國立高雄大學圖資館 |

Language: English

Back

Targeting the DNA damage response fo...

Curtin, Nicola.

Targeting the DNA damage response for anti-cancer therapy

Record Type:	Electronic resources : Monograph/item
Title/Author:	Targeting the DNA damage response for anti-cancer therapyedited by John Pollard, Nicola Curtin.
other author:	Pollard, John.
Published:	Cham :Springer International Publishing :2018.
Description:	ix, 401 p. :ill. (some col.), digital ;24 cm.
Contained By:	Springer eBooks
Subject:	CancerTreatment
Online resource:	http://dx.doi.org/10.1007/978-3-319-75836-7
ISBN:	9783319758367$q(electronic bk.)

Targeting the DNA damage response for anti-cancer therapy
Targeting the DNA damage response for anti-cancer therapy[electronic resource] /edited by John Pollard, Nicola Curtin. - Cham :Springer International Publishing :2018. - ix, 401 p. :ill. (some col.), digital ;24 cm. - Cancer drug discovery and development,2196-9906. - Cancer drug discovery and development..

Over 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.

ISBN: 9783319758367$q(electronic bk.)

Standard No.: 10.1007/978-3-319-75836-7doiSubjects--Topical Terms:

570466
Cancer
--Treatment

LC Class. No.: RC270.8 / .T374 2018

Dewey Class. No.: 616.99406

Targeting the DNA damage response for anti-cancer therapy
LDR:02659nmm a2200313 a 4500 001 539038
003 DE-He213
005 20181204094956.0
006 m d
007 cr nn 008maaau
008 190122s2018 gw s 0 eng d
020 $a 9783319758367$q(electronic bk.)
020 $a 9783319758343$q(paper)
024 7 $a 10.1007/978-3-319-75836-7 $2 doi
035 $a 978-3-319-75836-7
040 $a GP $c GP
041 0 $a eng
050 4 $a RC270.8 $b .T374 2018
072 7 $a MJCL $2 bicssc
072 7 $a MED062000 $2 bisacsh
082 0 4 $a 616.99406 $2 23
090 $a RC270.8 $b .T185 2018
245 0 0 $a Targeting the DNA damage response for anti-cancer therapy $h [electronic resource] / $c edited by John Pollard, Nicola Curtin.
260 $a Cham : $b Springer International Publishing : $b Imprint: Humana Press, $c 2018.
300 $a ix, 401 p. : $b ill. (some col.), digital ; $c 24 cm.
490 1 $a Cancer drug discovery and development, $x 2196-9906
520 $a Over 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.
650 0 $a Cancer $x Treatment $x Genetic aspects. $3 570466
650 0 $a DNA damage. $3 229562
650 1 4 $a Biomedicine. $3 273648
650 2 4 $a Cancer Research. $3 273660
650 2 4 $a Gene Therapy. $3 196467
700 1 $a Pollard, John. $3 816431
700 1 $a Curtin, Nicola. $3 816432
710 2 $a SpringerLink (Online service) $3 273601
773 0 $t Springer eBooks
830 0 $a Cancer drug discovery and development. $3 557535
856 4 0 $u http://dx.doi.org/10.1007/978-3-319-75836-7
950 $a Medicine (Springer-11650)