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Multi-omic Data Integration

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196487 Year: Pages: 135 DOI: 10.3389/978-2-88919-648-7 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Biology --- Genetics
Added to DOAB on : 2016-08-16 10:34:25
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Stable, predictive biomarkers and interpretable disease signatures are seen as a significant step towards personalized medicine. In this perspective, integration of multi-omic data coming from genomics, transcriptomics, glycomics, proteomics, metabolomics is a powerful strategy to reconstruct and analyse complex multi-dimensional interactions, enabling deeper mechanistic and medical insight. At the same time, there is a rising concern that much of such different omic data –although often publicly and freely available- lie in databases and repositories underutilised or not used at all. Issues coming from lack of standardisation and shared biological identities are also well-known. From these considerations, a novel, pressing request arises from the life sciences to design methodologies and approaches that allow for these data to be interpreted as a whole, i.e. as intertwined molecular signatures containing genes, proteins, mRNAs and miRNAs, able to capture inter-layers connections and complexity. Papers discuss data integration approaches and methods of several types and extents, their application in understanding the pathogenesis of specific diseases or in identifying candidate biomarkers to exploit the full benefit of multi-omic datasets and their intrinsic information content. Topics of interest include, but are not limited to: • Methods for the integration of layered data, including, but not limited to, genomics, transcriptomics, glycomics, proteomics, metabolomics;• Application of multi-omic data integration approaches for diagnostic biomarker discovery in any field of the life sciences;• Innovative approaches for the analysis and the visualization of multi-omic datasets;• Methods and applications for systematic measurements from single/undivided samples (comprising genomic, transcriptomic, proteomic, metabolomic measurements, among others);• Multi-scale approaches for integrated dynamic modelling and simulation;• Implementation of applications, computational resources and repositories devoted to data integration including, but not limited to, data warehousing, database federation, semantic integration, service-oriented and/or wiki integration;• Issues related to the definition and implementation of standards, shared identities and semantics, with particular focus on the integration problem. Research papers, reviews and short communications on all topics related to the above issues were welcomed.

Drug-Diagnostics Co-Development in Oncology

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193325 Year: Pages: 111 DOI: 10.3389/978-2-88919-332-5 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 idea of combining drugs and diagnostics in oncology is not new. When the selective estrogen receptor modulator tamoxifen was developed in the 1970’s for the treatment of breast cancer a positive correlation between receptor status and treatment outcome was found. As a result of this research, it was suggested to use the estrogen-receptor assay as a diagnostic test for selection of patients for tamoxifen treatment. Despite this suggestion was put forward nearly 40 years ago the adaptation of the drug-diagnostic co-development model has been relatively slow and it is only within the last decade that it has gained more widespread acceptance. The parallel development of the monoclonal antibody trastuzumab (Herceptin®, Roche/Genentech) and the immunohistochemistry assay for HER2 protein overexpression (HercepTest™, Dako) seems to have served as an inspiration to a number of stakeholders such as pharma and diagnostic companies, regulatory agencies, and academia. In recent years we have seen an increasing number of oncology drug development projects that have taken advantage of the drug-diagnostic co-development model, as outline below. Most of the new targeted anti-cancer drugs that have been introduced in recent years, such as BRAF-, ALK-, EGFR- and HER2-inhibitors, are more or less all a product of the drugdiagnostic co-development model. These drugs have shown remarkable high response rates in selected groups of patients within cancer diseases with great unmet medical needs. This Research Topic on Drug-Diagnostic Co-Development in Oncology aims to provide you with an insight into some of the diverse activities that constitute this new research area.

Current Challenges in Cardiovascular Molecular Diagnostics

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452811 Year: Pages: 128 DOI: 10.3389/978-2-88945-281-1 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General)
Added to DOAB on : 2018-02-27 16:16:44
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The field of cardiovascular genetics has tremendously benefited from the recent application of massive parallel sequencing technology also referred to as next generation sequencing (NGS). However, along with the discovery of additional genes associated with human cardiac diseases, the analysis of large dataset of genetic information uncovered a much more complex and variegated landscape, which often departs from the comfort zone of the monogenic Mendelian diseases image that clinical molecular geneticists have been well acquainted with for many decades. It is now clear that, in addition to highly penetrant genetic variants, which in isolation are able to recapitulate the full clinical presentation when expressed in animal models, we are now aware that a small but significant fraction of subjects presenting with cardiac muscle diseases such as cardiomyopathies or primary arrhythmias such as long QT syndrome (LQTS), may harbor at least two deleterious variants in the same gene (compound heterozygous) or in different gene (double heterozygous). Although the clinical presentation in subjects with more than one deleterious variant appears to be more severe and with an earlier disease onset, it somehow changes the viewpoint of clinical molecular geneticists whose aim is to identify all possible genetic contributors to a human condition. In this light, the employment in clinical diagnostics of the NGS technology, allowing the simultaneous interrogation of a DNA target spanning from large panel of genes up to the entire genome, will definitely aid at uncovering all such contributors, which will have to be tested functionally to confirm their role in human cardiac conditions. The uncovering of all clinically relevant deleterious changes associated with a cardiovascular disease would probably increase our understanding of the clinical variability commonly occurring among affected family relatives, and potentially provide with unexpected therapeutic targets for the treatment of symptoms related to the presence of “accessory” deleterious genetic variants other than the key molecular culprit. The objective of this Research Topic is to explore the current challenges presenting to the cardiovascular genetics providers, such as clinical geneticists, genetic counselors, clinical molecular geneticists and molecular pathologists involved in the diagnosis, counseling, testing and interpretation of genetic tests results for the comprehensive management of patients affected by cardiovascular genetic disorders.

Epigenetic Modifications and Viral Infections

Authors: --- --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195879 Year: Pages: 111 DOI: 10.3389/978-2-88919-587-9 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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Epigenetics is defined as the study of modifications of the genome, heritable during cell division that does not involve changes in DNA sequences. Up to date, epigenetic modifications involve at least three general mechanisms regulating gene expression: histone modifications, DNA methylation, and non-coding RNAs (ncRNAs). For the past two decades, an explosion in our interest and understanding of epigenetic mechanisms has been seen. This mainly based on the influence that epigenetic alterations have on an amazing number of biological processes, such as gene expression, imprinting, programmed DNA rearrangements, germ line silencing, developmentally cued stem cell division, and overall chromosomal stability and identity. It has become also evident that the constant exposure of living organisms to environment factors affects their genomes through epigenetic mechanisms. Viruses infecting animal cells are thought to play central roles in shaping the epigenetic scenario of infected cells. In this context it has become obvious that knowing the impact that viral infections have on the epigenetic control of their host cells will certainly lead to a better understanding of the interplay viruses have with animal cells. In fact, DNA viruses use host transcription factors as well as epigenetic regulators in such a way that they affect epigenetic control of gene expression that extends to host gene expression. At the same time, animal cells employ mechanisms controlling transcription factors and epigenetic processes, in order to eliminate viral infections. In summary, epigenetic mechanisms are involved in most virus-cell interactions. We now know that some viruses exhibit epigenetic immune evasion mechanisms to survive and propagate in their host; however, there is still much ambiguity over these epigenetic mechanisms of viral immune evasion, and most of the discovered mechanisms are still incomplete. Other animal viruses associated to cancer often deregulate cellular epigenetic mechanisms, silencing cellular tumor-suppressor genes and/or activating either viral or host cell oncogenes. In addition, in several cancers the down-regulation of tumor suppressor protein-coding genes and ncRNAs with growth inhibitory functions, such as miRNAs, have been closely linked to the presence of cell CpG island promoter hypermethylation. The goal of the aforementioned Research Topic is to bring together the key experimental and theoretical research, linking state-of-the-art knowledge about the epigenetic mechanisms involved in animal virus-cell interactions.

mTOR in Human Diseases

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ISBN: 9783039210602 / 9783039210619 Year: Pages: 480 DOI: 10.3390/books978-3-03921-061-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-06-26 08:44:06
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The mechanistic target of rapamycin (mTOR) is a major signaling intermediary that coordinates favorable environmental conditions with cell growth. Indeed, as part of two functionally distinct protein complexes, named mTORC1 and mTORC2, mTOR regulates a variety of cellular processes, including protein, lipid, and nucleotide synthesis, as well as autophagy. Over the last two decades, major molecular advances have been made in mTOR signaling and have revealed the complexity of the events implicated in mTOR function and regulation. In parallel, the role of mTOR in diverse pathological conditions has also been identified, including in cancer, hamartoma, neurological, and metabolic diseases. Through a series of articles, this book focuses on the role played by mTOR in cellular processes, metabolism in particular, and highlights a panel of human diseases for which mTOR inhibition provides or might provide benefits. It also addresses future studies needed to further characterize the role of mTOR in selected disorders, which will help design novel therapeutic approaches. It is therefore intended for everyone who has an interest in mTOR biology and its application in human pathologies.

Keywords

acute myeloid leukemia --- metabolism --- mTOR --- PI3K --- phosphorylation --- epithelial to mesenchymal transition --- mTOR inhibitor --- pulmonary fibrosis --- transcriptomics --- miRNome --- everolimus --- mTOR --- thyroid cancer --- sodium iodide symporter (NIS)/SLC5A5 --- dopamine receptor --- autophagy --- AKT --- mTOR --- AMPK --- mTOR --- Medulloblastoma --- MBSCs --- mTOR --- T-cell acute lymphoblastic leukemia --- targeted therapy --- combination therapy --- mTOR --- metabolic diseases --- glucose and lipid metabolism --- anesthesia --- neurotoxicity --- synapse --- mTOR --- neurodevelopment --- mTOR --- rapamycin --- autophagy --- protein aggregation --- methamphetamine --- schizophrenia --- tumour cachexia --- mTOR --- signalling --- metabolism --- proteolysis --- lipolysis --- mTOR --- mTORC1 --- mTORC2 --- rapamycin --- rapalogues --- rapalogs --- mTOR inhibitors --- senescence --- ageing --- aging --- cancer --- neurodegeneration --- immunosenescence --- senolytics --- biomarkers --- leukemia --- cell signaling --- metabolism --- apoptosis --- miRNA --- mTOR inhibitors --- mTOR --- tumor microenvironment --- angiogenesis --- immunotherapy --- fluid shear stress --- melatonin --- chloral hydrate --- nocodazole --- MC3T3-E1 cells --- primary cilia --- mTOR complex --- metabolic reprogramming --- cancer --- microenvironment --- nutrient sensor --- oral cavity squamous cell carcinoma (OSCC) --- NVP-BEZ235 --- mTOR --- p70S6K --- mTOR --- advanced biliary tract cancers --- mTOR --- NGS --- illumina --- IonTorrent --- eIFs --- mTOR --- autophagy --- Parkinson’s disease --- mTOR --- PI3K --- cancer --- inhibitor --- therapy --- mTOR --- laminopathies --- lamin A/C --- Emery-Dreifuss muscular dystrophy (EDMD) --- Hutchinson-Gilford progeria syndrome (HGPS) --- autophagy --- cellular signaling --- metabolism --- bone remodeling --- ageing --- mTOR --- fructose --- glucose --- liver --- lipid metabolism --- gluconeogenesis --- Alzheimer’s disease --- autophagy --- mTOR signal pathway --- physical activity --- microRNA --- mTOR --- spermatogenesis --- male fertility --- Sertoli cells --- n/a

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