LEADER 00912nam0 22002773i 450 001 UBO0095079 005 20231121125851.0 100 $a20191213d1988 ||||0itac50 ba 101 | $aita 102 $ait 181 1$6z01$ai $bxxxe 182 1$6z01$an 200 1 $a˜Il œgrande dizionario dei sogni$fLaura Tuan 210 $aMilano$cDe Vecchi$dc1988 215 $a409 p.$d24 cm 606 $aSogno$xInterpretazione$2FIR$3RMLC005051$9I 676 $a135.3$9$v21 700 1$aTuan$b, Laura$3CFIV115309$4070$01200980 801 3$aIT$bIT-01$c20191213 850 $aIT-FR0017 899 $aBiblioteca umanistica Giorgio Aprea$bFR0017 $eN 912 $aUBO0095079 950 0$aBiblioteca umanistica Giorgio Aprea$d 52MAG 2/932$e 52FSS0000018885 VMB A4 $fA $h20191213$i20191213 977 $a 52 996 $aGrande dizionario dei sogni$93639579 997 $aUNICAS LEADER 00971nam0 22002651i 450 001 UON00052554 005 20231205102232.532 100 $a20020107d1959 |0itac50 ba 101 $arus 102 $aSU 105 $a|||| 1|||| 200 1 $aBeludzi$fM. G. Pikulin 210 $aMoskva$cIzd. Vostocnoj Literatury$d1959 215 $a211 p.$d22 cm 606 $aPAKISTAN$xCULTURA E CIVILTA'$3UONC007288$2FI 620 $aRU$dMoskva$3UONL003152 686 $aSI I$cSUBCONT. INDIANO - GENERALIA$2A 700 1$aPIKULIN$bMixail Grigor'evic$3UONV029377$0649606 712 $aIzdatel'stvo Vosto?noj Literatury$3UONV246797$4650 801 $aIT$bSOL$c20241213$gRICA 899 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$2UONSI 912 $aUON00052554 950 $aSIBA - SISTEMA BIBLIOTECARIO DI ATENEO$dSI SI I 150 $eSI SA 37452 5 150 996 $aBeludzi$91145810 997 $aUNIOR LEADER 02373nam 2200409z- 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(EXLCZ)993800000000216181 100 $a20202102d2016 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$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 610 $aCancer 610 $acombination therapy 610 $aDNA Damage 610 $aDNA reapir 610 $aHomologous Recombination 610 $aPARP inhibitor 615 7$aMedicine 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