Relevant bibliographies by topics / Metastasis promotion

Academic literature on the topic 'Metastasis promotion'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Metastasis promotion"

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Kitamura, Takanori, Bin-Zhi Qian, and Jeffrey W. Pollard. "Immune cell promotion of metastasis." Nature Reviews Immunology 15, no. 2 (January 23, 2015): 73–86. http://dx.doi.org/10.1038/nri3789.

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Mathias, Alissa B., Eric P. Palmer, Nicole Kruh-Garcia, and Daniel P. Regan. "The role of osteosarcoma cell-derived exosomes in the promotion of lung metastasis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 242.44. http://dx.doi.org/10.4049/jimmunol.204.supp.242.44.

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Abstract Osteosarcoma (OS) is the most common primary tumor of bone and typically occurs in children and young adults. 30–40% of OS patients develop lung metastases after initial diagnosis, with only 20% of these patients surviving 4 years post-relapse. For over 30 years, there have been no improvements in the treatment of OS, and more importantly, no diagnostic tools that help identify those patients at high risk for lung metastases. Recent data has shown that in other tumor types, tumor-secreted extracellular vesicles (EVs) deliver biological cargo to distant sites, resulting in priming of non-malignant host cells for promotion of metastasis. The aim of this project is to understand how OS EVs influence the response of lung fibroblasts (LFs) and alveolar macrophages (AMs), and if their uptake of EVs results in pre-metastatic priming that can be detected via AM transcriptomic changes. Hypothesis LFs are primary targets of OS EVs, which will increase LF IL-6 production and cause paracrine STAT3 activation of AM’s into an M2 tumor-promoting phenotype. Results Flow cytometry and confocal microscopy demonstrated in vitro uptake of OS EVs by LF cells. In vitro ‘education’ of LFs with OS EVs induced significant production of IL-6, IL-8, and CCL2, with the greatest mean difference between EV-educated and naïve LFs observed with IL-6 secretion. Conclusion This data suggest that OS EVs efficiently prime LFs to induce IL-6 secretion, and this response may be associated with promotion of OS lung metastasis. Further data is being collected to determine the role of IL-6 in OS cell survival and lung metastatic colonization. RNA sequencing of AMs will be used to characterize phenotype which could serve as an effective cellular biomarker to predict lung metastasis.
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Solinas, Graziella, Federica Marchesi, Cecilia Garlanda, Alberto Mantovani, and Paola Allavena. "Inflammation-mediated promotion of invasion and metastasis." Cancer and Metastasis Reviews 29, no. 2 (April 24, 2010): 243–48. http://dx.doi.org/10.1007/s10555-010-9227-2.

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Lin, Richard J., Vahid Afshar-Kharghan, and Andrew I. Schafer. "Paraneoplastic thrombocytosis: the secrets of tumor self-promotion." Blood 124, no. 2 (July 10, 2014): 184–87. http://dx.doi.org/10.1182/blood-2014-03-562538.

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Abstract Paraneoplastic thrombocytosis is associated with many solid tumors and often correlates with reduced survival. Recent studies suggest that a pathogenic feed back loop may be operative between platelets and tumor cells, with reciprocal interactions between tumor growth/metastasis and thrombocytosis/platelet activation. Specific molecular pathways have been identified in which tumors can stimulate platelet production and activation; activated platelets can, in turn, promote tumor growth and metastasis. Taken together, these findings provide exciting new potential targets for therapeutic intervention.
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Bar-Yosef, Shahar, Rivka Melamed, Gayle G. Page, Guy Shakhar, Keren Shakhar, and Shamgar Ben-Eliyahu. "Attenuation of the Tumor-promoting Effect of Surgery by Spinal Blockade in Rats." Anesthesiology 94, no. 6 (June 1, 2001): 1066–73. http://dx.doi.org/10.1097/00000542-200106000-00022.

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Background The perioperative period is characterized by a state of immunosuppression, which was shown in animal studies to underlie the promotion of tumor metastasis by surgery. As this immunosuppression is partly ascribed to the neuroendocrine stress response, the authors hypothesized that spinal blockade, known to attenuate this response, may reduce the tumor-promoting effect of surgery. Methods Fischer-344 rats were subjected to a laparotomy during general halothane anesthesia alone or combined with either systemic morphine (10 mg/kg) or spinal block using bupivacaine (50 microg) with morphine (10 microg). Control groups were either anesthetized or undisturbed. Blood was drawn 5 h after surgery to assess number and activity of natural killer cells, or rats were inoculated intravenously with MADB106 adenocarcinoma cells, which metastasize only to the lungs. Metastatic development was assessed by quantifying lung retention of tumor cells 24 h after inoculation or by counting pulmonary metastases 3 weeks later. Results Laparotomy conducted during general anesthesia alone increased lung tumor retention up to 17-fold. The addition of spinal block reduced this effect by 70%. The number of metastases increased from 16.7 +/- 10.5 (mean +/- SD) in the control group to 37.2 +/- 24.4 after surgery and was reduced to 10.5 +/- 4.7 during spinal block. Systemic morphine also reduced the effects of surgery, but to a lesser degree. Natural killer cell activity was suppressed to a similar extent by surgery and by anesthesia alone. Conclusions The addition of spinal blockade to general halothane anesthesia markedly attenuates the promotion of metastasis by surgery.
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Reticker-Flynn, Nathan E., Weiruo Zhang, Julia A. Belk, Pamela A. Basto, Andrew J. Gentles, John B. Sunwoo, Ansuman K. Satpathy, Sylvia K. Plevritis, and Edgar G. Engleman. "Abstract PR013: Lymph node colonization promotes distant tumor metastasis through the induction of tumor-specific immune tolerance." Cancer Research 83, no. 2_Supplement_2 (January 15, 2023): PR013. http://dx.doi.org/10.1158/1538-7445.metastasis22-pr013.

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Abstract The majority of cancer-associated deaths result from distant organ metastasis, yet the mechanisms that enable this process remain poorly understood. For most solid tumors, colonization of regional or distant lymph nodes (LNs) typically precedes the formation of distant organ metastases, yet it remains unclear whether LN metastasis plays a functional role in disease progression. LNs are major sites of anti-tumor lymphocyte education, including in the context of immunotherapy, yet LN metastasis frequently correlates with further disease progression. Here, we find that LN metastasis represents a critical step in tumor progression through the capacity of such metastases to induce tumor-specific immune tolerance in a manner that promotes further dissemination of tumors to distant organs. Using an in vivo passaging approach of a non-metastatic syngeneic melanoma, we generated 300 unique cell lines exhibiting varying degrees of LN metastatic capacity. We show that the presence of these LN metastases enables distant organ seeding of metastases in a manner that the parental tumor cannot, and this effect is eliminated in mice lacking an adaptive immune response. Furthermore, this promotion of distant seeding by LN metastases is tumor specific. Using flow cytometry and single-cell sequencing to perform comprehensive immune profiling, we identify multiple cellular mediators of tolerance. In particular, we find that LN metastases have the capacity to both resist NK cell cytotoxicity and induce regulatory T cells (Tregs). Furthermore, depletion of NK cells in vivo enables non-metastatic tumors to disseminate to LNs, and ablation of Tregs using FoxP3-DTR mice eliminates the occurrence of lymphatic metastases. Adoptive transfer of Tregs from the LNs of mice bearing LN metastasis to naïve mice facilitates metastasis in a manner that Tregs from mice without LN metastases cannot, and we find that these Tregs are induced in an antigen-specific manner. Whole exome sequencing revealed that neither the metastatic proclivity nor immunosuppression evolve through the acquisition of driver mutations, loss of neoantigens, loss of MHC class I presentation, or decreases in melanoma antigen expression. Rather, by RNA-seq and ATAC-seq, we show that a conserved interferon signaling axis is upregulated in LN metastases and is rendered stable through epigenetic reprogramming of chromatin accessibility resulting from chronic exposure to interferons in vivo. Furthermore, using CRISPR/Cas9, we find that these pathways are required for LN metastatic seeding, and validate their conserved significance in additional mouse models of pancreatic ductal adenocarcinoma and head and neck squamous cell carcinoma and humans with LN metastatic disease. Together, these findings demonstrate a critical role for LN metastasis in promoting tumor-specific immunosuppression. Citation Format: Nathan E. Reticker-Flynn, Weiruo Zhang, Julia A. Belk, Pamela A. Basto, Andrew J. Gentles, John B. Sunwoo, Ansuman K. Satpathy, Sylvia K. Plevritis, Edgar G. Engleman. Lymph node colonization promotes distant tumor metastasis through the induction of tumor-specific immune tolerance [abstract]. In: Proceedings of the AACR Special Conference: Cancer Metastasis; 2022 Nov 14-17; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_2):Abstract nr PR013.
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Hirakawa, Satoshi, Lawrence F. Brown, Shohta Kodama, Karri Paavonen, Kari Alitalo, and Michael Detmar. "VEGF-C–induced lymphangiogenesis in sentinel lymph nodes promotes tumor metastasis to distant sites." Blood 109, no. 3 (October 10, 2006): 1010–17. http://dx.doi.org/10.1182/blood-2006-05-021758.

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Abstract The mechanisms by which tumors metastasize to sentinel and distant lymph nodes, and beyond, are poorly understood. We developed transgenic mice that overexpress vascular endothelial growth factor-C (VEGF-C) and green fluorescent protein specifically in the skin and studied the effects of chemically-induced skin carcinogenesis in this model. We found that in contrast to VEGF-A, VEGF-C does not increase the growth of primary tumors, but instead induces expansion of lymphatic networks within sentinel lymph nodes, even before the onset of metastasis. Once the metastatic cells arrived at the sentinel lymph nodes, the extent of lymphangiogenesis at these sites increased. Of importance, in mice with metastasis-containing sentinel lymph nodes, tumors that expressed VEGF-C were more likely to metastasize to additional organs, such as distal lymph nodes and lungs. No metastases were observed in distant organs in the absence of lymph node metastases. These findings indicate an important role of VEGF-C–induced lymph node lymphangiogenesis in the promotion of cancer metastasis beyond the sentinel lymph nodes. VEGF-C is therefore a good target to slow or even prevent the onset of metastasis.
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Wei, Qinyao, Yun Qian, Jun Yu, and Chi Chun Wong. "Metabolic rewiring in the promotion of cancer metastasis: mechanisms and therapeutic implications." Oncogene 39, no. 39 (August 24, 2020): 6139–56. http://dx.doi.org/10.1038/s41388-020-01432-7.

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Abstract Tumor metastasis is the major cause of mortality from cancer. Metabolic rewiring and the metastatic cascade are highly intertwined, co-operating to promote multiple steps of cancer metastasis. Metabolites generated by cancer cells influence the metastatic cascade, encompassing epithelial-mesenchymal transition (EMT), survival of cancer cells in circulation, and metastatic colonization at distant sites. A variety of molecular mechanisms underlie the prometastatic effect of tumor-derived metabolites, such as epigenetic deregulation, induction of matrix metalloproteinases (MMPs), promotion of cancer stemness, and alleviation of oxidative stress. Conversely, metastatic signaling regulates expression and activity of rate-limiting metabolic enzymes to generate prometastatic metabolites thereby reinforcing the metastasis cascade. Understanding the complex interplay between metabolism and metastasis could unravel novel molecular targets, whose intervention could lead to improvements in the treatment of cancer. In this review, we summarized the recent discoveries involving metabolism and tumor metastasis, and emphasized the promising molecular targets, with an update on the development of small molecule or biologic inhibitors against these aberrant situations in cancer.
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Erpenbeck, Luise, Bernhard Nieswandt, Margarete Schön, Miroslava Pozgajova, and Michael P. Schön. "Inhibition of Platelet GPIbα and Promotion of Melanoma Metastasis." Journal of Investigative Dermatology 130, no. 2 (February 2010): 576–86. http://dx.doi.org/10.1038/jid.2009.278.

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Orosz, Peter, Achim Krüger, Marcus Hubbe, Josef Rüschoff, Paul Von Hoegen, and Daniela N. Männel. "Promotion of experimental liver metastasis by tumor necrosis factor." International Journal of Cancer 60, no. 6 (March 16, 1995): 867–71. http://dx.doi.org/10.1002/ijc.2910600624.

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Dissertations / Theses on the topic "Metastasis promotion"

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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.
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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.
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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.
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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
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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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Books on the topic "Metastasis promotion"

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Jean, Cros, Etievant C, and Rustum Youcef M, eds. New concepts in cancer: Metastasis, oncogenes and growth factors. Basingstoke: Macmillan, 1990.

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New Concepts in Cancer. Palgrave Macmillan, 1990.

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Book chapters on the topic "Metastasis promotion"

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Steeg, Patricia S., Generoso Bevilacqua, Mark E. Sobel, and Lance A. Liotta. "Identification and Characterization of Differentially Expressed Genes in Tumor Metastasis: The nm23 Gene." In Boundaries between Promotion and Progression during Carcinogenesis, 355–61. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5994-4_29.

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Van Ginderachter, Jo, Yuanqing Liu, Nick Devoogdt, Wim Noël, Lea Brys, Gholamreza Hassanzadeh Gh., Geert Raes, et al. "Classical and alternative activation of macrophages: different pathways of macrophage-mediated tumor promotion." In Selected Aspects of Cancer Progression: Metastasis, Apoptosis and Immune Response, 139–56. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6729-7_9.

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Riaz, Ramish, Shah Rukh Abbas, and Maria Shabbir. "Adapting the Foreign Soil: Factors Promoting Tumor Metastasis." In 'Essentials of Cancer Genomic, Computational Approaches and Precision Medicine, 171–96. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1067-0_8.

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von Ardenne, Manfred. "Oxygen Multistep Immunostimulation as a Simple Process Against Cancer Metastasis — A Process Timed to the Metastasis Promoting Leukopenic and Oxygen Deficiency Phases of Established Cancer Therapies." In Cancer Management in Man, 188–99. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2536-6_16.

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Lin, Shu, and Lu-Zhe Sun. "Suppression of Premature Senescence and Promotion of Metastatic Transformation: Role of Reduced TGF-Beta Signaling in Human Cancer Progression." In Tumor Dormancy, Quiescence, and Senescence, Volume 2, 219–26. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7726-2_21.

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Sherbet, Gajanan V. "MTAs in EMT Activation and Tumour and Metastasis Promotion." In Molecular Approach to Cancer Management, 201–9. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-812896-1.00024-6.

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Dervan, Eoin, Dibyangana Bhattacharyya, and Sharon A. Glynn. "A review of RKIP promotion of tumor progression, metastasis and poor outcome in multiple solid tumor types." In Prognostic and Therapeutic Applications of RKIP in Cancer, 95–113. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-819612-0.00005-5.

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Basu, Bhaskar, and Subhajit Karmakar. "The Role of Extracellular Vesicles in the Progression of Tumors towards Metastasis." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101635.

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Extracellular vesicles (EVs) are cell-derived lipid membrane bound vesicles that serve as mediators of intercellular communication. EVs have been found to regulate a wide range of cellular processes through the transference of genetic, protein and lipid messages from the host cell to the recipient cell. Unsurprisingly, this major mode of intracellular communication would be abrogated in cancer. Ever increasing evidence points towards a key role of EVs in promoting tumor development and in contributing to the various stages of metastasis. Tumor released EVs have been shown to facilitate the transference of oncogenic proteins and nucleic acids to other tumor cells and to the surrounding stromal cells, thereby setting up a tumor permissive microenvironment. EVs released from tumor cells have been shown to promote extracellular matrix (ECM) remodeling through the modulation of neighboring tumor cells and stromal cells. EVs released from disseminated tumor cells have been reported to attract circulating tumor cells (CTCs) via chemotaxis and induce the production of specific extracellular matrix components from neighboring stromal cells so as to support the growth of metastatic cells at the secondary tumor site. Circulating levels of tumor derived EVs of patients have been correlated with incidence of metastasis and disease relapse.
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Mukhuty, Alpana. "Islet Inflammation: The Link between Type 2 Diabetes and Pancreatic Cancer." In Inflammation [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98538.

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The role of islet inflammation in type 2 diabetes (T2DM) and pancreatic ductal adenocarcinoma (PDAC) is complex. About 80% of pancreatic cancer patients have glucose intolerance or T2D. Chronic type 2 diabetes increases risk for pancreatic cancer, but the mechanisms are unknown. In this context two hypotheses exist: (i) pancreatic cancer causes diabetes and (ii) diabetes promotes the development of pancreatic cancer. Pancreatic ductal adenocarcinoma is the most common and deadly form of pancreatic cancer that is associated with diabetes. There are many possibilities by which obesity links to pancreatic cancer. These possibilities include insulin resistance, hyperinsulinemia and inflammation. Adipose tissue deposition near pancreas (peri-pancreatic depot) increase proinflammatory response to a high fat or high calorie containing diet. Inflammatory processes in the islets act as main mediators during the development and progression of pancreatic cancer. Recently, studies have been carried out to investigate the underlying mechanisms that contribute to tumorigenesis induced by inflammation. Tumor-elicited inflammation, secretion of pro-inflammatory cytokines and migration of immune cells play the key roles in initiation, promotion and progression of malignant metastasis in pancreatic cancer. Initiation and progression of islet inflammation in diabetes and pancreatic cancer occurs as a result of various protein–protein interactions and genetic events. The increase in pancreatic cancer cases may be attributed to the obesity endemic and obesity mediated Type 2 diabetes. The existence of link between islet inflammation in chronic diabetes and pancreatic cancer cannot be ignored, although the details about the underlying mechanisms are not clear, and must be studied in detail.
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Valdivia-Silva, J., J. Franco-Barraza, E. Cukierman, and E. A. Garcia-Zepe. "Novel Insights Into the Role of Inflammation in Promoting Breast Cancer Development." In Breast Cancer - Focusing Tumor Microenvironment, Stem cells and Metastasis. InTech, 2011. http://dx.doi.org/10.5772/21699.

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Conference papers on the topic "Metastasis promotion"

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Daenen, Laura G., Jeanine M. L. Roodhart, and Emile E. Voest. "Abstract 3429: Promotion of metastasis by frequently used chemotherapeutic agents." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3429.

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Tang, Xin, Tony Cappa, Theresa B. Kuhlenschmidt, Mark S. Kuhlenschmidt, and Taher A. Saif. "Studying the Mechanical Sensitivity of Human Colon Cancer Cells Through a Novel Bio-MEMS Force Sensor." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13237.

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Cancer deaths are primarily caused by metastases, not by the parent tumor. During the metastasis, malignant cancer cells detach from the parent tumor, and spread through the patient’s circulatory system to invade new tissues and organs [1]. To study the role played by the mechanical microenvironment on the cancer cell growth and malignancy promotion, we cultured human colon carcinoma (HCT-8) cells in vitro on substrates with varied mechanical stiffness, from the physiologically relevant 1 kPa, 20 kPa to very stiff 3.5 GPa. A novel and versatile micro-electromechanical systems (Bio-MEMS) force sensor [2] is developed to quantify the strength of non-specific adhesion between living cancer cells membrane and probe, an important hallmark of cancer cell malignancy level. Immunoflurescent staining and Confocal microscopy imaging are used to visualize the cellular organelle organization and cooperate to explore the underlying mechanism.
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Martinson, Holly, Sonail Jindal, Virginia Borges, and Pepper Schedin. "Abstract A31: Immune cell influx during postpartum mammary gland involution reveals immunosuppression and tumor promotion." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a31.

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Sonoshita, Masahiro, Yoshiro Itatani, Fumihiko Kakizaki, Yoshiharu Sakai, and M. Mark Taketo. "Abstract B65: Promotion of colorectal cancer invasion and metastasis through activation of Notch–Dab1–Abl–RhoGEF protein trio." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-b65.

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Cook, Leah M., Xuemei Cao, Alexander E. Dowell, Andra A. Frost, Renee A. Desmond, Mick D. Edmonds, Robert A. Kesterson, Douglas R. Hurst, and Danny R. Welch. "Abstract 3416: Ubiquitous Brms1 expression is critical for mammary carcinoma metastasis suppression via promotion of apoptosis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3416.

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Li, Bin, George Sai-Wah Tsao, Kwok-Wah Chan, and Annie Lai-Man Cheung. "Abstract 4361: Role of Id1-induced IGF2 in autocrine/endocrine promotion of esophageal cancer tumorigenesis and metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4361.

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Fornetti, Jaime, Peter Henson, Virginia Borges, and Pepper Schedin. "Abstract A12: A novel in vitro model to study the role of phagocytic mammary epithelial cells in postpartum breast cancer promotion." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a12.

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Pereira, S., L. Rodrigues, D. Castven, FL Mahn, S. Dooley, NM Meindl-Beinker, H. Lang, P. Grimminger, P. Galle, and J. Marquardt. "Dual role of Transforming Growth Factor Beta1&2 during Tumor Promotion and Metastasis in Primary Liver Cancer." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402231.

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Taketo, Mark. "Abstract 3254: Promotion of colon cancer invasion and metastasis via activation of Notch-Dab1-Abl-RhoGEF protein Trio." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3254.

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Mastri, Michalis, Amanda Tracz, Biao Liu, Christina R. Lee, and John ML Ebos. "Abstract 3251: A Senescence-like phenotype associates with rapid metastasis promotion following antiangiogenic drug resistance and therapy withdrawal." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3251.

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