Books: 'Cellular RNA'

1

Pitre, Liisa K. The application of RNA interference to cellular biotechnology. Sudbury, Ont: Laurentian University, 2003.

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2

Brasier, Allan R., Adolfo García-Sastre, and Stanley M. Lemon, eds. Cellular Signaling and Innate Immune Responses to RNA Virus Infections. Washington, DC, USA: ASM Press, 2008. http://dx.doi.org/10.1128/9781555815561.

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3

Kekkonen, Viktoria. Characterization of bacterial RNA and DNA signalling pathways that induce cellular dysfunction. Sudbury, Ont: Laurentian University, 2006.

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4

Post-transcriptional regulation by STAR proteins : control of RNA metabolism in development and disease. New York: Springer Science+Business Media, LLC, 2010.

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5

Wingender, Edgar. Gene regulation in eukaryotes. Weinheim: VCH, 1993.

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6

Mallick, Bibekanand. Regulatory RNAs: Basics, Methods and Applications. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012.

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7

Tax, Frans. Receptor-like Kinases in Plants: From Development to Defense. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012.

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8

Farrell, Robert E. RNA methodologies: A laboratory guide for isolation and characterization. 2nd ed. San Diego: Academic Press, 1998.

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9

Divan, Aysha, and Janice A. Royds. 3. RNA. Oxford University Press, 2016. http://dx.doi.org/10.1093/actrade/9780198723882.003.0003.

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The first RNA molecules to be discovered were those involved in protein synthesis, mRNA, transfer RNA (tRNA), and ribosomal RNA (rRNA). In recent years, a vast number of additional RNA molecules have been identified. ‘RNA’ explains that these are non-coding RNAs that are not involved in protein synthesis, but influence many normal cellular and disease processes by regulating gene expression. RNA interference (RNAi) as one of the main ways in which gene expression is regulated is described with applications to therapy. Classes of RNA, including long non-coding RNAs and catalytic RNAs, are explained along with RNA techniques used to study RNA molecule and gene function.

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10

Grimm, Dirk. Cellular RNA Interference Mechanisms. Elsevier Science & Technology Books, 2011.

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11

Grimm, Dirk. Cellular RNA Interference Mechanisms. Elsevier Science & Technology Books, 2011.

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12

Cellular RNA Interference Mechanisms. Elsevier, 2011. http://dx.doi.org/10.1016/c2011-0-04281-3.

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13

Masquida, Benoît, and Fabrice Leclerc. Looking at Ribozymes: From Atomic to Molecular and Cellular Scales. Elsevier, 2019.

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14

Masquida, Benoît, and Fabrice Leclerc. Looking at Ribozymes: From Atomic to Molecular and Cellular Scales. Elsevier, 2019.

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15

Gunaratne, Preethi, and Matthew L. Anderson. MicroRNAs in Health and Disease. Taylor & Francis Group, 2014.

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16

R, Brasier Allan, García-Sastre Adolfo, and Lemon Stanley M, eds. Cellular signaling and innate immune responses to RNA virus infections. Washington, D.C: ASM Press, 2009.

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17

Lemon, Stanley M., Allan R. Brasier, and Adolfo Garcia-Sastre. Cellular Signaling and Innate Immune Responses to RNA Virus Infections. Wiley & Sons, Limited, John, 2014.

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18

Replication of Viral and Cellular Genomes: Molecular events at the origins of replication and biosynthesis of viral and cellular genomes. Springer, 2011.

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19

Becker, Yechiel. Replication of Viral and Cellular Genomes: Molecular Events at the Origins of Replication and Biosynthesis of Viral and Cellular Genomes. Springer London, Limited, 2012.

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20

Becker, Yechiel. Replication of Viral and Cellular Genomes: Molecular Events at the Origins of Replication and Biosynthesis of Viral and Cellular Genomes. Springer, 2011.

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21

Reckman, Yolan J., and Yigal M. Pinto. The role of non-coding RNA/microRNAs in cardiac disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0031.

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In the past two decades, our knowledge about non-coding DNA has increased tremendously. While non-coding DNA was initially discarded as ‘junk DNA’, we are now aware of the important and often crucial roles of RNA transcripts that do not translate into protein. Non-coding RNAs (ncRNAs) play important functions in normal cellular homeostasis and also in many diseases across all organ systems. Among the different ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have been studied the most. In this chapter we discuss the role of miRNAs and lncRNAs in cardiac disease. We present examples of miRNAs with fundamental roles in cardiac development (miR-1), hypertrophy (myomiRs, miR-199, miR-1/133), fibrosis (miR-29, miR-21), myocardial infarction (miR-15, miR17~92), and arrhythmias/conduction (miR-1). We provide examples of lncRNAs related to cardiac hypertrophy (MHRT, CHRF), myocardial infarction (ANRIL, MIAT), and arrhythmias (KCNQ1OT1). We also discuss miRNAs and lncRNAs as potential therapeutic targets or biomarkers in cardiac disease.

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22

Molecular biology of RNA: Proceedings of a Director's Sponsors-UCLA Symposium, held at Keystone, Colorado, April 4-10, 1988 (UCLA symposia on molecular and cellular biology). Liss, 1989.

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23

Erickson, Robert P. Gene Regulation: Biology of Antisense Rna and DNA (Raven Press Series on Molecular and Cellular Biology). Raven Pr, 1991.

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24

Becker, Yechiel. Molecular Evolution of Viruses - Past and Present: Evolution Of Viruses By Acquisition Of Cellular Rna And Dna. Springer, 2012.

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25

Yechiel, Becker, and Darai Gholamreza, eds. Molecular evolution of viruses-past and present: Evolution of viruses by acquisition of cellular RNA and DNA. Boston: Kluwer Academic Publishers, 2000.

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26

Becker, Yechiel, and Gholamreza Darai. Molecular Evolution of Viruses -- Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA. Springer London, Limited, 2012.

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27

(Editor), Y. Becker, and Gholamreza Darai (Editor), eds. Molecular Evolution of Viruses - Past and Present: Evolution of Viruses by Acquisition of Cellular RNA and DNA (VIRUS GENES). Springer, 2007.

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28

Jeffrey, Wilusz, ed. Post-transcriptional gene regulation. Totowa, N.J: Humana Press, 2008.

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29

Post-Transcriptional Gene Regulation. Humana Press, 2007.

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30

Wilusz, Jeffrey. Post-Transcriptional Gene Regulation. Humana Press, 2010.

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31

Short And Long Distance Signaling. Springer, 2011.

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32

Mallick, Bibekanand, and Zhumur Ghosh. Regulatory RNAs: Basics, Methods and Applications. Springer, 2012.

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33

Mallick, Bibekanand, and Zhumur Ghosh. Regulatory RNAs: Basics, Methods and Applications. Springer, 2014.

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34

Methylation, Hoffmann-LA Roche-UCLA Colloquium on Nucleic Acid, Dawn B. Willis, Arthur Weissbach, and Gary A. Clawson. Nucleic Acid Methylation: Proceedings of a Hoffman-LA Roche-UCLA Colloquium on Nucleic Acid Methylation Held at Frisco, Colorado, March 31-April 7, (Ucla ... and Cellular Biology, New Ser., V. 128). Wiley-Liss, 1989.

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35

Vaheri, Antti, James N. Mills, Christina F. Spiropoulou, and Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.

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36

Signal Transduction: Pathways, Mechanisms and Diseases. Springer, 2009.

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37

Hughes, Alis, and Lesley Jones. Pathogenic Mechanisms. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0013.

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Huntington’s disease (HD) pathogenesis is complex. In the two decades since the gene and its mutation were discovered, there has been extensive exploration of how the expanded CAG repeat in HTT leads to neurodegeneration in HD. This chapter focuses on the mechanisms that potentially contribute to the dysfunction and death of cells in HD. These include repeat instability and RNA toxicity and the production, processing, modification, and degradation of mutant huntingtin. The effects of mutant HTT on cellular processes such as transcription, transport, neurotransmission, and protein clearance are also described. The interdependence and individual importance of these mechanisms in disease etiology remains to be clarified; however, consideration of each could be important for the development of therapeutic interventions in HD.

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38

Kemmerling, Birgit, and Frans Tax. Receptor-like Kinases in Plants: From Development to Defense. Springer, 2014.

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39

Choi, Sangdun. Encyclopedia of Signaling Molecules. Springer, 2017.

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40

Choi, Sangdun. Encyclopedia of Signaling Molecules. Springer, 2017.

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41

Encyclopedia Of Signaling Molecules. Springer, 2012.

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42

Choi, Sangdun. Encyclopedia of Signaling Molecules. Springer, 2013.

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43

Webster, Jessica Lynn, and Marco Vignuzzi. Viral evolution and impact for public health strategies in low-income countries. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789833.003.0007.

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Viruses, the simplest organisms, obligate parasites that encode structural proteins and replicative functions requiring the cellular machinery of the host to ensure their propagation. Viruses are masters of evolution. An analysis of infectious diseases emerging since the 1980s revealed that most were caused by viruses, especially those with RNA genomes. New viral emergences are generally the result of intrinsic changes in the genetics of the virus to increase transmission, virulence or host range, and environmental or ecological changes that favor contacts between viruses and humans or other hosts. We describe the molecular mechanisms of viruses that ensure their rapid adaptation and evolution. We describe instances where viral evolution appears partially responsible for recent outbreaks and discuss the challenges in identifying the cause or consequence of viral evolution in the context of resource-rich versus -limited countries.

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44

Benarroch, Eduardo E. Neuroscience for Clinicians. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.001.0001.

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The aim of this book is to provide the clinician with a comprehensive and clinical relevant survey of emerging concepts on the organization and function of the nervous system and neurologic disease mechanisms, at the molecular, cellular, and system levels. The content of is based on the review of information obtained from recent advances in genetic, molecular, and cell biology techniques; electrophysiological recordings; brain mapping; and mouse models, emphasizing the clinical and possible therapeutic implications. Many chapters of this book contain information that will be relevant not only to clinical neurologists but also to psychiatrists and physical therapists. The scope includes the mechanisms and abnormalities of DNA/RNA metabolism, proteostasis, vesicular biogenesis, and axonal transport and mechanisms of neurodegeneration; the role of the mitochondria in cell function and death mechanisms; ion channels, neurotransmission and mechanisms of channelopathies and synaptopathies; the functions of astrocytes, oligodendrocytes, and microglia and their involvement in disease; the local circuits and synaptic interactions at the level of the cerebral cortex, thalamus, basal ganglia, cerebellum, brainstem, and spinal cord transmission regulating sensory processing, behavioral state, and motor functions; the peripheral and central mechanisms of pain and homeostasis; and networks involved in emotion, memory, language, and executive function.

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45

Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.

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46

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.

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47

Simpson, A., E. Aarons, and R. Hewson. Marburg and Ebola viruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0038.

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Infection with Marburg and Ebola viruses cause haemorrhagic fevers that are characterized by organ malfunction, bleeding complications, and high mortality. The viruses are members of the family Filoviridae, a group of membrane-enveloped filamentous RNA viruses. Five distinct species of the genus Ebolavirus have been reported; the genus Marburgvirus contains only one species. Both Marburg and Ebola virus diseases are zoonotic infections whose primary hosts are thought to be bats. The initial human infection is acquired from wildlife and subsequent person-to-person spread propagates the outbreak until it is brought under control. Ebola and Marburg viruses are classified as hazard or risk group 4 pathogens because of the very high case fatality rates observed for Ebola and Marburg virus diseases, the frequency of person-to-person transmission and community spread, and the lack of an approved vaccine or antiviral therapy. This mandates that infectious materials are handled and studied in maximum containment laboratory facilities. Epidemics have occurred sporadically since the discovery of Marburg in 1967 and Ebola virus in 1976. While some of these outbreaks have been relatively large, infecting a few hundreds of individuals, they have generally occurred in rural settings and have been controlled relatively easily. However, the 2013–2016 epidemic of Ebola virus disease in West Africa was different, representing the first emergence of the Zaire species of Ebola in a high-density urban location. Consequently, this has been the largest recorded filovirus outbreak in both the number of people infected and the range of geographical spread. Many of the reported and confirmed cases were among people living in high-density and impoverished urban environments. The chapter summarizes the most up-to-date taxonomic status of the family Filoviridae. It focuses on Marburg and Ebola viruses in a historical context, culminating in the 2013–2016 outbreak of Ebola virus in West Africa. Virus biology of the most well-studied member is described, with details of the viral genome and the protein machinery necessary to propagate viruses at the molecular and cellular level. This information is used to build a wider-scale virus–host perspective with detail on the pathology and pathogenesis of Ebola virus disease. The consequences of cell infection are examined, together with our current understanding of the immune response to Ebola virus, leading to a broader description of the clinical features of disease. The chapter closes by drawing information together in a section on diagnosis, ecology, prevention, and control.

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48

Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.

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49

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.

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50

Rice-Evans, C. A., A. T. Diplock, and M. C. R. Symons. Techniques in Free Radical Research (Laboratory Techniques in Biochemistry and Molecular Biology). Elsevier Science, 1991.

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Books on the topic 'Cellular RNA'

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