LEADER 01514nam a2200301 i 4500 001 991003676369707536 005 20020509130215.0 008 980701s1965 de ||| | ger 035 $ab1119733x-39ule_inst 035 $aPARLA186389$9ExL 040 $aDip. di Filol. Class. e di Scienze Filosofiche$bita 082 0 $a780.901 100 1 $aAristoxenus : Tarentinus$0474179 245 10$aMelik und Rhythmik des classischen Hellenentums /$cAristoxenos von Tarent ; Uebersetzt und erläutert von R. Westphal 260 $aHildesheim :$bOlms,$c1965 300 $a2 v. ;$c21 cm 600 04$aAristosseno :$cdi Taranto 650 4$aMusica$zGrecia antica 700 1 $aWestphal, Rudolf 907 $a.b1119733x$b02-04-14$c01-07-02 912 $a991003676369707536 945 $aLE007 880.1 Aristoxenus Tarentinus WES 01.01 $cv. 1$g1$i2007000051245$lle007$o-$pE0.00$q-$rl$s- $t0$u0$v0$w0$x0$y.i11347508$z01-07-02 945 $aLE007 880.1 Aristoxenus Tarentinus WES 01.01 $cv. 2$g1$i2007000051252$lle007$o-$pE0.00$q-$rl$s- $t0$u0$v0$w0$x0$y.i1134751x$z01-07-02 945 $aLE007 880.1 Aristoxenus Tarentinus WES 01.01$cv. 1 $g2$i2007000100264$lle007$op$pE0.00$q-$rl$s- $t0$u0$v0$w0$x0$y.i14205609$z14-03-06 945 $aLE007 880.1 Aristoxenus Tarentinus WES 01.01 $cv. 2 $g2$i2007000100271$lle007$op$pE0.00$q-$rl$s- $t0$u1$v0$w1$x0$y.i14205610$z14-03-06 996 $aMelik und Rhythmik des classischen Hellenentums$9870997 997 $aUNISALENTO 998 $ale007$b01-01-98$cm$da $e-$fger$gde $h0$i2 LEADER 02484nam 2200445z- 450 001 9910220059703321 005 20210211 035 $a(CKB)3800000000216181 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/50258 035 $a(oapen)doab50258 035 $a(oapen)50258 035 $a(EXLCZ)993800000000216181 100 $a20202102d2016 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 10$aInhibiting PARP as a Strategic Target in Cancer 210 $cFrontiers Media SA$d2016 215 $a1 online resource (97 p.) 225 1 $aFrontiers Research Topics 311 08$a2-88919-955-X 330 $aPoly-ADP ribose polymerase (PARP) proteins are critical mediators of DNA repair. Many traditional anti-cancer chemotherapy agents overwhelm a cell's ability to repair DNA damage in order to kill proliferating malignant cells. Recent evidence suggests that cancers within and across tissue types have specific defects in DNA repair pathways, and that these defects may predispose for sensitivity and resistance to various classes of cytotoxic agents. Breast, ovarian and other cancers develop in the setting of inherited DNA repair deficiency, and these cancers may be more sensitive to cytotoxic agents that induce DNA strand breaks, as well as to inhibitors of PARP activity. A series of recent clinical trials has tested whether PARP inhibitors can achieve synthetic lethality in hereditary DNA repair-deficient tumors. At the current time, mutation of BRCA serves as a potential, but not comprehensive, biomarker to predict response to PARP inhibitor therapy. Mechanisms of resistance to PARP inhibitors are only recently being uncovered. Future studies seek to identify sporadic cancers that harbor genomic instability rendering susceptibility to PARP inhibitors that compound lethal DNA damage. 606 $aMedicine$2bicssc 606 $aMedicine and Nursing$2bicssc 610 $aCancer 610 $acombination therapy 610 $aDNA Damage 610 $aDNA reapir 610 $aHomologous Recombination 610 $aPARP inhibitor 615 7$aMedicine 615 7$aMedicine and Nursing 700 $aKristin Zorn$4auth$01311554 702 $aChristina Annunziata$4auth 906 $aBOOK 912 $a9910220059703321 996 $aInhibiting PARP as a Strategic Target in Cancer$93030415 997 $aUNINA