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Journal articles on the topic 'Epithelial-mesenchymal transition'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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

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2

Han, Myung Woul, Jong Cheol Lee, Young Min Kim, et al. "Epithelial-Mesenchymal Transition." Otolaryngology–Head and Neck Surgery 152, no. 1 (2014): 80–86. http://dx.doi.org/10.1177/0194599814556061.

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3

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

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4

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

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5

Kamlund, Sofia, Birgit Janicke, Kersti Alm, Robert L. Judson-Torres, and Stina Oredsson. "Quantifying the Rate, Degree, and Heterogeneity of Morphological Change during an Epithelial to Mesenchymal Transition Using Digital Holographic Cytometry." Applied Sciences 10, no. 14 (2020): 4726. http://dx.doi.org/10.3390/app10144726.

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Cells in complex organisms can transition between epithelial and mesenchymal phenotypes during both normal and malignant physiological events. These two phenotypes are not binary, but rather describe a spectrum of cell states along an axis. Mammalian cells can undergo dynamic and heterogenous bidirectional interconversions along the epithelial–mesenchymal phenotypic (EMP) spectrum, and such transitions are marked by morphological change. Here, we exploit digital holographic cytometry (DHC) to develop a tractable method for monitoring the degree, kinetics, and heterogeneity of epithelial and me

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6

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

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7

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

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8

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

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9

Shcherbakov, V., T. Ryabichenko, G. Skosyreva, and A. Trunov. "EPITHELIAL-MESENCHYMAL AND MESENCHYMAL-EPITHELIAL TRANSITION, PATHOGENESIS, REGULATION, THERAPY." Problems in oncology 64, no. 1 (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 transfor

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10

Ishida, Mitsuaki, Akie Takebayashi, Fuminori Kimura, et al. "Induction of the epithelial-mesenchymal transition in the endometrium by chronic endometritis in infertile patients." PLOS ONE 16, no. 4 (2021): e0249775. http://dx.doi.org/10.1371/journal.pone.0249775.

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Background The purpose of the present study was to evaluate the relationship between chronic endometritis and the epithelial-mesenchymal transition in the endometrium of infertile patients in the implantation phase. Methods Endometrial biopsy specimens from 66 infertility patients were analyzed. The presence of chronic endometritis was investigated by immunostaining for CD138. Immunohistochemical staining for E-cadherin, N-cadherin, Slug, and Snail was performed, and the expression profiles were statistically analyzed according to the presence of chronic endometritis. When the loss of E-cadher

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11

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 (2013): 970–77. http://dx.doi.org/10.5352/jls.2013.23.8.970.

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12

Thomson, Timothy M., Cristina Balcells, and Marta Cascante. "Metabolic Plasticity and Epithelial-Mesenchymal Transition." Journal of Clinical Medicine 8, no. 7 (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 si

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13

Manfioletti, Guidalberto, and Monica Fedele. "Epithelial–Mesenchymal Transition (EMT) 2021." International Journal of Molecular Sciences 23, no. 10 (2022): 5848. http://dx.doi.org/10.3390/ijms23105848.

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14

Shevlyuk, N. N. "Epithelial-mesenchymal transition: the history of the concept, debatable issues." Journal of Anatomy and Histopathology 12, no. 2 (2023): 90–98. http://dx.doi.org/10.18499/2225-7357-2023-12-2-90-98.

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The paper discusses diverse aspects of the concept of epithelial-mesenchymal transition and compares the basics of this concept with the classical concepts of tissue biology. The idea of the epithelial-mesenchymal transition was first suggested by Elizabeth Hay (1927–2007) in 1968 based on the analysis of tridermogenesis in the development and growth of the avian embryo. In the late 80s – early 90s of the twentieth century, the concept of epithelial–mesenchymal transition won supporters-pathomorphologists in our country who applied the concept to explain mechanisms of multiple pathological pro

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15

Stunf Pukl, Spela. "MicroRNA of Epithelial to Mesenchymal Transition in Fuchs’ Endothelial Corneal Dystrophy." Genes 13, no. 10 (2022): 1711. http://dx.doi.org/10.3390/genes13101711.

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Aim: a review of miRNA expression connected to epithelial mesenchymal transition studies in Fuchs’ endothelial corneal dystrophy (FECD). Methods: literature search strategy—PubMed central database, using “miRNA” or “microRNA“ and “epithelial mesenchymal transition” or “EMT“ and “Fuchs’ endothelial corneal dystrophy” or “FECD” as keywords. Experimental or clinical studies on humans published in English regarding miRNA profiles of epithelial mesenchymal transition in Fuchs’ endothelial corneal dystrophy published between 2009 and 2022 were included. Conclusion: The publications regarding the miR

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16

Bhatia, Monkman, Blick, et al. "Interrogation of Phenotypic Plasticity between Epithelial and Mesenchymal States in Breast Cancer." Journal of Clinical Medicine 8, no. 6 (2019): 893. http://dx.doi.org/10.3390/jcm8060893.

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Dynamic interconversions between transitional epithelial and mesenchymal states underpin the epithelial mesenchymal plasticity (EMP) seen in some carcinoma cell systems. We have delineated epithelial and mesenchymal subpopulations existing within the PMC42-LA breast cancer cell line by their EpCAM expression. These purified but phenotypically plastic states, EpCAMHigh (epithelial) and EpCAMLow (mesenchymal), have the ability to regain the phenotypic equilibrium of the parental population (i.e., 80% epithelial and 20% mesenchymal) over time, although the rate of reversion in the mesenchymal dir

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17

Mitchell, Brendon, Jagdish K. Dhingra, and Meera Mahalingam. "BRAF and Epithelial-Mesenchymal Transition." Advances In Anatomic Pathology 23, no. 4 (2016): 244–71. http://dx.doi.org/10.1097/pap.0000000000000113.

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18

Sheng, Wang, Guizhi Wang, David P. La Pierre, et al. "Versican Mediates Mesenchymal-Epithelial Transition." Molecular Biology of the Cell 17, no. 4 (2006): 2009–20. http://dx.doi.org/10.1091/mbc.e05-10-0951.

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Versican is a large extracellular chondroitin sulfate proteoglycan that belongs to the family of lecticans. Alternative splicing of versican generates at least four isoforms named V0, V1, V2, and V3. We show here that ectopic expression of versican V1 isoform induced mesenchymal-epithelial transition (MET) in NIH3T3 fibroblasts, and inhibition of endogenous versican expression abolished the MET in metanephric mesenchyme. MET in NIH3T3 cells was demonstrated by morphological changes and dramatic alterations in both membrane and cytoskeleton architecture. Molecular analysis showed that V1 promot

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19

Eger, Andreas, and Wolfgang Mikulits. "Models of epithelial–mesenchymal transition." Drug Discovery Today: Disease Models 2, no. 1 (2005): 57–63. http://dx.doi.org/10.1016/j.ddmod.2005.04.001.

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20

Quarta, S., L. Vidalino, C. Turato, et al. "SERPINB3 induces epithelial mesenchymal transition." Digestive and Liver Disease 41, no. 5 (2009): A1—A2. http://dx.doi.org/10.1016/j.dld.2009.02.012.

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21

Sleeman, Jonathan P., and Jean Paul Thiery. "SnapShot: The Epithelial-Mesenchymal Transition." Cell 145, no. 1 (2011): 162–162. http://dx.doi.org/10.1016/j.cell.2011.03.029.

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22

Moustakas, Aristidis, and Antonio Garcia de Herreros. "Epithelial-mesenchymal transition in cancer." Molecular Oncology 11, no. 7 (2017): 715–17. http://dx.doi.org/10.1002/1878-0261.12094.

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23

Quarta, Santina, Laura Vidalino, Cristian Turato, et al. "SERPINB3 induces epithelial-mesenchymal transition." Journal of Pathology 221, no. 3 (2010): 343–56. http://dx.doi.org/10.1002/path.2708.

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24

Deng, Junjian, and Ximing Xu. "Epithelial-mesenchymal transition and cancermetastasis." Chinese-German Journal of Clinical Oncology 10, no. 3 (2011): 125–33. http://dx.doi.org/10.1007/s10330-011-0740-8.

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25

Zhao, Min, Lin Ang, Jin Huang, and Jin Wang. "MicroRNAs regulate the epithelial–mesenchymal transition and influence breast cancer invasion and metastasis." Tumor Biology 39, no. 2 (2017): 101042831769168. http://dx.doi.org/10.1177/1010428317691682.

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MicroRNAs are small RNA molecules that play a major role in the post-transcriptional regulation of genes and influence the development, differentiation, proliferation, and apoptosis of cells and the development and progression of tumors. The epithelial–mesenchymal transition is a process by which epithelial cells morphologically transform into cells with a mesenchymal phenotype. The epithelial–mesenchymal transition plays a highly important role in tumor invasion and metastasis. Increasing evidence indicates that microRNAs are tightly associated with epithelial–mesenchymal transition regulatio

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26

Enderle-Ammour, Kathrin, Moritz Bader, Theresa Dorothee Ahrens, et al. "Form follows function: Morphological and immunohistological insights into epithelial–mesenchymal transition characteristics of tumor buds." Tumor Biology 39, no. 5 (2017): 101042831770550. http://dx.doi.org/10.1177/1010428317705501.

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In cancer biology, the architectural concept “form follows function” is reflected by cell morphology, migration, and epithelial–mesenchymal transition protein pattern. In vivo, features of epithelial–mesenchymal transition have been associated with tumor budding, which correlates significantly with patient outcome. Hereby, the majority of tumor buds are not truly detached but still connected to a major tumor mass. For detailed insights into the different tumor bud types and the process of tumor budding, we quantified tumor cells according to histomorphological and immunohistological epithelial

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27

Rapanotti, Maria Cristina, Elisa Cugini, Maria Giovanna Scioli, et al. "The Clinical Relevance of Epithelial-to-Mesenchymal Transition Hallmarks: A Cut-Off-Based Approach in Healthy and Cancerous Cell Lines." International Journal of Molecular Sciences 26, no. 8 (2025): 3617. https://doi.org/10.3390/ijms26083617.

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The atypical activation of the epithelial-to-mesenchymal transition represents one of the main mechanisms driving cancer cell dissemination. It enables epithelial cancer cells to detach from the primary tumor mass and gain survival advantages in the bloodstream, significantly contributing to the spread of circulating tumor cells. Notably, epithelial-to-mesenchymal transition is not a binary process but rather leads to the formation of a wide range of cell subpopulations characterized by the simultaneous expression of both epithelial and mesenchymal markers. Therefore, analyzing the modulation

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28

Jayan, Lekshmy, R. Bharanidharan, and Ramya Ramdas. "Epithelial-Mesenchymal Interactions in Embryogenesis and Head and Neck Tumors." Journal of Surgical Case Reports and Images 2, no. 1 (2019): 01–08. http://dx.doi.org/10.31579/2690-1897/007.

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Epithelial mesenchymal interactions are one of the most important process taking place in the body. It is an indispensable mechanism that mediates the development of numerous organs and organ systems especially tooth, salivary gland etc. It has been long implicated in the causation of numerous pathogenic processes especially cancer. The mechanism of epithelial mesenchymal interactions are a forerunner for epithelial mesenchymal transition, which is an important pathological process in the development of cancer. In this review, we have highlighted the role of epithelial mesenchymal interactions

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29

Jayan, Lekshmy. "Epithelial-Mesenchymal Interactions in Embryogenesis and Head and Neck Tumors." Journal of Surgical Case Reports and Images 1, no. 2 (2019): 01–08. http://dx.doi.org/10.31579/jscr/2019/007.

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Epithelial mesenchymal interactions are one of the most important process taking place in the body. It is an indispensable mechanism that mediates the development of numerous organs and organ systems especially tooth, salivary gland etc. It has been long implicated in the causation of numerous pathogenic processes especially cancer. The mechanism of epithelial mesenchymal interactions are a forerunner for epithelial mesenchymal transition, which is an important pathological process in the development of cancer. In this review, we have highlighted the role of epithelial mesenchymal interactions

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30

Varankar, Sagar S., Madhuri More, Ancy Abraham, et al. "Functional balance between Tcf21–Slug defines cellular plasticity and migratory modalities in high grade serous ovarian cancer cell lines." Carcinogenesis 41, no. 4 (2019): 515–26. http://dx.doi.org/10.1093/carcin/bgz119.

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Abstract Cellular plasticity and transitional phenotypes add to complexities of cancer metastasis that can be initiated by single cell epithelial to mesenchymal transition (EMT) or cooperative cell migration (CCM). Our study identifies novel regulatory cross-talks between Tcf21 and Slug in mediating phenotypic and migration plasticity in high-grade serous ovarian adenocarcinoma (HGSC). Differential expression and subcellular localization associate Tcf21, Slug with epithelial, mesenchymal phenotypes, respectively; however, gene manipulation approaches identify their association with additional

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31

Desai, Krisha, Radhika Aiyappa, Jyothi S. Prabhu, et al. "HR+HER2− breast cancers with growth factor receptor–mediated EMT have a poor prognosis and lapatinib downregulates EMT in MCF-7 cells." Tumor Biology 39, no. 3 (2017): 101042831769502. http://dx.doi.org/10.1177/1010428317695028.

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Despite an overall good prognosis, a significant proportion of patients with hormone receptor positive human epidermal growth factor receptor 2 negative breast cancers develop distant metastases. The metastatic potential of epithelial cells is known to be regulated by tumor–stromal interaction and mediated by epithelial-to-mesenchymal transition. Hormone receptor positive human epidermal growth factor receptor 2 negative tumors were used to estimate markers of epithelial-to-mesenchymal transition, and the luminal breast cancer cell line MCF-7 was used to examine the interactions between integr

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32

Kucuksayan, Hakan, and Hakan Akca. "The crosstalk between p38 and Akt signaling pathways orchestrates EMT by regulating SATB2 expression in NSCLC cells." Tumor Biology 39, no. 9 (2017): 101042831770621. http://dx.doi.org/10.1177/1010428317706212.

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Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators. Special AT-rich sequence-binding protein 2 is an epigenetic regulator involved in epithelial–mesenchymal transition and osteoblastic differentiation. It has been reported that the crosstalk between several pathways is responsible for the regulation of epithelial–mesenchymal transition in cancer cells. However, crosstalks between p38 and Akt pathways involved in epithelial–me

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33

Shimoda, Tomonari, Kazuhiro Takahashi, Kei Asayama, Ryota Matsuoka, and Tatsuya Oda. "Intrahepatic Cholangiocarcinoma With Sarcomatous Transformation: Demonstrating the Transition Zone." ACG Case Reports Journal 11, no. 10 (2024): e01523. http://dx.doi.org/10.14309/crj.0000000000001523.

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ABSTRACT Intrahepatic cholangiocarcinoma with sarcomatous transformation (ICC-S) is a rare, aggressive neoplasm with epithelial and sarcomatous elements. We report a rapid progression of ICC-S in a 66-year-old woman. Initially, a seemingly benign 8-cm mass was observed. However, the tumor doubled to 16 cm within 3 months during follow-up. Partial hepatectomy confirmed ICC-S and histopathological examination showed cytokeratin 7 and vimentin positivity in epithelial and sarcomatous components, respectively. An analysis of transition zone indicated epithelial–mesenchymal transition as a mechanis

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34

Kovacic, Jason C., Nadia Mercader, Miguel Torres, Manfred Boehm, and Valentin Fuster. "Epithelial-to-Mesenchymal and Endothelial-to-Mesenchymal Transition." Circulation 125, no. 14 (2012): 1795–808. http://dx.doi.org/10.1161/circulationaha.111.040352.

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35

Dong, Feng, Tingting Liu, Hao Jin та Wenbo Wang. "Chimaphilin inhibits human osteosarcoma cell invasion and metastasis through suppressing the TGF-β1-induced epithelial-to-mesenchymal transition markers via PI-3K/Akt, ERK1/2, and Smad signaling pathways". Canadian Journal of Physiology and Pharmacology 96, № 1 (2018): 1–7. http://dx.doi.org/10.1139/cjpp-2016-0522.

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Epithelial-to-mesenchymal transition is a cellular process associated with cancer invasion and metastasis. However, the antimetastatic effects of chimaphilin remain elusive. In this study, we attempted to investigate the potential use of chimaphilin as an inhibitor of TGF-β1-induced epithelial-to-mesenchymal transition in U2OS cells. We found that TGF-β1 induced epithelial-to-mesenchymal transition to promote U2OS cell invasion and metastasis. Western blotting demonstrated that chimaphilin inhibited U2OS cell invasion and migration, increased the expression of the epithelial phenotype marker E

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36

Kushwaha, Sandhya, Deepti Jindal, Sonia Joshi, Ashwini P., and Poorva Tiwari. "Exploring the Role of Cadherins in Epithelial–Mesenchymal Transition and Mesenchymal–Epithelial Transition-Associated Tumorigenesis." Dental Journal of Advance Studies 6, no. 02/03 (2018): 045–52. http://dx.doi.org/10.1055/s-0038-1673588.

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AbstractThe malignant tumors develop when tumor cells overcome the cell–cell adhesion and invade the surrounding tissue. The epithelium consists of E-cadherin as the main adhesion molecule, which is mainly implicated in the carcinogenesis as it is frequently lost in the human epithelial tumors. Epithelial–mesenchymal transition (EMT) and its reverse mesenchymal–epithelial transition (MET) have been suggested to play crucial roles in metastatic dissemination of carcinomas. E-cadherin loss may promote invasion, and re-expression may facilitate cell survival within metastatic deposits. The mechan

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37

Font-Clos, Francesc, Stefano Zapperi, and Caterina A. M. La Porta. "Topography of epithelial–mesenchymal plasticity." Proceedings of the National Academy of Sciences 115, no. 23 (2018): 5902–7. http://dx.doi.org/10.1073/pnas.1722609115.

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The transition between epithelial and mesenchymal states has fundamental importance for embryonic development, stem cell reprogramming, and cancer progression. Here, we construct a topographic map underlying epithelial–mesenchymal transitions using a combination of numerical simulations of a Boolean network model and the analysis of bulk and single-cell gene expression data. The map reveals a multitude of metastable hybrid phenotypic states, separating stable epithelial and mesenchymal states, and is reminiscent of the free energy measured in glassy materials and disordered solids. Our work no

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38

Calabrò, Maria Luisa, Nayana Lazzari, Giulia Rigotto, Marco Tonello, and Antonio Sommariva. "Role of Epithelial–Mesenchymal Plasticity in Pseudomyxoma Peritonei: Implications for Locoregional Treatments." International Journal of Molecular Sciences 21, no. 23 (2020): 9120. http://dx.doi.org/10.3390/ijms21239120.

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The mechanisms by which neoplastic cells disseminate from the primary tumor to metastatic sites, so-called metastatic organotropism, remain poorly understood. Epithelial–mesenchymal transition (EMT) plays a role in cancer development and progression by converting static epithelial cells into the migratory and microenvironment-interacting mesenchymal cells, and by the modulation of chemoresistance and stemness of tumor cells. Several findings highlight that pathways involved in EMT and its reverse process (mesenchymal–epithelial transition, MET), now collectively called epithelial–mesenchymal p

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39

Guerra, A., D. J. Rodriguez, S. Montero, et al. "Phase transitions in tumor growth VI: Epithelial–Mesenchymal transition." Physica A: Statistical Mechanics and its Applications 499 (June 2018): 208–15. http://dx.doi.org/10.1016/j.physa.2018.01.040.

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40

Maier, Harald J., Thomas Wirth, and Hartmut Beug. "Epithelial-Mesenchymal Transition in Pancreatic Carcinoma." Cancers 2, no. 4 (2010): 2058–83. http://dx.doi.org/10.3390/cancers2042058.

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41

Hashem, Hala. "Epithelial Mesenchymal Transition and Tissue Healing." Journal of Medical Histology 2, no. 2 (2019): 81–102. http://dx.doi.org/10.21608/jmh.2019.7401.1046.

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42

Menju, Toshi, and Hiroshi Date. "Lung cancer and epithelial-mesenchymal transition." General Thoracic and Cardiovascular Surgery 69, no. 5 (2021): 781–89. http://dx.doi.org/10.1007/s11748-021-01595-4.

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43

van Zijl, Franziska, Gudrun Zulehner, Michaela Petz, et al. "Epithelial–mesenchymal transition in hepatocellular carcinoma." Future Oncology 5, no. 8 (2009): 1169–79. http://dx.doi.org/10.2217/fon.09.91.

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Broster, Seth A., and Natasha Kyprianou. "Epithelial–mesenchymal transition in prostatic disease." Future Oncology 11, no. 23 (2015): 3197–206. http://dx.doi.org/10.2217/fon.15.253.

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ZHAO, YA-LEI, RONG-TAO ZHU, and YU-LING SUN. "Epithelial-mesenchymal transition in liver fibrosis." Biomedical Reports 4, no. 3 (2016): 269–74. http://dx.doi.org/10.3892/br.2016.578.

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46

Kogan, Samuel. "The Mesenchymal-Epithelial Transition and Metaplasia." Journal of Undergraduate Life Sciences 16, no. 1 (2022): 4. http://dx.doi.org/10.33137/juls.v16i1.38941.

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47

Wu, Yanyuan, Marianna Sarkissyan, and Jaydutt Vadgama. "Epithelial-Mesenchymal Transition and Breast Cancer." Journal of Clinical Medicine 5, no. 2 (2016): 13. http://dx.doi.org/10.3390/jcm5020013.

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48

Son, Hwa-Jin, and Aree Moon. "Epithelial-mesenchymal Transition and Cell Invasion." Toxicological Research 26, no. 4 (2010): 245–52. http://dx.doi.org/10.5487/tr.2010.26.4.245.

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49

Venkov, Christo, David Plieth, Terri Ni, et al. "Transcriptional Networks in Epithelial-Mesenchymal Transition." PLoS ONE 6, no. 9 (2011): e25354. http://dx.doi.org/10.1371/journal.pone.0025354.

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50

Zhao, Li-Jin, and Fang Wang. "Epithelial-to-mesenchymal transition and hepatolithiasis." World Chinese Journal of Digestology 24, no. 8 (2016): 1153. http://dx.doi.org/10.11569/wcjd.v24.i8.1153.

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