000 04411nam a22006015i 4500
001 978-1-4020-3764-1
003 DE-He213
005 20161121230657.0
007 cr nn 008mamaa
008 100301s2005 ne | s |||| 0|eng d
020 _a9781402037641
_9978-1-4020-3764-1
024 7 _a10.1007/1-4020-3764-3
_2doi
050 4 _aRC261-271
072 7 _aMJCL
_2bicssc
072 7 _aMED062000
_2bisacsh
082 0 4 _a614.5999
_223
245 1 0 _aGenome Instability in Cancer Development
_h[electronic resource] /
_cedited by Nathan Back, Irun R. Cohen, David Kritchevsky, Abel Lajtha, Rodolfo Paoletti, Erich A. Nigg.
264 1 _aDordrecht :
_bSpringer Netherlands,
_c2005.
300 _aXVI, 512 p.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
490 1 _aAdvances in Experimental Medicine and Biology,
_x0065-2598 ;
_v570
505 0 _aThe Multiplicity of Mutations in Human Cancers -- Monitoring Chromosome Rearrangements -- Nucleotide Excision Repair and its Connection with Cancer and Ageing -- DNA Mismatch Repair and Colon Cancer -- Base Excision Repair -- Genomic Instability in Cancer Development -- Translesion Synthesis And Errorprone Polymerases -- The INK4A/Arf Network — Cell Cycle Checkpoint or Emergency Brake? -- DNA Replication and Genomic Instability -- The Dream of Every Chromosome: Equal Segregation for a Healthy Life of the Host -- Telomere Structural Dynamics in Genome Integrity Control and Carcinogenesis -- Gene Amplification Mechanisms -- DNA Methylation and Cancer-associated Genetic Instability -- Deregulation of the Centrosome Cycle and the Origin of Chromosomal Instability in Cancer -- Mammalian DNA Damage Response Pathway -- ATM and Cellular Response to DNA Damage -- Mitotic Checkpoint, Aneuploidy and Cancer.
520 _aResearch over the past decades has firmly established the genetic basis of cancer. In particular, studies on animal tumour viruses and chromosome rearrangements in human tumours have concurred to identify so-called ‘proto-oncogenes’ and ‘tumour suppressor genes’, whose deregulation promotes carcinogenesis. These important findings not only explain the occurrence of certain hereditary tumours, but they also set the stage for the development of anti-cancer drugs that specifically target activated oncogenes. However, in spite of tremendous progress towards the elucidation of key signalling pathways involved in carcinogenesis, most cancers continue to elude currently available therapies. This stands as a reminder that “cancer” is an extraordinarily complex disease: although some cancers of the haematopoietic system show only a limited number of characteristic chromosomal aberrations, most solid tumours display a myriad of genetic changes and considerable genetic heterogeneity. This is thought to reflect a trait commonly referred to as ‘genome instability’, so that no two cancers are ever likely to display the exact same genetic alterations. Numerical and structural chromosome aberrations were recognised as a hallmark of human tumours for more than a century. Yet, the causes and consequences of these aberrations still remain to be fully understood. In particular, the question of how genome instability impacts on the development of human cancers continues to evoke intense debate.
650 0 _aMedicine.
650 0 _aCancer research.
650 0 _aOncology.
650 0 _aPathology.
650 0 _aLife sciences.
650 0 _aCell biology.
650 1 4 _aBiomedicine.
650 2 4 _aCancer Research.
650 2 4 _aPathology.
650 2 4 _aCell Biology.
650 2 4 _aOncology.
650 2 4 _aBiomedicine general.
650 2 4 _aLife Sciences, general.
700 1 _aBack, Nathan.
_eeditor.
700 1 _aCohen, Irun R.
_eeditor.
700 1 _aKritchevsky, David.
_eeditor.
700 1 _aLajtha, Abel.
_eeditor.
700 1 _aPaoletti, Rodolfo.
_eeditor.
700 1 _aNigg, Erich A.
_eeditor.
710 2 _aSpringerLink (Online service)
773 0 _tSpringer eBooks
776 0 8 _iPrinted edition:
_z9781402037634
830 0 _aAdvances in Experimental Medicine and Biology,
_x0065-2598 ;
_v570
856 4 0 _uhttp://dx.doi.org/10.1007/1-4020-3764-3
912 _aZDB-2-SBL
950 _aBiomedical and Life Sciences (Springer-11642)
999 _c502321
_d502321