00945nam0-2200325---450-99000994524040332120150309082825.0000994524FED01000994524(Aleph)000994524FED0100099452420150306d1953----km-y0itay50------bagerDEc-------001yyGeschichte und Altes Testamentaufsätze von W.F. Albright [et al.]TübingenMohr1953223 p.[1] ritratto24 cmBeiträge zur historischen Theologie16Alt,Albrecht<1883-1956>Protestantesimo284Albright,William Foxwell<1891-1971>ITUNINARICAUNIMARCBK990009945240403321284 ALB 1Bibl. 33455FLFBCFLFBCGeschichte und Altes Testament820748UNINA02408nam0 2200529 i 450 VAN010390720220221030801.95N978-3-319-08693-420151130d2014 |0itac50 baengCH|||| |||||Introduction to noncommutative algebraMatej BrešarChamSpringer2014XXXVII, 199 p.24 cm001VAN00245062001 Universitext210 Berlin [etc]Springer1930-VAN0241043Introduction to noncommutative algebra140985516PxxChain conditions, growth conditions, and other forms of finiteness for associative rings and algebra [MSC 2020]VANC021288MF16KxxDivision rings and semisimple Artin rings [MSC 2020]VANC022015MF16SxxAssociative rings and algebras arising under various constructions [MSC 2020]VANC025059MF16DxxModules, bimodules and ideals in associative algebras [MSC 2020]VANC031386MF16NxxRadicals and radical properties of associative rings [MSC 2020]VANC031387MF16RxxRings with polynomial identity [MSC 2020]VANC031388MF16UxxConditions on elements [MSC 2020]VANC031389MFDivision RingKW:KModuleKW:KNoncommutative Rings and AlgebrasKW:KPolynomial IdentityKW:KPrime RingKW:KPrimitive RingKW:KRadicalKW:KRings of QuotientsKW:KSemiprime RingKW:KSimple RingKW:KStructure of Rings and AlgebrasKW:KTensor ProductKW:KCHChamVANL001889BrešarMatejVANV080994721264Springer <editore>VANV108073650ITSOL20240614RICAhttp://dx.doi.org/10.1007/978-3-319-08693-4E-book – Accesso al full-text attraverso riconoscimento IP di Ateneo, proxy e/o ShibbolethBIBLIOTECA CENTRO DI SERVIZIO SBAVAN15NVAN0103907BIBLIOTECA CENTRO DI SERVIZIO SBA15CONS SBA EBOOK 4531 15EB 4531 20191106 Introduction to noncommutative algebra1409855UNICAMPANIA05025nam 22006495 450 991073482170332120251008163530.09783031325731303132573710.1007/978-3-031-32573-1(MiAaPQ)EBC30606181(Au-PeEL)EBL30606181(DE-He213)978-3-031-32573-1(PPN)272273066(CKB)27195821400041(OCoLC)1388361987(EXLCZ)992719582140004120230624d2023 u| 0engurcnu||||||||txtrdacontentcrdamediacrrdacarrierEvolutionary Dynamics of Malignancy The Genetic and Environmental Causes of Cancer /by Robert C. Jackson1st ed. 2023.Cham :Springer International Publishing :Imprint: Springer,2023.1 online resource (271 pages)Print version: Jackson, Robert C. Evolutionary Dynamics of Malignancy Cham : Springer International Publishing AG,c2023 9783031325724 Chapter 1: Cancer as a Disease of Cell Proliferation -- Chapter 2: Genetic and Chromosomal Instability -- Chapter 3: Cancer as a Disease of Defective Cell Cycle Checkpoint Function -- Chapter 4: The DNA Damage Checkpoint -- Chapter 5: Dynamics of the Spindle Assembly Checkpoint -- Chapter 6: Cancer as a Disease of Complexity: The Dynamics of Drug Resistance -- Chapter 7: Chronic Myeloid Leukaemia: a One-Hit Malignancy -- Chapter 8: Chronic Myelomonocytic Leukaemia: a Three-Hit Malignancy -- Chapter 9: The Cancer Stem Cell and Tumour Progression -- Chapter 10: Evading the antitumour immune response -- Chapter 11: Implications of Evolutionary Dynamics for Cancer Treatment and Prevention -- Chapter 12: In science, all conclusions are provisional.Advances in cancer genomics are transforming our understanding of cancer, and have profound implications for its prevention, diagnosis, and treatment. Evolutionary dynamics suggests that as few as two mutations can cause transformation of normal cells into cancer stem cells. A process of Darwinian selection, involving a further three or more mutations, taking place over a period of years, can then result in progression to a life-threatening tumour. In many cases the immune response can recognise and eliminate the mutant cells, but most advanced tumours have mutations that activate immune checkpoints and enable the tumour to hide from the immune system. For the most hard-to-treat tumours, future progress will require molecular diagnostics to detect cancer-causing mutations in healthy subjects, and new drugs or vaccines that prevent the progression process. Chapters of this book deal with the signalling pathways that control cell division, and changes in these pathways in cancer cells.Three cell cycle checkpoints that are often mutated in cancer are analysed in detail. A discussion of chronic myeloid leukaemia illustrates the role of reactive oxygen species in driving progression from a chronic to an acute condition. A single drug that suppresses reactive oxygen can prevent disease progression and turn an otherwise deadly disease into a condition that can be managed to enable many years of normal life. Another chapter discusses chronic myelomonocytic leukaemia, a disease that involves both genetic and epigenetic change. Tumour progression is discussed as a multi-stage process in which cancer stem cells evolve into genetically unstable, invasive, metastatic, drug-resistant growths. Each of these stages can act as targets for drugs or immunomodulators, but the future of cancer treatment lies in understanding tumour dynamics, and arresting malignancy at the earliest possible stage. Evolutionary dynamics is a primarily mathematical technique, but the target readership will be tumour biologists, clinicians, and drug developers. Computational detail is provided in an online supplement, but the main text emphasises the implications of the dynamics for an understanding of tumour biology and does not require mathematical expertise.CancerCancerAnimal modelsCancerTreatmentCancerGenetic aspectsCancer BiologyCancer ModelsCancer TherapyCancer Genetics and GenomicsCancer MicroenvironmentCancer.CancerAnimal models.CancerTreatment.CancerGenetic aspects.Cancer Biology.Cancer Models.Cancer Therapy.Cancer Genetics and Genomics.Cancer Microenvironment.616.994042Jackson Robert C303859MiAaPQMiAaPQMiAaPQBOOK9910734821703321Evolutionary Dynamics of Malignancy3404534UNINA