Now showing items 1-7 of 7

    • Ataxia Telangiectasia Mutated Protein Loss and Benefit From Oxaliplatin-based Chemotherapy in Colorectal Cancer. 

      Sundar, R; Miranda, S; Rodrigues, DN; Chénard-Poirier, M; Dolling, D; Clarke, M; Figueiredo, I; Bertan, C; Yuan, W; Ferreira, A; Chistova, R; Boysen, G; Perez, DR; Tunariu, N; Mateo, J; Wotherspoon, A; Chau, I; Cunningham, D; Valeri, N; Carreira, S; de Bono, J (2018-12)
      BACKGROUND: Loss of ataxia telangiectasia mutated (ATM), a key protein regulating DNA repair signaling, has been suggested to increase sensitivity to DNA damaging agents. We conducted a study analyzing the loss of ATM ...
    • ATR inhibitors as a synthetic lethal therapy for tumours deficient in ARID1A. 

      Williamson, CT; Miller, R; Pemberton, HN; Jones, SE; Campbell, J; Konde, A; Badham, N; Rafiq, R; Brough, R; Gulati, A; Ryan, CJ; Francis, J; Vermulen, PB; Reynolds, AR; Reaper, PM; Pollard, JR; Ashworth, A; Lord, CJ (2016-12-13)
      Identifying genetic biomarkers of synthetic lethal drug sensitivity effects provides one approach to the development of targeted cancer therapies. Mutations in ARID1A represent one of the most common molecular alterations ...
    • ATR Is a Therapeutic Target in Synovial Sarcoma. 

      Jones, SE; Fleuren, EDG; Frankum, J; Konde, A; Williamson, CT; Krastev, DB; Pemberton, HN; Campbell, J; Gulati, A; Elliott, R; Menon, M; Selfe, JL; Brough, R; Pettitt, SJ; Niedzwiedz, W; van der Graaf, WTA; Shipley, J; Ashworth, A; Lord, CJ (2017-12-15)
      Synovial sarcoma (SS) is an aggressive soft-tissue malignancy characterized by expression of SS18-SSX fusions, where treatment options are limited. To identify therapeutically actionable genetic dependencies in SS, we ...
    • DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer. 

      Mateo, J; Carreira, S; Sandhu, S; Miranda, S; Mossop, H; Perez-Lopez, R; Nava Rodrigues, D; Robinson, D; Omlin, A; Tunariu, N; Boysen, G; Porta, N; Flohr, P; Gillman, A; Figueiredo, I; Paulding, C; Seed, G; Jain, S; Ralph, C; Protheroe, A; Hussain, S; Jones, R; Elliott, T; McGovern, U; Bianchini, D; Goodall, J; Zafeiriou, Z; Williamson, CT; Ferraldeschi, R; Riisnaes, R; Ebbs, B; Fowler, G; Roda, D; Yuan, W; Wu, YM; Cao, X; Brough, R; Pemberton, H; A'Hern, R; Swain, A; Kunju, LP; Eeles, R; Attard, G; Lord, CJ; Ashworth, A; Rubin, MA; Knudsen, KE; Feng, FY; Chinnaiyan, AM; Hall, E; de Bono, JS
      Prostate cancer is a heterogeneous disease, but current treatments are not based on molecular stratification. We hypothesized that metastatic, castration-resistant prostate cancers with DNA-repair defects would respond to ...
    • Elevated APOBEC3B expression drives a kataegic-like mutation signature and replication stress-related therapeutic vulnerabilities in p53-defective cells. 

      Nikkilä, J; Kumar, R; Campbell, J; Brandsma, I; Pemberton, HN; Wallberg, F; Nagy, K; Scheer, I; Vertessy, BG; Serebrenik, AA; Monni, V; Harris, RS; Pettitt, SJ; Ashworth, A; Lord, CJ (2017-06-27)
      BACKGROUND: Elevated APOBEC3B expression in tumours correlates with a kataegic pattern of localised hypermutation. We assessed the cellular phenotypes associated with high-level APOBEC3B expression and the influence of p53 ...
    • A multi-centre phase I trial of the PARP inhibitor olaparib in patients with relapsed chronic lymphocytic leukaemia, T-prolymphocytic leukaemia or mantle cell lymphoma. 

      Pratt, G; Yap, C; Oldreive, C; Slade, D; Bishop, R; Griffiths, M; Dyer, MJS; Fegan, C; Oscier, D; Pettitt, A; Matutes, E; Devereux, S; Allsup, D; Bloor, A; Hillmen, P; Follows, G; Rule, S; Moss, P; Stankovic, T (2018-08)
    • Sp1 phosphorylation by ATM downregulates BER and promotes cell elimination in response to persistent DNA damage. 

      Fletcher, SC; Grou, CP; Legrand, AJ; Chen, X; Soderstrom, K; Poletto, M; Dianov, GL (2018-02-28)
      ATM (ataxia-telangiectasia mutated) is a central molecule for DNA quality control. Its activation by DNA damage promotes cell-cycle delay, which facilitates DNA repair prior to replication. On the other hand, persistent ...