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      Emerging role of tumor cell plasticity in modifying therapeutic response


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          Resistance to cancer therapy is a major barrier to cancer management. Conventional views have proposed that acquisition of resistance may result from genetic mutations. However, accumulating evidence implicates a key role of non-mutational resistance mechanisms underlying drug tolerance, the latter of which is the focus that will be discussed here. Such non-mutational processes are largely driven by tumor cell plasticity, which renders tumor cells insusceptible to the drug-targeted pathway, thereby facilitating the tumor cell survival and growth. The concept of tumor cell plasticity highlights the significance of re-activation of developmental programs that are closely correlated with epithelial–mesenchymal transition, acquisition properties of cancer stem cells, and trans-differentiation potential during drug exposure. From observations in various cancers, this concept provides an opportunity for investigating the nature of anticancer drug resistance. Over the years, our understanding of the emerging role of phenotype switching in modifying therapeutic response has considerably increased. This expanded knowledge of tumor cell plasticity contributes to developing novel therapeutic strategies or combination therapy regimens using available anticancer drugs, which are likely to improve patient outcomes in clinical practice.

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          Immunity, inflammation, and cancer.

          Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis. Inflammation also affects immune surveillance and responses to therapy. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. This review outlines the principal mechanisms that govern the effects of inflammation and immunity on tumor development and discusses attractive new targets for cancer therapy and prevention. 2010 Elsevier Inc. All rights reserved.
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            Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.
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              Epithelial-mesenchymal transitions in development and disease.

              The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.

                Author and article information

                Signal Transduct Target Ther
                Signal Transduct Target Ther
                Signal Transduction and Targeted Therapy
                Nature Publishing Group UK (London )
                7 October 2020
                7 October 2020
                : 5
                : 228
                [1 ]GRID grid.13291.38, ISNI 0000 0001 0807 1581, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, and West China School of Basic Medical Sciences and Forensic Medicine, , Sichuan University, and Collaborative Innovation Center for Biotherapy, ; 610041 Chengdu, People’s Republic of China
                [2 ]GRID grid.263817.9, School of Medicine, , Southern University of Science and Technology Shenzhen, ; Shenzhen, Guangdong 518055 People’s Republic of China
                [3 ]Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen, Guangdong People’s Republic of China
                [4 ]GRID grid.1002.3, ISNI 0000 0004 1936 7857, Department of Biochemistry and Molecular Biology, , Monash University, ; Clayton, VIC Australia
                [5 ]GRID grid.411304.3, ISNI 0000 0001 0376 205X, School of Basic Medical Sciences, , Chengdu University of Traditional Chinese Medicine, ; 1166 Liutai Road, 611137 Chengdu, People’s Republic of China
                [6 ]GRID grid.410570.7, ISNI 0000 0004 1760 6682, State Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, , Third Military Medical University (Army Medical University), ; Chongqing, People’s Republic of China
                [7 ]Chongqing Key Laboratory for Disease Proteomics, Chongqing, People’s Republic of China
                Author information
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                : 19 June 2020
                : 25 August 2020
                : 30 August 2020
                Funded by: Supported by Project of the State Key Laboratory of Trauma, Burn and Combined Injury, Third Military Medical University;SKLJYJF20;
                Review Article
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                cancer therapy
                cancer therapy


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