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Interaction Between Hyaluronic Acid and Its Receptors (CD44, RHAMM) Regulates the Activity of Inflammation and Cancer

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199136 Year: Pages: 218 DOI: 10.3389/978-2-88919-913-6 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2016-01-19 14:05:46
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The biological outcome of Hyaluronan (also hyaluronic acid, abbreviated HA) interaction with its CD44 or RHAMM receptors recently attracted much attention within the scientific community owing to a Nature article by Tian X et al. (Nature 2013; 499:346-9). The article described a life span exceeding 30 years in naked mole rats, whereas the maximal lifespan of mice, to which the naked mole rat is related, is only 4 years. This observation is accompanied by the finding that the naked mole rat, in contrast to the mouse, does not develop spontaneous tumors during this exceptional longevity. The article provides evidence that interaction of long tissue HA (6000-12,000 kDa) of the naked mole rat with cell surface CD44, in contrast to the interaction of short tissue HA (less than 3000 kDa) with the mouse CD44, makes the difference. More specifically, this communication shows that the interaction of short HA with fibroblasts’ CD44 imposes on them susceptibility for malignant transformation, whereas the corresponding interaction with long HA imposes on the fibroblasts a resistance to malignant transformation. The article does not explain the mechanism that underlines these findings. However, the articles, that will be published in the proposed Research Topic in the Inflammation section of Frontiers in Immunology, can bridge not only this gap, but also may explain why interaction between short HA and cell surface CD44 (or RHAMM, an additional HA receptor) enhances the development of inflammatory and malignant diseases. Furthermore, the articles included in the proposed Frontiers Research Topic will show that cancer cells and inflammatory cells share several properties related to the interaction between short HA and cell surface CD44 and/or RHAMM. These shared properties include: 1. Support of cell migration, which allows tumor metastasis and accumulation of inflammatory cells at the inflammation site; 2. Delivery of intracellular signaling, which leads to cell survival of either cancer cells or inflammatory cells; 3. Delivery of intracellular signaling, which activates cell replication and population expansion of either cancer cells or inflammatory cells; and 4. Binding of growth factors to cell surface CD44 of cancer cells or inflammatory cells (i.e., the growth factors) and their presentation to cells with cognate receptors (endothelial cells, fibroblasts), leading to pro-malignant or pro-inflammatory activities. Going back to the naked mole rat story, we may conclude from the proposed articles of this Frontiers Research Topic that the long HA, which displays anti-malignant effect, interferes with the above described pro-malignant potential of the short HA (perhaps by competing on the same CD44 receptor). Extrapolating this concept to Inflammation, the same mechanism (competition?) may be valid for inflammatory (and autoimmune) activities. If this is the case, long HA may be used for therapy of both malignant and inflammatory diseases. Moreover, targeting the interaction between short HA and CD44 (e.g. by anti-CD44 blocking antibodies) may display also a therapeutic effect on both malignant and inflammatory diseases, an issue that encourages not only fruitful exchange of views, but also practical experimental collaboration.

Mesothelioma Heterogeneity: Potential Mechanisms

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ISBN: 9783038974734 / 9783038974741 Year: Pages: 204 DOI: 10.3390/books978-3-03897-474-1 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology --- Oncology
Added to DOAB on : 2019-01-11 11:18:51
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Mesothelioma is a rare aggressive cancer that develops from the mesothelium. Recent molecular analyses have defined four different types of mesothelioma based on gene expression and two major molecularly-defined groups based on prognosis. In this volume, potential mechanisms causing this heterogeneity are explored. The different chapters include heterogeneity learned from experimental animal models in NF2/Hippo pathway signaling, stem cell signaling pathways, the tumor microenvironment, and micro RNA secretome. Novel aspects deserving attention such as the implication of long, non-coding RNA in disease heterogeneity are described. The volume also includes the description of tools useful to address some specific questions such as an assessment of the copy number variations of two tumor suppressors frequently mutated in mesothelioma or an investigation of Macrophage Inhibition Factor signaling in mesothelioma.

Ways to improve tumor uptake and penetration of drugs into solid tumors

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193509 Year: Pages: 129 DOI: 10.3389/978-2-88919-350-9 Language: English
Publisher: Frontiers Media SA
Subject: Oncology --- Medicine (General) --- Therapeutics --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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The main scope of this topic is to give an update on pharmacologic and non-pharmacologic approaches to enhance uptake and penetration of cancer drugs into tumors. Inadequate accumulation of drugs in tumors has emerged over the last decade as one of the main problems underlying therapeutic failure and drug resistance in the treatment of cancer. Insufficient drug uptake and penetration is causally related to the abnormal tumor architecture. Thus, poor vascularization, increased resistance to blood flow and impaired blood supply represent a first obstacle to the delivery of antitumor drugs to tumor tissue. Decreased or even inverted transvascular pressure gradients compromise convective delivery of drugs. Eventually, an abnormal extracellular matrix offers increased frictional resistance to tumor drug penetration. Abnormal tumor architecture also changes the biology of tumor cells, which contributes to drug resistance through several different mechanisms. The variability in vessel location and structure can make many areas of the tumor hypoxic, which causes the tumor cells to become quiescent and thereby resistant to many antitumor drugs. In addition, the abnormally long distance of part of the tumor cell population from blood vessels provides a challenge to delivering cancer drugs to these cells. We have recently proposed additional mechanisms of tumor drug resistance, which are also related to abnormal tumor architecture. First, increased interstitial fluid pressure can by itself induce drug resistance through the induction of resistance-promoting paracrine factors. Second, the interaction of drug molecules with vessel- proximal tumor cell layers may also induce the release of these factors, which can spread throughout the cancer, and induce drug resistance in tumor cells distant from blood vessels. As can be seen, abnormal tumor architecture, inadequate drug accumulation and tumor drug resistance are tightly linked phenomena, suggesting the need to normalize the tumor architecture, including blood vessels, and/or increase the accumulation of cancer drugs in tumors in order to increase therapeutic effects. Indeed, several classes of drugs (that we refer to as promoter drugs) have been described, that promote tumor uptake and penetration of antitumor drugs, including those that are vasoactive, modify the barrier function of tumor vessels, debulk tumor cells, and overcome intercellular and stromal barriers. In addition, also non-pharmacologic approaches have been described that enhance tumor accumulation of effector drugs (e.g. convection-enhanced delivery, hyperthermia, etc.). Some drugs that have already received regulatory approval (e.g. the anti-VEGF antibody bevacizumab) exert antitumor effects at least in part through normalization of the tumor vasculature and enhancement of the accumulation of effector drugs. Other drugs, acting through different mechanisms of action, are now in clinical development (e.g. NGR-TNF in phase II/III studies) and others are about to enter clinical investigation (e.g. JO-1).

Tumor Hypoxia: Impact in Tumorigenesis, Diagnosis, Prognosis and Therapeutics

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450640 Year: Pages: 113 DOI: 10.3389/978-2-88945-064-0 Language: English
Publisher: Frontiers Media SA
Subject: Biology --- Science (General) --- Oncology --- Medicine (General)
Added to DOAB on : 2017-07-06 13:27:36
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Hypoxic regions have been identified within tumors and its presence has been linked to malignant progression, metastasis, resistance to therapy, and poor clinical outcomes following treatment. Acute and chronic hypoxia are integral components of tumor microenvironment and conduce to metabolic adaptations of tumor cells leading to genetic instability, intratumor heterogeneity and malignant progression. On the success of our fight against cancer, the continued adaptability of tumors to their microenvironmental stresses, such as hypoxia, must be considered. Tumor cells are endowed with a very high plasticity and capacity to adapt. It is our challenge to find populations and conditions of the tumor microenvironment germane for target success. Interdisciplinary work will be the key for achievement of these goals. This e-book is a compendium of original reports and review articles contributed by world-class experts in the field of tumor hypoxia. This material will be useful to foster discussion and increase understanding of the involvement of hypoxia in tumorigenesis, biomarker development, and therapeutics.Hypoxic regions have been identified within tumors and its presence has been linked to malignant progression, metastasis, resistance to therapy, and poor clinical outcomes following treatment. Acute and chronic hypoxia are integral components of tumor microenvironment and conduce to metabolic adaptations of tumor cells leading to genetic instability, intratumor heterogeneity and malignant progression. On the success of our fight against cancer, the continued adaptability of tumors to their microenvironmental stresses, such as hypoxia, must be considered. Tumor cells are endowed with a very high plasticity and capacity to adapt. It is our challenge to find populations and conditions of the tumor microenvironment germane for target success. Interdisciplinary work will be the key for achievement of these goals. This e-book is a compendium of original reports and review articles contributed by world-class experts in the field of tumor hypoxia. This material will be useful to foster discussion and increase understanding of the involvement of hypoxia in tumorigenesis, biomarker development, and therapeutics.

Keywords

hypoxia --- tumor --- microenvironment --- HIF --- pH --- stress --- Stem Cells --- Leukemia --- biomarkers --- therapy

Cancer Metabolism: Molecular Targeting and Implications for Therapy

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453221 Year: Pages: 114 DOI: 10.3389/978-2-88945-322-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2018-02-27 16:16:45
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Development of an effective anticancer therapeutic necessitates the selection of cancer-related or cancer-specific pathways or molecules that are sensitive to intervention. Several such critical yet sensitive molecular targets have been recognized, and their specific antagonists or inhibitors validated as potential therapeutics in preclinical models. Yet, majority of anticancer principles or therapeutics show limited success in the clinical translation. Thus, the need for the development of an effective therapeutic strategy persists. “Altered energy metabolism” in cancer is one of the earliest known biochemical phenotypes which dates back to the early 20th century. The German scientist, Otto Warburg and his team (Warburg, Wind, Negelein 1926; Warburg, Wind, Negelein 1927) provided the first evidence that the glucose metabolism of cancer cells diverge from normal cells. This phenomenal discovery on deregulated glucose metabolism or cellular bioenergetics is frequently witnessed in majority of solid malignancies. Currently, the altered glucose metabolism is used in the clinical diagnosis of cancer through positron emission tomography (PET) imaging. Thus, the “deregulated bioenergetics” is a clinically relevant metabolic signature of cancer cells, hence recognized as one of the hallmarks of cancer (Hanahan and Weinberg 2011). Accumulating data unequivocally demonstrate that, besides cellular bioenergetics, cancer metabolism facilitates several cancer-related processes including metastasis, therapeutic resistance and so on. Recent reports also demonstrate the oncogenic regulation of glucose metabolism (e.g. glycolysis) indicating a functional link between neoplastic growth and cancer metabolism. Thus, cancer metabolism, which is already exploited in cancer diagnosis, remains an attractive target for therapeutic intervention as well. The Frontiers in Oncology Research Topic “Cancer Metabolism: Molecular Targeting and Implications for Therapy” emphases on recent advances in our understanding of metabolic reprogramming in cancer, and the recognition of key molecules for therapeutic targeting. Besides, the topic also deliberates the implications of metabolic targeting beyond the energy metabolism of cancer. The research topic integrates a series of reviews, mini-reviews and original research articles to share current perspectives on cancer metabolism, and to stimulate an open forum to discuss potential challenges and future directions of research necessary to develop effective anticancer strategies.

Microenvironment-Derived Stem Cell Plasticity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453443 Year: Pages: 114 DOI: 10.3389/978-2-88945-344-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology --- Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
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Plasticity is the hallmark of stem cells. At the same time, stem cells, like any other cell type, are influenced by their microenvironment and respond to it accordingly. A specific microenvironment is defined by a variety of factors, including biological and chemical factors, cell-cell interactions, but also metabolic and mechanical cues. Such dynamic and specialized microenvironment where the stem cells reside is considered a stem cell niche. Tissue injury as well as malignant tissue alterations lead to changes in the niche influencing the plasticity and biology of residing stem cells. Similarly, the niche changes upon tissue damage, which eventually induces differentiation of stem cells and ultimately regeneration of the tissue.

Self-Eating on Demand: Autophagy in Cancer and Cancer Therapy

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454228 Year: Pages: 111 DOI: 10.3389/978-2-88945-422-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Oncology
Added to DOAB on : 2018-11-16 17:17:57
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Macroautophagy, the major lysosomal pathway for recycling intracellular components including whole organelles, has emerged as a key process modulating tumorigenesis, tumor–stroma interactions, and cancer therapy. An impressive number of studies over the past decade have unraveled the plastic role of autophagy during tumor development and dissemination. The discoveries that autophagy may either support or repress neoplastic growth and contextually favor or weaken resistance and impact antitumor immunity have spurred efforts from many laboratories trying to conceptualize the complex role of autophagy in cancer using cellular and preclinical models. This complexity is further accentuated by recent findings highlighting that various autophagy-related genes have roles beyond this catabolic mechanism and interface with oncogenic pathways, other trafficking and degradation mechanisms and the cell death machinery. From a therapeutic perspective, knowledge of how autophagy modulates the tumor microenvironment is crucial to devise autophagy-targeting strategies using smart combination of drugs or anticancer modalities. This eBook contains a collection of reviews by autophagy researchers and provides a background to the state-of-the-art in the field of autophagy in cancer, focusing on various aspects of autophagy regulation ranging from its molecular components to its cell autonomous role, e.g. in cell division and oncogenesis, miRNAs regulation, cross-talk with cell death pathways as well as cell non-autonomous role, e.g. in secretion, interface with tumor stroma and clinical prospects of autophagy-based biomarkers and autophagy modulators in anticancer therapy. This eBook is part of the TransAutophagy initiative to better understand the clinical implications of autophagy in cancer.

Targeting thyroid cancer microenvironment and epigenetic signalling: new frontiers in cancer endocrinology basic and clinical research

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192403 Year: Pages: 131 DOI: 10.3389/978-2-88919-240-3 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Internal medicine --- Oncology
Added to DOAB on : 2015-11-16 15:44:59
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This Research Topic is devoted to the understanding of molecular mechanisms of Human Thyroid Cancers. Original research describing functional studies of genetic mutations that shed novel insights into the aetiology and pathogenesis of these cancers, as well as angiogenesis and tumor microenvironment, mouse models studies that describe mechanisms or novel potential therapeutic targets and biomarkers for these endocrine cancers are presented. Scopes: The scope of this Research Topic was to cover the entire field of thyroid cancers: the main focus of this topic is translational, with an emphasis on bench to bedside research. Experimental, pre-clinical and clinical research addressing the following aspects is included in this Research Topic: 1) Investigation of specific molecular patterns of thyroid tumorigenesis, which could allow the development of new directions in the field of pharmacotherapy research; 2) Emphasis on animal studies (preclinical models of human anaplastic thyroid cancers) for the validation of biomarkers with the potential to lead to clinical trials, and studies of targetable mechanisms of oncogenesis, progression of these malignancies, tumor microenvironment and extracellular matrix, and metastatic disease; 3) Assessment of biomarkers to predict the potential response or resistance to drug treatment (targeted cancer therapies) or to guide the follow-up of treated patients; 4) Investigation of new laboratory molecular tests (e.g. molecular techniques and applications of thyroid fine-needle aspiration biopsy) to translate in the clinical practice; In summary, specific areas of interest include: thyroid cancer genetics; genome-wide analysis; clinical and translational research; orthotopic mouse models of metastatic thyroid carcinoma; tumor microenvironment; epigenetic; biological insights of personalized medicine; novel applications of bioinformatics; large scale molecular characterization of tumors; diagnostic or prognostic biomarkers; endocrine pathology studies; thyroid fine-needle aspiration.

The Tumor Microenvironment of High Grade Serous Ovarian Cancer

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ISBN: 9783038975540 / 9783038975557 Year: Pages: 434 DOI: 10.3390/books978-3-03897-555-7 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology --- Oncology
Added to DOAB on : 2019-02-06 09:22:42
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The Special Issue on high grade serous ovarian cancer (HGSOC) and the contribution of the tumor microenviroment (TME) consists of reviews contributed by leaders in the OC field. As HGSOC metastases have a highly complex TME, there is an urgent need to better understand the TME in general, its distinct components in particular, and the role of the TME in the context of disease recurrence and development of chemoresistance. The Special Issue incorporates the current understanding of the different parts of thd TME components, including the cancer cells themselves, the cells surrounding the cancer cells or stromal cells, and the cells of the immune system, which are attracted to the site of metastases. In addition to these cells of the TME, the role of various cellular factors made by the cells of the TME are also the subject of the reviews. In addition, reviews in this Special Issue cover the complex relationships between the molecular mechanisms of HGSOC progression, including genomic, epigenomic and transcriptomic changes and changes in the immune cell landscape, as these may provide attractive new molecular targets for HGSOC therapy.

Breaking the cycle: Attacking the malaria parasite in the liver

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196951 Year: Pages: 173 DOI: 10.3389/978-2-88919-695-1 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General) --- Microbiology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Despite significant progress in the global fight against malaria, this parasitic infection is still responsible for nearly 300 million clinical cases and more than half a million deaths each year, predominantly in African children less than 5 years of age. The infection starts when mosquitoes transmit small numbers of parasites into the skin. From here, the parasites travel with the bloodstream to the liver where they undergo an initial round of replication and maturation to the next developmental stage that infects red blood cells. A vaccine capable of blocking the clinically silent liver phase of the Plasmodium life cycle would prevent the subsequent symptomatic phase of this tropical disease, including its frequently fatal manifestations such as severe anemia, acute lung injury, and cerebral malaria. Parasitologists, immunologists, and vaccinologists have come to appreciate the complexity of the adaptive immune response against the liver stages of this deadly parasite. Lymphocytes play a central role in the elimination of Plasmodium infected hepatocytes, both in humans and animal models, but our understanding of the exact cellular interactions and molecular effector mechanisms that lead to parasite killing within the complex hepatic microenvironment of an immune host is still rudimentary. Nevertheless, recent collaborative efforts have led to promising vaccine approaches based on liver stages that have conferred sterile immunity in humans – the University of Oxford's Ad prime / MVA boost vaccine, the Naval Medical Research Center’s DNA prime / Ad boost vaccine, Sanaria Inc.'s radiation-attenuated whole sporozoite vaccine, and Radboud University Medical Centre’s and Sanaria's derived chemoprophylaxis with sporozoites vaccines. The aim of this Research Topic is to bring together researchers with expertise in malariology, immunology, hepatology, antigen discovery and vaccine development to provide a better understanding of the basic biology of Plasmodium in the liver and the host’s innate and adaptive immune responses. Understanding the conditions required to generate complete protection in a vaccinated individual will bring us closer to our ultimate goal, namely to develop a safe, scalable, and affordable malaria vaccine capable of inducing sustained high-level protective immunity in the large proportion of the world’s population constantly at risk of malaria.

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