Search results: Found 12

Listing 1 - 10 of 12 << page
of 2
>>
Sort by
Mesothelioma Heterogeneity: Potential Mechanisms

Author:
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

Cancer Metabolism: Molecular Targeting and Implications for Therapy

Author:
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

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

Authors: ---
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

The Tumor Microenvironment of High Grade Serous Ovarian Cancer

Authors: --- --- ---
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

Cross Talk between Lymph Node Lymphatic Endothelial Cells and T Cells in Inflammation and Cancer

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453511 Year: Pages: 100 DOI: 10.3389/978-2-88945-351-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:45
License:

Loading...
Export citation

Choose an application

Abstract

Lymphocytes constantly survey the lymph nodes in search for potential infection by a pathogen. They enter the afferent lymphatic vessel that serves as a conduit to transport the motile lymphocytes to the draining lymph node. Lymphatic vessels (LVs) are present in most vascularized tissues. They are traditionally regarded as passive conduits for soluble antigens and leukocytes. Afferent LVs begin as blind ended capillaries, which give rise to collecting vessels that merge and connect with draining lymph nodes (dLNs). Initial lymphatic capillaries are composed of Lymphatic Endothelial Cells (LECs) connected by discontinuous cell junctions, which join to form larger collecting lymphatic vessels, and ultimately feed into the LN subcapsular sinus. Within the LN, LECs are localized to the subcapsular, cortical, and medullary sinuses, where they interact with incoming and exiting leukocytes. LECs, and in general LN stromal cells, have emerged in the recent years as active players in the immune response. In support to this,studies have shown that the immune response generated during inflammation and under pathologic conditions is accompanied by modeling of the LVs and generation of new lymphatics, a process known as lymphangiogenesis. These facts strongly suggest that LECs and stromal LN cells in general, are not inert players but rather are part of the immune response by organizing immune cells movement, exchanging information and supplying survival factors. The purpose of this research topic is to review the role of the LECs during immune homeostasis and cancer. Considering the critical role of lymphangiogenesis in many pathologies like chronic and acute inflammation, autoimmunity, wound healing, graft rejection, and tumor metastasis, it is important to understand the molecular mechanisms that govern the cross talks between the LECs and immune cells during homeostasis and inflammation.

Immune Checkpoint Molecules and Cancer Immunotherapy

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889457328 Year: Pages: 197 DOI: 10.3389/978-2-88945-732-8 Language: English
Publisher: Frontiers Media SA
Subject: Oncology --- Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2019-01-23 14:53:43
License:

Loading...
Export citation

Choose an application

Abstract

For the faultless function of the immune system, tight regulation of immune cell activation, immuno-suppression and the strength and efficiency of the immune response is essential. Immune checkpoint (ICP) molecules can amplify or dampen signals that lead to the modulation of specific immune activities. Under physiological conditions, immune checkpoints are essential to prevent autoimmune manifestations and to preserve self-tolerance. They help modulate immune responses by either promoting or inhibiting T-cell activation. However, in the context of cancer, malignant cells can dysregulate the expression of immune checkpoint proteins on immune cells in order to suppress anti-tumor immune responses and to gain immune resistance. Moreover, tumor cells themselves can also express some checkpoints proteins, thereby enabling these cells to externally orchestrate immune regulatory mechanisms. Several recent studies have confirmed that the expression of immune checkpoints could be an important prognostic parameter for cancer development and for patient outcome. Therefore, cancer immunotherapy based on the modulation of immune checkpoint molecules alone, or in combination with conventional tumor therapy (chemo- or/and radiotherapy), is now in focus as a means of developing new therapeutic strategies for different types of cancer. The two well-known molecules – CTLA4 and PD-1 - serve as important examples of such checkpoint proteins of important therapeutic potential. Thus far, inhibitors of CTLA4 and PD-1 have been approved to treat only a limited number of malignancies (e.g. malignant Melanoma, Non-Small Cell Lung Cancer). Many others are currently under investigation and the list of immune checkpoint molecules for potential therapeutic targeting is still growing. However, the clinical response to inhibitors of checkpoint molecules is not sufficient in all cases. Therefore, further studies are needed to improve our knowledge of such immunomodulatory proteins and their associated signaling pathways. Several key signaling pathways which are involved in the regulation of expression of checkpoint molecules in immune cells and in cancer cells have already been identified including MAPK, PI3K, NF-kB, JAKs and STATs. These (and future discovered) signaling pathways could give rise to the development of new strategies for modulating the expression of ICPs and thereby, improving anti-cancer immune responses. The main aim of the Research Topic is to collect novel findings from scientists involved in basic research on immune checkpoints as well as in translational studies investigating the use of checkpoint inhibtors in immunotherapy in experimental settings. We welcome the submission of Review, Mini-Review and Original Research articles that cover the following topics: 1. Molecular mechanisms underlying regulation of ICP expression in immune and/or cancer cells.2. Characterization of signaling pathways downstream ICP molecules.3. Cellular responses to ICP blockade.4. Identification of new compounds interfering with ICP expression and/or signaling.5. ICP-mediated interactions between cancer cells and immune cells. 6. Functional links between ICP and cytokines/chemokines.7. Molecular mechanisms of ICP inhibition in the context of experimental cancer immunotherapy.

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)

Authors: --- ---
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

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

Author:
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
License:

Loading...
Export citation

Choose an application

Abstract

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

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

Author:
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
License:

Loading...
Export citation

Choose an application

Abstract

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.

Carbonic Anhydrases and Metabolism

Author:
ISBN: 9783038978008 9783038978015 Year: Pages: 184 DOI: 10.3390/books978-3-03897-801-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-04-25 16:37:17
License:

Loading...
Export citation

Choose an application

Abstract

Carbonic anhydrases (CAs; EC 4.2.1.1) are metalloenzymes present in all kingdoms of life, as they equilibrate the reaction between three simple but essential chemical species: CO2, bicarbonate, and protons. Discovered more than 80 years ago, in 1933, these enzymes have been extensively investigated due to the biomedical application of their inhibitors, but also because they are an extraordinary example of convergent evolution, with seven genetically distinct CA families that evolved independently in Bacteria, Archaea, and Eukarya. CAs are also among the most efficient enzymes known in nature, due to the fact that the uncatalyzed hydration of CO2 is a very slow process and the physiological demands for its conversion to ionic, soluble species is very high. Inhibition of the CAs has pharmacological applications in many fields, such as antiglaucoma, anticonvulsant, antiobesity, and anticancer agents/diagnostic tools, but is also emerging for designing anti-infectives, i.e., antifungal, antibacterial, and antiprotozoan agents with a novel mechanism of action. Mitochondrial CAs are implicated in de novo lipogenesis, and thus selective inhibitors of such enzymes may be useful for the development of new antiobesity drugs. As tumor metabolism is diverse compared to that of normal cells, ultimately, relevant contributions on the role of the tumor-associated isoforms CA IX and XII in these phenomena have been published and the two isoforms have been validated as novel antitumor/antimetastatic drug targets, with antibodies and small-molecule inhibitors in various stages of clinical development. CAs also play a crucial role in other metabolic processes connected with urea biosynthesis, gluconeogenesis, and so on, since many carboxylation reactions catalyzed by acetyl-coenzyme A carboxylase or pyruvate carboxylase use bicarbonate, not CO2, as a substrate. In organisms other than mammals, e.g., plants, algae, and cyanobacteria, CAs are involved in photosynthesis, whereas in many parasites (fungi, protozoa), they are involved in the de novo synthesis of important metabolites (lipids, nucleic acids, etc.). The metabolic effects related to interference with CA activity, however, have been scarcely investigated. The present Special Issue of Metabolites aims to fill this gap by presenting the latest developments in the field of CAs and their role in metabolism.

Listing 1 - 10 of 12 << page
of 2
>>
Sort by
Narrow your search