000 02202nam a2200241 a 4500
020 _a1402037635 (hardcover)
020 _a9781402037634 (hardcover)
082 _a614.5999 Nigg 27639 V.570,1st 2005 Genetics
100 _aNigg, Erich A.
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245 1 0 _aGenome Instability in Cancer Development
250 _a2005th ed.
260 _aNetherlands, :
_bSpringer,
_c2005.
300 _a512 p. ;
490 1 _aAdvances in experimental medicine and biology.
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
650 _aCancer--Genetic aspects
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650 _aGenomics
_97309
650 _aMedicine
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650 _aOncology
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650 _aLife sciences
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650 _aTumors--Etiology
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942 _cBK
999 _c1443
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