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Cellular and Phenotypic Plasticity in Cancer

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196623 Year: Pages: 77 DOI: 10.3389/978-2-88919-662-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2016-08-16 10:34:25
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The process of Epithelial-Mesenchymal-Transition (EMT) is known to result in a phenotype change in cells from a proliferative state to a more invasive state. EMT has been reported to drive the metastatic spread of various cancers and has also been associated with drug resistance to cytotoxics and targeted therapeutics. Recently phenotype switching akin to EMT has been reported in non-epithelial cancers such as metastatic melanoma. This process involves changes in EMT-Transcription Factors (EMT-TFs), suggesting that phenotype-switching may be common to several tumour types. It remains unclear as to whether the presence of both Epilthelial-like and Mesenchymal-like cells are a pre-requisite for phenotype switching within a tumour, how this heterogeneity is regulated, and if alteration of cell phenotype is sufficient to mediate migratory changes, or whether drivers of cell migration result in an associated phenotype switch in cancer cells. Similarly it has yet to be clarified if cells in an altered phenotype can be refractory to drug therapy or whether mediators of drug resistance induce a concurrent phenotypic change. Little is known today about the underlying genetic, epigenetic and transient changes that accompany this phenotypic switch and about the role for the tumor micro-environment in influencing it. Hence this is currently an area of speculation and keen interest in the Oncology field with wide-ranging translational implications. In this Frontiers Research Topic, we discuss our current understanding of these concepts in various cancer types including breast cancer, colorectal cancer and metastatic melanoma. This topic covers how these processes of cellular and phenotypic plasticity are regulated and how they relate to cancer initiation, progression, dormancy, metastases and response to cytotoxics or targeted therapies.

The Epithelial-to-Mesenchymal Transition (EMT) in Cancer

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ISBN: 9783038427933 9783038427940 Year: Pages: VI, 254 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-04-27 16:09:54
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The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process with multiple transitional states, by which epithelial cells can convert into a mesenchymal phenotype. This process involves loss of cellular adhesion and cellular polarity, and an improvement in migratory and invasive properties. It occurs during normal embryonic development, tissue regeneration, organ fibrosis, and wound healing. It is also involved in tumor progression with metastatic expansion, and plays a major role in resistance to cancer treatment. In cancers, EMT inducers are hypoxia, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, metabolic changes, innate and adaptive immune responses, and treatment with antitumor drugs. Switch in gene expression from epithelial to mesenchymal phenotype is triggered by complex regulatory networks involving transcriptional control, non-coding RNAs, chromatin remodeling and epigenetic modifications, alternative splicing, post-translational regulation, protein stability and subcellular localization. Reversion of EMT, the mesenchymal-to-epithelial transition (MET), affects circulating cancer cells when they reach a desirable metastatic niche to develop secondary tumors. More knowledge and control of EMT to MET is necessary and will be beneficial for patients for cancer treatment. This current Special Issue entitled “Epithelial to Mesenchymal Transition in Cancer” will address these questions.

Pleiotropic Action of Selenium in the Prevention and Treatment of Cancer, and Related Diseases

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ISBN: 9783038976929 Year: Pages: 166 DOI: 10.3390/books978-3-03897-693-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology --- Science (General)
Added to DOAB on : 2019-04-05 11:07:22
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This book will cover topics related to the preparation and use of heterogeneous catalytic systems for the transformation of renewable sources, as well as of materials deriving from agro-industrial wastes and by-products. At the same time, the ever-increasing importance of bioproducts, due to the acceptance and request of consumers, makes the upgrade of biomass into chemicals and materials not only an environmental issue, but also an economical advantage.

Towards New Promising Discoveries for Lung Cancer Patients: A Selection of Papers from the First Joint Meeting on Lung Cancer of the FHU OncoAge (Nice, France) and the MD Anderson Cancer Center (Houston, TX, USA)

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ISBN: 9783039214518 / 9783039214525 Year: Pages: 230 DOI: 10.3390/books978-3-03921-452-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2019-12-09 11:49:15
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This Special Issue of Cancers (Basel) is mainly dedicated to selecting papers from the talks given during the first Joint Meeting on Lung Cancer (JMLC) between the MD Anderson Cancer Center (Houston, Texas USA) and the Hospital University Federation (HUF) OncoAge (University Côte d’Azur, Nice, France) (Nice, September 2018). The central theme of JMLC is to discuss new advances and exchange ideas regarding lung cancer. Notably, the talks covered different topics on new therapeutic strategies (targeted therapy and immuno-oncology), molecular and cellular biology, biomarkers, and the epidemiology of lung cancer. Special attention was also given to lung cancer in elderly patients. The articles published in this Special Issue covered subjects such as the assessment of new biomarkers and new approaches for the early detection of lung cancer, epidemiological data, and emphasized a place for the newly characterized cellular pathways in lung cancer, which opens room for therapeutic perspectives for lung cancer patients.

Disease and the Hippo Pathway: Cellular and Molecular Mechanisms

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ISBN: 9783039217762 / 9783039217779 Year: Pages: 226 DOI: 10.3390/books978-3-03921-777-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-12-09 11:49:16
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The Hippo pathway is a highly dynamic cellular signaling nexus that plays central roles in multiple cell types and regulates regeneration, metabolism, and development. The Hippo pathway integrates mechanotransduction, cell polarity, inflammation, and numerous types of paracrine signaling. If not tightly regulated, dysregulated Hippo pathway signaling drives the onset and progression of a range of diseases, including fibrosis and cancer. The molecular understanding of the Hippo pathway is rapidly evolving. This Special Issue contains ten articles contributed by established and up-and-coming Hippo pathway experts that, as a whole, provides an up-to-date overview of how dysregulated Hippo pathway activity is a common driver of specific diseases. The articles have a particular focus on the underlying molecular and cellular mechanisms that cause the Hippo pathway to go awry, and especially how this drives disease. The articles analyze disease-specific as well as common themes, which provides valuable insights into the fundamental molecular mechanisms in the dysfunctioning Hippo pathway, and thereby offer practical insights into potential future therapeutic intervention strategies.

Links between Fibrogenesis and Cancer: Mechanistic and Therapeutic Challenges: Mechanistic and Therapeutic Challenges

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ISBN: 9783039217069 / 9783039217076 Year: Pages: 348 DOI: 10.3390/books978-3-03921-707-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2019-12-09 11:49:16
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Tissue fibrosis may occur for unknown causes or be the consequence of many pathological conditions including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection, or malignancy. On the other hand, malignant tumors have been identified in fibrotic tissues decades ago, and now accumulating evidence suggests that fibrotic lesions enhance the risk of cancer in several organs such as liver, lungs, and breast. Disruption of an organ parenchymal cells and of its normal structural scaffold during tissue fibrogenesis appears to induce loss of cell polarity, promoting uncontrolled cell proliferation that may eventually lead to cancer development. Many cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications have been proposed to explain this link between fibrogenesis and carcinogenesis. However, the precise mechanisms of this fibrosis-to-cancer transition remain unclear. This book presents a collection of reviews and original articles summarizing recent advances in understanding the molecular mechanisms of cancer development in fibrotic organs.

Keywords

lung cancer --- renal injury --- fibrosis --- crizotinib --- anaplastic lymphoma kinase --- cystic formation --- pulmonary fibrosis --- butylidenephthalide --- SOX2 --- type I collagen --- bleomycin --- YAP --- TAZ --- Hippo pathway --- fibrosis --- cancer --- mechanotransduction --- TGF-? --- Wnt --- uterine fibroid --- leiomyoma --- tumor --- tumor necrosis factor ? --- cytokine --- growth factor --- inflammation --- clinical symptoms --- pathophysiology --- therapy --- hepatocellular carcinoma --- cirrhosis --- regeneration --- inflammation --- cytokines --- genetic instability --- reactive oxygen species --- idiopathic pulmonary fibrosis (IPF) --- lung cancer (LC) --- non-small cell lung cancer (NSCLC) --- acute lung injury --- protein S --- apoptosis --- signal pathway --- Erk1/2 --- lipopolysaccharide --- uterine fibroid --- leiomyoma --- smooth muscle tumor of uncertain malignant potential --- leiomyosarcoma --- myometrium --- immunohistochemistry --- marker --- pathology --- tumor --- diagnosis --- cancer-associated fibroblasts --- tumor microenvironment --- nanoparticles --- breast cancer --- antitumor efficacy --- cirrhosis --- HBV --- HCV --- hepatocellular carcinoma --- idiopathic pulmonary fibrosis --- lung cancer --- pathogenesis --- common pathways --- hepatocellular carcinoma (HCC) --- fibrosis --- cancer-associated fibroblasts (CAFs) --- hepatic stellate cells (HSCs) --- tumor microenvironment --- hepatocellular carcinoma --- non-alcoholic steatohepatitis --- fibrosis --- hepatic stellate cells --- extracellular matrix --- carcinogenesis --- angiogenesis --- cancer-associated fibroblasts --- extracellular matrix --- fibrosis --- heterogeneity --- interstitial fluid pressure --- metabolic reprogramming --- transforming growth factor-? --- tumor stiffness --- GPR40 --- GPR120 --- DHA --- omega-3 fatty acid --- SREBP-1 --- hepatocytes --- EMT --- lncRNA --- metastasis --- miRNA --- SMAD --- TGF-? --- targeted therapy --- tumor microenvironment --- n/a

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