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Matricellular Receptors as Potential Targets in Anti-Cancer Therapeutic Strategies

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450244 Year: Pages: 129 DOI: 10.3389/978-2-88945-024-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Therapeutics
Added to DOAB on : 2018-02-27 16:16:44
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The invasive character of a primary cancer is greatly dependent on numerous interactions between tumor cells and their extracellular surroundings. Matricellular receptors are defined as (cell-surface) receptors that bind extracellular matrix (ECM) structural proteins and soluble factors dynamically acting on ECM homeostasis. Matricellular receptors mediate numerous signalings from the extracellular environment to cell nucleus and drive main biological functions that are cell growth, survival and migration. Numerous data from the last decade evidence that matricellular receptors are biosensors that allow to a tumor cell answering to microenvironmental variations, and in this sense they are important contributors to tumor cell malignancy. Matricellular receptors represent thus valuable targets for the development of original anti-cancer strategies. Original reports, bibliographic reviews or hypotheses are welcome to improve the basic knowledge of matricellular receptor properties, their spatio-temporal regulation, the dynamic formation of complex receptors and the impact of such interactions on the invasive properties of tumor cells. Biological, biophysical and pharmacological, as well as in silico contributions will be appreciated.

Keywords

Anti-cancer target --- disco

Cancer-associated defects in the DNA damage response: drivers for malignant transformation and potential therapeutic targets

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199495 Year: Pages: 107 DOI: 10.3389/978-2-88919-949-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Genetics
Added to DOAB on : 2016-01-19 14:05:46
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For this eBook, and the associated Research Topic in Frontiers in Genetics, entitled: ‘Cancer-associated defects in the DNA damage response: drivers for malignant transformation and potential therapeutic targets’ we have selected 10 papers that each discusses important, yet distinct aspects of the response to DNA damage in normal cells and cancer cells. Using an evolutionary conserved signaling network called the ‘DNA damage response (DDR)’ cells maintain the integrity of their genome, and thus safeguard cellular functioning and the ability to create viably progeny. Initially, the DDR appeared to consist of few linear kinase-driven pathways. However, research over the past decades in model organisms, as well as in the human system has revealed that the DDR is a complex signaling network, wired by multiple parallel pathways and displaying extensive crosstalk. Besides phosphorylation, multiple other post-translational modifications, including ubiquitination and sumoylation, are involved to achieve chromatin remodeling and initiation of DNA repair. Also, rather than being a cell-intrinsic phenomenon, we increasingly appreciate that cell-cell communication is involved. The recognition and repair of DNA damage is essential to maintain normal physiology. Multiple pathological conditions have been attributed to defective DNA repair, most notably accelerated aging, neurodegeneration and cancer. In the context of cancer, through repair of DNA damage or elimination of irreparably damaged cells, the DDR clearly has a tumor-suppressive role. Indeed, many tumor cells show partially inactivated DDR signaling, which allows proliferation in the context of DNA damage-inducing oncogenes. Simultaneously, loss of specific DDR signaling nodes creates a specific dependence of tumor cells on their remaining DDR components, and thus creates therapeutic opportunities. Especially in the context of cancer treatment, numerous targeted agents are under investigation, either to potentiate the cytotoxic effects of chemo-radiotherapy, or to induce synthetic lethality with cancer-specific alterations, with the treatment of BRCA1/2 mutant cancers with PARP1 inhibitors as a prototype example. We have selected four review articles that provide insight into the key components and the wiring of the DDR and DNA repair. Torgovnick and Schumacher review the involvement of DNA repair in the initiation and treatment of cancer, Brinkmann et al., describe the involvement of ubiquitination in DNA damage signaling and Jaiswal and Lindqvist discuss how cell-extrinsic signaling participates in communication of DNA damage to neighboring cells. In addition, Shatneyeva and colleagues review the connection between the cellular response to DNA damage and escape from immune surveillance. Concerning the therapeutic application of targeting the DDR and DNA repair, three articles were included. Krajewska and van Vugt review the wiring of homologous recombination and how this offers therapeutic opportunities. Additionally, Knittel and colleagues describe how genetic loss of the central DDR component ATM in chronic lymphocytic leukemia can be exploited therapeutically by targeting certain parallel DNA repair pathways. Syljuasen and colleagues report on how targeting of the DDR can be used as a therapeutic strategy in lung cancer. Finally, three chapters describe newly identified regulators of the cellular response to DNA damage. Von Morgen et al. describe the R2TP complex, Lezzi and Fanciluuli review the involvement of Che-1/AATF in the DDR, and Ohms and co-authors describe how retrotransposons are at the basis of increased genomic instability. Altogether, these articles describe how defective responses to DNA damage underlie disease - and especially in the context of cancer -can be exploited to better treat disease.

Dendritic Cell Control of Immune Responses

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198689 Year: Pages: 121 DOI: 10.3389/978-2-88919-868-9 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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Dendritic cells (DC) are among the first cells to encounter pathogens and damage in peripheral tissues and, upon activation, DC migrate to lymph nodes where they activate and educate T cells to initiate and shape the immune response. DC present pathogen-derived antigen to T cells and drive T cell differentiation into particular effector cells through the expression and secretion of co-stimulatory molecules and cytokines respectively. The study of DC biology has included the identification of multiple DC subsets in tissues and lymphoid organs, the differentiation and plasticity of DC subsets, the functional consequences of DC interaction with pathogen, control of DC migratory properties and the impact of DC on T cell activation and differentiation. In recent years sophisticated systems biology approaches have been developed to deepen our understanding of DC function. These studies have identified differences between DC subsets located in various tissues and critical factors that drive the outcome of the interaction between DC and T cells. DC are currently being used in in various clinical therapeutic settings, including as vaccines for cancer and autoimmune disease. A clear understanding of DC factors that contribute to specific immune responses is vital to the success of DC based therapies. This research topic will give a comprehensive overview of current issues in DC biology and provides an update on the clinical uses of DC in the therapy of autoimmunity and cancer.

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.

Adrenal Cortex: From Physiology to Disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199198 Year: Pages: 89 DOI: 10.3389/978-2-88919-919-8 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Internal medicine --- Science (General) --- Biology
Added to DOAB on : 2016-01-19 14:05:46
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The adrenal gland plays essential roles in the control of body homeostasis, stress and immune responses. The adrenal cortex represents up to 90% of the gland and is specialised in the production of mineralocorticoids, glucocorticoids and adrenal androgens. This production is tightly coordinated and results from a unique zonal organisation. Although our knowledge of the molecular mechanisms controlling adrenal steroidogenesis is quite extensive, for decades, the mechanisms of adrenal cortex development, cellular homeostasis and renewal have remained elusive. The advent of new high-throughput technologies and sophisticated genetic approaches has brought tremendous progress in our understanding of how the adrenal cortex achieves and maintains its particular organisation. The aim of this Frontiers in Endocrinology Topic is to provide readers with a snapshot of our current knowledge on adrenal physiology and how deregulations of these processes result in adrenal diseases. This includes but is not limited to, basic research on adrenal development, cell lineage identification, progenitor cells, tissue renewal, control of differentiation and zonation and clinical research on the identification of disease-related genes.

Molecular Function and Regulation of Non-coding RNAs in Multifactorial Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450022 Year: Pages: 71 DOI: 10.3389/978-2-88945-002-2 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Our understanding of the mechanisms underlying the development of multifactorial diseases such as diabetes, autism, Alzheimer's disease, and cancer has been greatly advanced. Non-coding RNAs (ncRNAs), generally including microRNAs and long non-coding RNAs, have recently been found to have potential roles in these diseases, and provide new opportunities for developing both specific biomarkers and therapeutic targets. However, the molecular function and regulation of these RNAs still remains challenging. Numerous studies are focusing on this field in order to fully appreciate the role and regulation of these molecules in human medicine and biology. This e-book aims to bring together new findings on Non-coding RNAs in different complex diseases. It will highlight the characterization, roles, mechanism, and mode of action of these RNAs in complex disorders. We believe that the publications on this topic would be exponentially extended in future. The improved approaches at multiple levels may pave the way for designing and applying new biomarker and therapeutic targets for specific diseases based on these attractive molecules.

Tumor Metastasis

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ISBN: 9789535126300 9789535126317 9789535141815 Year: Pages: 266 DOI: 10.5772/61798 Language: English
Publisher: IntechOpen
Subject: Oncology
Added to DOAB on : 2019-10-03 07:51:49

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Metastasis is the major cause of cancer-related death. It is a multistep process. The mechanism underlying metastasis is complicated and poorly understood. Recent advances in tumor metastasis research have led to improved diagnosis and clinical management of cancer. However, new strategies on metastasis treatment are urgently needed, especially the novel biomarkers discovery and targeted therapy. This book is designed to present the most recent advances in tumor metastasis.

Free Radicals and Diseases

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ISBN: 9789535127468 9789535127475 9789535141655 Year: Pages: 386 DOI: 10.5772/61358 Language: English
Publisher: IntechOpen
Subject: Oncology
Added to DOAB on : 2019-10-03 07:51:49

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The current volume entitled, ""Free Radicals and Diseases"" integrates knowledge in free radical-associated diseases from the basic level to the advanced level, and from the bench side to bed side. The chapters in this book provide an extensive overview of the topic, including free radical formations and clinical interventions.

Advances in Epithelial Ovarian Cancer: Model Systems, Microenvironmental Influences, Therapy, and Origins

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197699 Year: Pages: 176 DOI: 10.3389/978-2-88919-769-9 Language: English
Publisher: Frontiers Media SA
Subject: Oncology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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This eBook provides a compendium of the current state-of-the-art in research tools for, and understanding of, the critical research areas in epithelial ovarian cancer (EOC) with a strong emphasis on (HG-SOC). Research areas covered include therapy response and development, microenvironmental influences and the etiology and progression of EOC. Ten articles detail established and novel in vivo and in vitro model systems. These include primary and immortalized cell culture in 2D and 3D as well as genetically engineered, transgenic, spontaneous, syngeneic, classical xenograft and patient derived xenograft mouse models. The generation of genetically engineered mouse models of HG-SOC has been a major dilemma as models with the oncogenic aberrations common in the human malignancy do not accurately recapitulate HG-SOC. Conversely, commonly used HG-SOC cell lines have been found to not harbor the expected genetic changes. These issues as well as the rapid acceptance of patient derived xenograft models are reviewed. Five articles discuss different aspects of the tumor microenvironment including its role in therapy resistance, disease progression and metastasis. Mutation of BRCA1/2 continues to be the best defined risk factor for HG-SOC. Three articles discuss BRCA-loss in the context of disease development, targeted therapies and changes in preventative measures proposed for mutation carriers in light of the recent advances in knowledge regarding the origins of this malignancy. An image of HG-SOC with patchy BRCA1 expression is featured on the cover (image by VM Howell). A major clinical issue for patients with HG-SOC is the development of therapy resistance. Five articles focus on therapy resistance and different ways to overcome resistance. Overall, this eBook is an outstanding resource to aid researchers design their programs of research and determine the most appropriate and up-to-date EOC model systems to address their research questions.

Immunogenic Cell Death in Cancer: From Benchside Research to Bedside

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198382 Year: Pages: 145 DOI: 10.3389/978-2-88919-838-2 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Oncology
Added to DOAB on : 2017-02-07 16:12:31
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Classically, anti-cancer therapies have always been applied with the primary aim of tumor debulking achieved through widespread induction of cancer cell death. While the role of host immune system is frequently considered as host protective in various (antigen-bearing) pathologies or infections yet in case of cancer overtime it was proposed that the host immune system either plays no role in therapeutic efficacy or plays a limited role that is therapeutically unemployable. The concept that the immune system is dispensable for the efficacy of anticancer therapies lingered on for a substantial amount of time; not only because evidence supporting the claim that anti-cancer immunity played a role were mainly contradictory, but also largely because it was considered acceptable (and sometimes still is) to test anticancer therapies in immunodeficient mice (i.e. SCID/athymic mice lacking adaptive immune system). This latter practice played a detrimental role in appreciating the role of anticancer immunity in cancer therapy. This scenario is epitomized by the fact that for a long time the very existence of cancer-associated antigens or cancer-associated ‘danger signaling’ remained controversial. However, over last several years this dogmatic view has been considerably modified. The existence of cancer-associated antigens and ‘danger signaling’ has been proven to be incontrovertible. These developments have together paved way for the establishment of the attractive concept of “immunogenic cell death” (ICD). It has been established that a restricted class of chemotherapeutics/targeted therapeutics, radiotherapy, photodynamic therapy and certain oncolytic viruses can induce a form of cancer cell death called ICD which is accompanied by spatiotemporally defined emission of danger signals. These danger signals along with other factors help cancer cells undergoing ICD to activate host innate immune cells, which in turn activate T cell-based immunity that helps eradicate live (or residual) surviving cancer cells. The emergence of ICD has been marred by some controversy. ICD has been criticized to be either experimental model or setting-specific or mostly a concept based on rodent studies that may have very limited implications for clinical application. However, in recent times it has emerged (through mainly retrospective or prognostic studies) that ICD can work in various human clinical settings hinting towards clinical applicability of ICD. However a widespread consensus on this issue is still transitional. In the current Research Topic we aimed to organize and intensify a discussion that strives to bring together the academic and clinical research community in order to provide a background to the current state-of-the-art in ICD associated bench-side research and to initiate fruitful discussions on present and future prospects of ICD translating towards the clinical, bedside reality.

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