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008			180526s2018 gw | s |||| 0|eng d
020			_a9783319758367
024	7		_a10.1007/978-3-319-75836-7 _2doi
040			_aES-MaUEC _bspa _dES-VaUE
050		4	_aRC270.8 _b.T37 2018 EB
245	1	0	_aTargeting the DNA Damage Response for Anti-Cancer Therapy _cedited by John Pollard, Nicola Curtin.
264		1	_aCham _bSpringer International Publishing : _bImprint: Humana Press _c2018.
300			_a1 recurso en línea (IX, 401 páginas 80 ilustraciones, 52 ilustraciones a color)
336			_2rdacontent _aTexto (visual) _btxt
337			_2rdamedia _aelectrónico _bc
338			_2rdacarrier _arecurso electrónico _bcr
347			_atext file _bPDF
490	0		_aCancer Drug Discovery and Development _x2196-9906
490	0		_aMedicine (Springer-11650)
520	3		_aOver the past decade a complex role for DNA damage response (DDR) in tumorigenesis has emerged. A proficient DDR has been shown to be a primary cause for cellular resistance to the very many DNA damaging drugs, and IR, that are widely used as standard-of-care across multiple cancer types. It has also been shown that defects in this network, predominantly within the ATM mediated signaling pathway, are commonly observed in cancers and may be a primary event during tumorigenesis. Such defects may promote a genomically unstable environment, facilitating the persistence of mutations, any of which may provide a growth or survival advantage to the developing tumor. In addition, these somatic defects provide opportunities to exploit a reliance on remaining repair pathways for survival, a process which has been termed synthetic lethality. As a result of all these observations there has been a great interest in targeting the DDR to provide anti-cancer agents that may have benefit as monotherapy in cancers with high background DNA damage levels or as a means to increase the efficacy of DNA damaging drugs and IR. In this book we will review a series of important topics that are of great interest to a broad range of academic, industrial and clinical researchers, including  the basic science of the DDR, its role in tumorigenesis and in dictating response to DNA damaging drugs and IR. Additionally, we will focus on the several proteins that have been targeted in attempts to provide drug candidates, each of which appear to have quite distinct profiles and could represent very different opportunities to provide patient benefit.
988			_aEBSPRINGER_2018
650		7	_aOncología _9139207 _2embne
650		7	_aCáncer _xTratamiento _9174085 _2embne
700	1		_aPollard, John. _eeditor literario _0http://id.loc.gov/authorities/names/nb2011000301 _0http://viaf.org/viaf/20057638
700	1		_aCurtin, Nicola. _eeditor literario _0http://viaf.org/viaf/196144647702368380090
710	2		_aSpringerLink (Online service) _0http://id.loc.gov/authorities/names/no2005046756 _0http://viaf.org/viaf/148105729 _9106996
776	0	8	_iEdición impresa: _z9783319758343
776	0	8	_iEdición impresa: _z9783319758350
856	4	0	_uhttps://go.openathens.net/redirector/universidadeuropea.es?url=https://doi.org/10.1007/978-3-319-75836-7 _zAcceso a este recurso digital (usuarios Universidad Europea de Valencia)
942			_2lcc _cLE
998			_db _feng _ggw _h0