Relevant bibliographies by topics / Epithelial-mesenchymal transition

Academic literature on the topic 'Epithelial-mesenchymal transition'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Epithelial-mesenchymal transition"

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Klymkowsky, Michael W., and Pierre Savagner. "Epithelial-Mesenchymal Transition." American Journal of Pathology 174, no. 5 (May 2009): 1588–93. http://dx.doi.org/10.2353/ajpath.2009.080545.

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Han, Myung Woul, Jong Cheol Lee, Young Min Kim, Hee Jeong Cha, Jong-Lyel Roh, Seung-Ho Choi, Soon Yuhl Nam, Kyung-Ja Cho, Seong Who Kim, and Sang Yoon Kim. "Epithelial-Mesenchymal Transition." Otolaryngology–Head and Neck Surgery 152, no. 1 (November 11, 2014): 80–86. http://dx.doi.org/10.1177/0194599814556061.

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Zavadil, Jiri, John Haley, Raghu Kalluri, Senthil K. Muthuswamy, and Erik Thompson. "Epithelial-Mesenchymal Transition." Cancer Research 68, no. 23 (December 1, 2008): 9574–77. http://dx.doi.org/10.1158/0008-5472.can-08-2316.

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Radisky, D. C. "Epithelial-mesenchymal transition." Journal of Cell Science 118, no. 19 (September 13, 2005): 4325–26. http://dx.doi.org/10.1242/jcs.02552.

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Sharma, Anil K., and Rolf D. Hubmayr. "Epithelial to mesenchymal transition." Critical Care Medicine 40, no. 2 (February 2012): 682–83. http://dx.doi.org/10.1097/ccm.0b013e318232d1a8.

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Luft, Friedrich C. "Targeting epithelial–mesenchymal transition." Journal of Molecular Medicine 93, no. 7 (June 14, 2015): 703–5. http://dx.doi.org/10.1007/s00109-015-1302-2.

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Manfioletti, Guidalberto, and Monica Fedele. "Epithelial–Mesenchymal Transition (EMT)." International Journal of Molecular Sciences 24, no. 14 (July 13, 2023): 11386. http://dx.doi.org/10.3390/ijms241411386.

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Shcherbakov, V., T. Ryabichenko, G. Skosyreva, and A. Trunov. "EPITHELIAL-MESENCHYMAL AND MESENCHYMAL-EPITHELIAL TRANSITION, PATHOGENESIS, REGULATION, THERAPY." Problems in oncology 64, no. 1 (January 2, 2018): 62–72. http://dx.doi.org/10.37469/0507-3758-2018-64-1-62-72.

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The review considered the issues of epithelial-mesenchymal transition (EMT) and its role in inflammation, fibrosis, tumor growth. There were analyzed mechanisms and classification of EMT. A comparison of different forms of EMTs was performed. The important role of EMT in the formation of metastasis-initiating cells was noted. There were presented data on the role of fibroblasts in fibrosis of the lung, carcinogenesis. Stimulators and inhibitors of EMTs were summarized. There were considered intracellular paths that were associated with the development of the EMT under the influence of transforming growth factor ß1 (TGF - ß1). It also induced the development of local hypothyroidism, for easy expression of oncofetal genes, which was especially important in tumor growth. Therapy EMT was associated with blocking the actions of TGF - ß1 and was an important area in anticancer therapy.
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Jeon, Hyun Min, Su Yeon Lee, Min Kyung Ju, Hye Gyeong Park, and Ho Sung Kang. "Early Growth Response 1 Induces Epithelial-to-mesenchymal Transition via Snail." Journal of Life Science 23, no. 8 (August 30, 2013): 970–77. http://dx.doi.org/10.5352/jls.2013.23.8.970.

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Thomson, Timothy M., Cristina Balcells, and Marta Cascante. "Metabolic Plasticity and Epithelial-Mesenchymal Transition." Journal of Clinical Medicine 8, no. 7 (July 3, 2019): 967. http://dx.doi.org/10.3390/jcm8070967.

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A major transcriptional and phenotypic reprogramming event during development is the establishment of the mesodermal layer from the ectoderm through epithelial-mesenchymal transition (EMT). EMT is employed in subsequent developmental events, and also in many physiological and pathological processes, such as the dissemination of cancer cells through metastasis, as a reversible transition between epithelial and mesenchymal states. The remarkable phenotypic remodeling accompanying these transitions is driven by characteristic transcription factors whose activities and/or activation depend upon signaling cues and co-factors, including intermediary metabolites. In this review, we summarize salient metabolic features that enable or instigate these transitions, as well as adaptations undergone by cells to meet the metabolic requirements of their new states, with an emphasis on the roles played by the metabolic regulation of epigenetic modifications, notably methylation and acetylation.
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Dissertations / Theses on the topic "Epithelial-mesenchymal transition"

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Qiao, Bin. "Epithelial-Mesenchymal Transition and Mesenchymal-Epithelial Transition in Oral Stem Cell Carcinogenesis." Thesis, Griffith University, 2011. http://hdl.handle.net/10072/367467.

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Oral squamous cell carcinoma (OSCC), derived from normal oral epithelium transformation, remains a major public health problem world-wide. The prognosis of OSCCs that occur on lips is good, while other sites of oral mucosa where OSCC appears are more progressive, invasive and metastatic. A small subset of cells within a malignant neoplasm, named cancer stem cells (CSCs) or tumour initiating cells are thought to be capable of initiating the neoplasm itself, and of driving its growth and recurrance after treatment. The precise origin of CSCs is an ambiguous issue at present. The first proposal of the origin of CSCs is that CSCs develop from tumour cells themselves via cellular dedifferentiation. The secondary hypothesis for the origin of CSCs proposes that CSCs are the product of malignant transformation of adult stem cells. In this Ph.D thesis, we tried to demonstrate that CSCs in OSCC may be produced from those pathways.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medicine
Griffith Health
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Robson, Ewan John Douglas. "Characterisation of epithelial-mesenchymal transition in murine mammary epithelial cells." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616130.

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Millanes, Romero Alba 1986. "Heterochromatin dynamics during epithelial-to-mesenchymal transition." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/129339.

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Although heterochromatin is enriched with repressive traits, it is actively transcribed, giving rise to large amounts of non-coding RNAs. These transcripts are responsible for the formation and maintenance of heterochromatin, but little is known about how their transcription is regulated. In this thesis we show that Snail1 transcription factor represses mouse pericentromeric transcription and regulates heterochromatin organization through the action of the H3K4 deaminase LOXL2. Snail1 has a key role in epithelial-to-mesenchymal transition (EMT). We show that, also during this process, Snail1 is responsible for pericentromeric transcription regulation. At the onset of EMT, one of the major structural heterochromatin proteins, HP1α, is transiently released from heterochromatin foci in a Snail1/LOXL2 dependent manner, concomitantly with a down-regulation of major satellite transcription. Moreover, prevention of major satellite transcripts down-regulation compromises the migratory and invasive behaviour of EMT resulting mesenchymal cells. We propose that Snail1 and LOXL2 regulate heterochromatin during this process, which may be crucial to allow the genome reorganization required to complete EMT.
Tot i estar enriquida en marques repressores, l’heterocromatina es transcriu activament i dóna lloc a grans quantitats d’ARNs no codificants. Aquests trànscrits són responsables de la formació i el manteniment de l’heterocromatina, però com es regula la seva transcripció segueix sent quelcom poc clarificat. En aquesta tesi demostrem que el factor de transcripció Snail1 reprimeix la transcripció pericentromèrica en cèl·lules de ratolí i regula l’organització de l’heterocromatina a través de l’acció de la LOXL2, que deamina l’H3K4. Snail1 té un paper clau en la transició epiteli-mesènquima (EMT). Aquí demostrem que, també durant aquest procés, Snail1 és responsable de la regulació de la transcripció pericentromèrica. A l’inici de l’EMT, l’HP1α, una de les principals proteïnes estructurals de l’heterocromatina, es desprèn de forma transitòria de l’heterocromatina. Aquest esdeveniment està regulat per Snail1 i LOXL2 i coincideix amb una disminució de la transcripció pericentromèrica. El bloqueig de la baixada dels trànscrits durant l’EMT compromet les capacitats migratòries i invasives de les cèl·lules mesenchimals que en resulten. Així doncs, proposem que Snail1 i LOXL2 regulen l’heterocromatina durant aquest procés, i així permeten que tingui lloc la reorganització genòmica que deu ser necessària per tal que es completi la EMT.
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Tan, E.-Jean. "Transcriptional and Epigenetic Regulation of Epithelial-Mesenchymal Transition." Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-206120.

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The transforming growth factor beta (TGFβ) is a cytokine that regulates a plethora of cellular processes such as cell proliferation, differentiation, migration and apoptosis. TGFβ signals via serine/threonine kinase receptors and activates the Smads to regulate gene expression. Enigmatically, TGFβ has a dichotomous role as a tumor suppressor and a tumor promoter in cancer. At early stages of tumorigenesis, TGFβ acts as a tumor suppressor by exerting growth inhibitory effects and inducing apoptosis. However, at advanced stages, TGFβ contributes to tumor malignancy by promoting invasion and metastasis. The pro-tumorigenic TGFβ potently triggers an embryonic program known as epithelial-mesenchymal transition (EMT). EMT is a dynamic process whereby polarized epithelial cells adapt a mesenchymal morphology, thereby facilitating migration and invasion. Downregulation of cell-cell adhesion molecules, such as E-cadherin and ZO-1, is an eminent feature of EMT. TGFβ induces EMT by upregulating a non-histone chromatin factor, high mobility group A2 (HMGA2). This thesis focuses on elucidating the molecular mechanisms by which HMGA2 elicits EMT. We found that HMGA2 regulates a network of EMT transcription factors (EMT-TFs), such as members of the Snail, ZEB and Twist families, during TGFβ-induced EMT. HMGA2 can interact with Smad complexes to synergistically induce Snail expression. HMGA2 also directly binds and activates the Twist promoter. We used mouse mammary epithelial cells overexpressing HMGA2, which are mesenchymal in morphology and highly invasive, as a constitutive EMT model. Snail and Twist have complementary roles in HMGA2-mesenchymal cells during EMT, and tight junctions were restored upon silencing of both Snail and Twist in these cells. Finally, we also demonstrate that HMGA2 can epigenetically silence the E-cadherin gene. In summary, HMGA2 modulates multiple reprogramming events to promote EMT and invasion.
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Cheung, Pak-yan, and 張柏欣. "Esophageal carcinogenesis: immortalization, transformation and epithelial-mesenchymal transition." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41290379.

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Abdulla, Tariq. "Advances in modelling of epithelial to mesenchymal transition." Thesis, Loughborough University, 2013. https://dspace.lboro.ac.uk/2134/12744.

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Epithelial to Mesenchymal Transition (EMT) is a cellular transformation process that is employed repeatedly and ubiquitously during vertebrate morphogenesis to build complex tissues and organs. Cellular transformations that occur during cancer cell invasion are phenotypically similar to developmental EMT, and involve the same molecular signalling pathways. EMT processes are diverse, but are characterised by: a loss of cell-cell adhesion; a gain in cell-matrix adhesion; an increase in cell motility; the secretion of proteases that degrade basement membrane proteins; an increased resistance to apoptosis; a loss of polarisation; increased production of extracellular matrix components; a change from a rounded to a fibroblastic morphology; and an invasive phenotype. This thesis focuses explicitly on endocardial EMT, which is the EMT that occurs during vertebrate embryonic heart development. The embryonic heart initially forms as a tube, with myocardium externally, endocardium internally, with these tissue layers separated by a thick extracellular matrix termed the cardiac jelly. Some of the endocardial cells in specific regions of the embryonic heart tube undergo EMT and invade the cardiac jelly. This causes cellularised swellings inside the embryonic heart tube termed the endocardial cushions. The emergence of the four chambered double pump heart of mammals involves a complex remodelling that the endocardial cushions play an active role in. Even while heart remodelling is taking place, the heart tube is operating as a single-circulation pump, and the endocardial cushions are performing a valve-like function that is critical to the survival of the embryo (Nomura-Kitabayashi et al. 2009). As the endocardial cushions grow and remodel, they become the valve leaflets of the foetal heart. The endocardial cushions also contribute tissue to the septa (walls) of the heart. Their correct formation is thus essential to the development of a fully functional, fully divided, double-pump system. It has been shown that genetic mutations that cause impaired endocardial EMT lead to the development of a range of congenital heart defects (Fischer et al. 2007). An extensive review is conducted of existing experimental investigations into endocardial EMT. The information extracted from this review is used to develop a multiscale conceptual model of endocardial EMT, including the major protein signalling pathways involved, and the cellular phenotypes that they induce or inhibit. After considering the requirements for computational simulations of EMT, and reviewing the various techniques and simulation packages available for multi-cell modelling, cellular Potts modelling is selected as having the most appropriate combination of features. The open source simulation platform Compucell3D is selected for model development, due to the flexibility, range of features provided and an existing implementation of multiscale models; that include subcellular models of reaction pathways. Based on the conceptual model of endocardial EMT, abstract computational simulations of key aspects are developed, in order to investigate qualitative behaviour under different simulated conditions. The abstract simulations include a 2D multiscale model of Notch signalling lateral induction, which is the mechanism by which the embryonic heart tube is patterned into cushion and non-cushion forming regions. Additionally, a 3D simulation is used to investigate the possible role of contact-inhibited mitosis, upregulated by the VEGF protein, in maintaining an epithelial phenotype. One particular in vitro investigation of endocardial EMT (Luna-Zurita et al. 2010) is used to develop quantitative simulations. The quantitative data used for fitting the simulations consist of cell shape metrics that are derived from simple processing of the imaging results. Single cell simulations are used to investigate the relationship between cell motility and cell shape in the cellular Potts model. The findings are then implemented in multi-cell models, in order to investigate the relationship between cell-cell adhesion, cell-matrix adhesion, cell motility and cell shape during EMT.
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Cheung, Pak-yan. "Esophageal carcinogenesis : immortalization, transformation and epithelial-mesenchymal transition /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41290379.

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De, Arpan. "Circadian clock regulation of epithelial-mesenchymal and mesenchymal-epithelial transitions in glioma and breast cancer cells." Bowling Green State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1566494866910786.

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Ilter, Didem. "The Role of ERK2 in Regulating Epithelial-Mesenchymal Transition." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11407.

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Epithelial-mesenchymal transition (EMT) is a fundamental developmental program, which is believed to be reactivated during the progression of in situ carcinoma to aggressive metastatic cancers. Ras-ERK pathway has been shown to play a crucial role in EMT. We have previously shown that ERK2, but not ERK1, is necessary for RasV12-induced EMT and overexpression of ERK2 is sufficient to promote EMT. ERK2 promotes EMT by regulating several factors, including the upregulation of transcription factors ZEB1/2. ZEB1/2 repress expression of E-cadherin, which is necessary for polar epithelial tissue formations.
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Dubois-Marshall, Sylvie. "Understanding epithelial to mesenchymal transition in human breast cancer." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/24541.

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Background and aims: Increasing evidence suggests that epithelial to mesenchymal transition (EMT) has a key role in breast cancer progression, underlying invasion, metastatic dissemination and acquisition of therapeutic resistance. However, this role is predominantly inferred from in vitro and animal studies and controversy regarding EMT in human cancer remains. This thesis has two principle aims. Firstly, to clarify the role of EMT in human breast cancer at the protein level. Secondly, to develop a three-dimensional in vitro assay to investigate cell invasion. Experimental Design: Two independent patient cohorts of high-grade, invasive ductal breast cancer were interrogated for their expression of key EMT proteins using quantitative immunofluorescence. This analysis was extended to paired lymph node metastases for a subset of cases. EMT-related cell lines were selected based on gene and protein expression data. These lines were investigated using lightmicroscopy, immunohistochemistry and immunofluorescence in a three-dimensional assay that models invasion across the basement membrane. Results: Two transcriptionally-driven EMT programmes were identified. One comprises vimentin, Snail and Slug and is uncoupled from E-cadherin downregulation. A second is characterised by up-regulation of WT1, Snail and Slug and down-regulation of E-cadherin. Importantly, acquisition of this phenotype in lymph node metastases predicts poor outcome. Some aspects of these programmes were recapitulated in vitro. Conclusions: These results suggest that EMT does occur in human breast cancer but in a manner distinct to that seen in vitro. The examination of primary tumours with their paired lymph node metastases may significantly contribute to understanding EMT. Lastly, in vitro models can reflect aspects of tumour biology and may prove invaluable in identifying clinically relevant, targetable pathways.
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Books on the topic "Epithelial-mesenchymal transition"

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Campbell, Kyra, and Eric Theveneau, eds. The Epithelial-to Mesenchymal Transition. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0779-4.

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Pierre, Savagner, ed. Rise and fall of epithelial phenotype: Concepts of epithelial-mesenchymal transition. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2005.

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Cheung, Albert. Pax3 and PAX3/FKHR induces cell aggregation and morphogenic mesenchymal-epithelial transition. Ottawa: National Library of Canada, 2002.

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Muthuswamy, Senthil, John Douglas Haley, and Raghu Kalluri. Abstracts of papers presented at the 2008 meeting on epithelial-mesenchymal transition: March 17-March 20, 2008. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2008.

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Sivasubramaniyan, Kavitha. A novel antibody directed against SSEA-4 defines spontaneous epithelial-to-mesenchymal cell transition in human prostate cancer. [S.l: s.n.], 2014.

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Sŏnggyun'gwan Taehakkyo (Seoul, Korea). Sanhak Hyŏmnyŏktan. TGF-beta e ŭihan oncogenic Epithelial-Mesenchymal Transition (EMT) yubal inja rosŏ hangsanhwa tanbaekchildŭl ŭi yŏkhal kyumyŏng kwa kijŏn yŏn'gu =: Molecular characterization of distinct roles of anti-oxidative proteins and their signaling mechanism in the oncogenic epithelial-mesenchymal transition by TGF-beta. [Seoul]: Pogŏn Pokchi Kajokpu, 2009.

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Thompson, Erik W. Epithelial-mesenchymal transitions: new advances in development, fibrosis and cancer: 9 tables. Basel: Karger, 2011.

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Campbell, Kyra, and Eric Theveneau. Epithelial-To Mesenchymal Transition: Methods and Protocols. Springer, 2021.

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Campbell, Kyra, and Eric Theveneau. Epithelial-To Mesenchymal Transition: Methods and Protocols. Springer, 2020.

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Savagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer London, Limited, 2008.

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Book chapters on the topic "Epithelial-mesenchymal transition"

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Rajasekaran, Ayyappan K., and Sigrid A. Langhans. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_1962-2.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Epithelial to Mesenchymal Transition." In Encyclopedia of Signaling Molecules, 574. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100399.

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Rajasekaran, Ayyappan K., and Sigrid A. Langhans. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1593–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-46875-3_1962.

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Rajasekaran, Ayyappan K., and Sigrid A. Rajasekaran. "Epithelial-to-Mesenchymal Transition." In Encyclopedia of Cancer, 1292–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1962.

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Choi, Yoon Jin, and Hyeon Jang. "Gastric Cancer: Epithelial Mesenchymal Transition." In Helicobacter pylori, 275–91. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-287-706-2_25.

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Kim, Nayoung, Yoon Jin Choi, and Hyeon Jang. "Gastric Cancer: Epithelial-Mesenchymal Transition." In Helicobacter pylori, 327–45. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-97-0013-4_26.

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Karakas, E., J. Waldmann, G. Feldmann, K. Schlosser, A. König, A. Ramaswamy, D. K. Bartsch, and V. Fendrich. "Epithelial-mesenchymal transition in parathyroid neoplasms." In Deutsche Gesellschaft für Chirurgie, 39–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_16.

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Schmalhofer, Otto, Simone Brabletz, and Thomas Brabletz. "Epithelial-Mesenchymal Transition in Colorectal Cancer." In Metastasis of Colorectal Cancer, 147–72. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-8833-8_6.

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Mittal, Vivek. "Epithelial Mesenchymal Transition in Aggressive Lung Cancers." In Lung Cancer and Personalized Medicine: Novel Therapies and Clinical Management, 37–56. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-24932-2_3.

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Wu, Yadi, and Binhua P. Zhou. "Epithelial–Mesenchymal Transition in Development and Diseases." In The Tumor Microenvironment, 187–211. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6615-5_9.

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Conference papers on the topic "Epithelial-mesenchymal transition"

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Brockmeyer, T., L. Pham, K. Zscheppang, S. Murray, Z. Borok, H. Nielsen, and C. Dammann. "Epithelial-Mesenchymal Transition in Fetal Type-II Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5299.

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Wu, Tsung-Hsien, Jen-I. Liang, Yu-Wei Chiu, Ming-Long Yeh, and Chia-Hsin Chen. "Mechanical quantification of the Epithelial mesenchymal transition." In 2011 IEEE International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2011. http://dx.doi.org/10.1109/nems.2011.6017391.

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Yamauchi, Y., T. Kohyama, S. Kamitani, S. Kawasaki, M. Desaki, K. Takami, H. Takizawa, and T. Nagase. "Epithelial Mesenchymal Transition Modulates the Cell Proliferation of Lung Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5306.

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Nagel, D., R. M. Kottmann, and D. Hocking. "Elastin Degradation Products Cause Epithelial to Mesenchymal Transition." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2187.

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Sporn, Peter H. S., Naizhen Wang, and Aisha Nair. "MicroRNA Profile Of Epithelial-Mesenchymal Transition In Normal Human Bronchial Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2488.

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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Mason, CA, and LS Brown. "Acetaldehyde Promoted Epithelial-Mesenchymal Transition through Increased TGF-β." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4971.

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Weinberg, R. "Breast Cancer Stem Cells and the Epithelial-Mesenchymal Transition." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-a1-1.

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Inayat, Huma, Scott Tsai, and Andras Kapus. "Investigation Of Epithelial-To-Mesenchymal Transition Through Microcontact Printing." In 2018 Canadian Society for Mechanical Engineering (CSME) International Congress. York University Libraries, 2018. http://dx.doi.org/10.25071/10315/35348.

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Wang, Fangfang, and Handong Jiang. "Salvianolate can attenuate bleomycin-induced pulmonary epithelial-mesenchymal transition." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4806.

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Reports on the topic "Epithelial-mesenchymal transition"

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Krause, Silva. Promotion of Epithelial to Mesenchymal Transition by Hyaluronan. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada462484.

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Krause, Silva. Promotion of Epithelial to Mesenchymal Transition by Hyaluronan. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada463843.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada541945.

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Thompson, Erik W. Functional Genomics for Epithelial-Mesenchymal Transition in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada542255.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada504655.

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Tyner, Angela L. Regulation of the Epithelial-Mesenchymal Transition in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada594294.

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Kah, Kong J. Signature and Mechanism of the Epithelial-to-Mesenchymal Transition. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada549247.

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Thompson, Erik. Functional Genomics for Epithelial-Mesenchymal Transition in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada554588.

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Range, Ryan C., and Davis R. McClay. A Normal Epithelial-Mesenchymal Transition as a Model for Studying Metastatic Onset. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada416671.

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Keckesova, Zuzana. The Role of Epithelial-Mesenchymal Transition in the Formation of Normal and Neoplastic Mammary Epithelial Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada554127.

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