involved in acquired resistance of tumors to various therapies. The tumor microenvironment refers to the interaction between the tumor and its surrounding cells. Among them, M2 type macrophages have anti-inflammatory and tumor-promoting ability, therefore, it is very important to inhibit the tumor microenvironment regulated by M2 type macrophages and to hinder the growth and metastasis of colorectal cancer cells. Piceatannol (PIC) is a natural product commonly found in peanut, grapes, myrtle and passion fruit and has been shown to have anti-tumor effects. Therefore, this study used phorbol 12-myristate 13-acetate (PMA) to induce human monocytic cell THP-1 to differentiate into M2 type macrophages, and co-culture with human colorectal cancer cell SW480. We aimed to evaluate the efficacy of PIC in inhibiting M2 macrophage-induced tumor metastasis microenvironment and the underlying molecular mechanisms. The results of in vitro co-culture experiment showed that PIC at maximium non-toxic concentrations significantly inhibited the differentiation of THP-1 into M2 macrophages, therefore, suppression of M2 type macrophage activation in colorectal cancer cells. transforming growth factor beta (TGF-β) / drosophila mothers against decapentaplegic protein 2/3 (Smad2/3) signal pathway and downstream regulation of the transfer factors matrix metallopeptidase 9 (MMP-9) and monocyte chemoattractant protein-1 (MCP-1) in colorectal cancer, thereby inhibiting their mobility potency. Consistent with in vitro findings, the intraperitoneal (i.p.) injection of 50 mg/kg piceatannol significantly decreased the subcutaneous tumor growth and pulmonary metastases by inhibiting the M2-macrophage polarization and TGF-β secretion in the tumor microenvironment of SW480 xenograft mouse model. Taken together, our results suggest that PIC has the potential to prevent or treat colorectal cancer, and these findings provide important riches for future development PIC as functional foods or adjuvant therapeutic agents.
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Shang-MeiWeng and 翁尚楣. "Identification of exosomal proteins in promoting non-small cell lung cancer metastasis." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/6wp9gp.
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Shan-Fu and 王山富. "In vitro promoting effect of humic acid on metastasis of A549 lung cancer cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/27621044849829418499.
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碩士中山醫學大學
生化暨生物科技研究所
96
Humic acid (HA), a group of high-molecular weight polymer, resulting from the decompositing of organic matter has been implicated as a possible etiologic factor for Blackfoot disease and cancers. In this study, we observed that humic acid exerted a dose- and time-dependent promoting effect on the motility and invasion ability of a highly metastatic A549 cells under non-cytotoxic concentrations. In vitro wound-healing assay, cell invasion and migration assay, the results showed that A549 cells with HA pretreatment increased the migrating growth. HA was shown to enhance activation of adhesion molecules in A549 cells. In A549 cells migration and invasion processes, matrix-degrading proteinase are required. A549 cells with HA treatment at various concentrations showed increasing activates of ECM proteinase including matrix metalloproteinases (MMP-9 and MMP-2) by using gelatin and casein zymography analysis. The upstream mediators, FAK, PAK, ERK1/2, Jun, P38 MAPK and Akt were activated by increased phosphorylation of the proteins. Our results suggest that HA may promote a metastic effect involving (1) integrin signaling, (2) mitogen-activated protein kinase (MAPK) and PI3K/Akt signaling pathway to regulate the expression of progelatinase in human A549 lung cells.
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CHIAO, LI-KANG, and 喬立綱. "Evaluation of the potential role of tumor suppressor gene ZAC1/PLAGL1 in promoting tumor metastasis." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/zx9pdw.
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碩士國防醫學院
生物化學研究所
107
Previous studies have suggested the potential function of Zac1/PLAGL1 as a tumor suppressor gene associated with p53 activity and cell cycle inhibition. When tumor cell transformation was occurred in normal cervical tissue, the expression of the Zac1/PLAGL1 gene will be reduced correspondingly, it is also considered to be one reason of the causes of uncontrolled cell cycle and continued proliferation of cancer cells. However, in the TCGA clinical data of cervical cancer, the population of Zac1/PLAGL1 with high expression had a significantly poorer prognosis. To disclose the contradictory between clinical and basic research, the bioinformatic analysis of clinical survival rates extracted from TCGA and the comparison of normal and cervical carcinoma was combined with the microarray data from Hela cell line expressing amplified Zac1/PLAGL1 in this project. The consistency of oncogenic signature among these three sources was analyzed in GSEA and found that Zac1/PLAGL1 may play important role in promoting TGFβ signaling pathway activation, inhibiting cancer cell apoptosis by downregulating PTEN activity, and activating epithelial-mesenchymal transition (EMT) by LEF1 related pathway. Moreover, it was found that the excessive expression of the Zac1/PLAGL1 gene did promote the occurrence of EMT in cervical cancer cells and speed up its migration. The analysis of the downstream targets of PTEN and Akt shows that although the ectopically amplified expression of Zac1 reduces the phosphorylation of Akt, the Gsk3β ser9 phosphorylation considered to be one of its targets was increased in reverse, indicating that Zac1 may result in GSK3β phosphorylation through another signaling pathway. Our study found that Zac1 may potentially contribute to the deterioration of cancer in the event of excessive expression of cancer cells, and this transformation will also likely provide us with a new biomarker for the disease progression of cervical cancer as well as a potential novel goal for future treatment strategies of cervical cancer therapy.