Now showing items 1-6 of 6

    • APOBEC3B-mediated corruption of the tumor cell immunopeptidome induces heteroclitic neoepitopes for cancer immunotherapy. 

      Driscoll, CB; Schuelke, MR; Kottke, T; Thompson, JM; Wongthida, P; Tonne, JM; Huff, AL; Miller, A; Shim, KG; Molan, A; Wetmore, C; Selby, P; Samson, A; Harrington, K; Pandha, H; Melcher, A; Pulido, JS; Harris, R; Evgin, L; Vile, RG (2020-02-07)
      APOBEC3B, an anti-viral cytidine deaminase which induces DNA mutations, has been implicated as a mediator of cancer evolution and therapeutic resistance. Mutational plasticity also drives generation of neoepitopes, which ...
    • DNA replication stress mediates APOBEC3 family mutagenesis in breast cancer. 

      Kanu, N; Cerone, MA; Goh, G; Zalmas, L-P; Bartkova, J; Dietzen, M; McGranahan, N; Rogers, R; Law, EK; Gromova, I; Kschischo, M; Walton, MI; Rossanese, OW; Bartek, J; Harris, RS; Venkatesan, S; Swanton, C (2016-09-15)
      <h4>Background</h4>The APOBEC3 family of cytidine deaminases mutate the cancer genome in a range of cancer types. Although many studies have documented the downstream effects of APOBEC3 activity through next-generation ...
    • 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)
      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 status on ...
    • Evaluation of APOBEC3B Recognition Motifs by NMR Reveals Preferred Substrates. 

      Liu, M; Mallinger, A; Tortorici, M; Newbatt, Y; Richards, M; Mirza, A; van Montfort, RLM; Burke, R; Blagg, J; Kaserer, T (2018-09)
      APOBEC3B (A3B) deamination activity on ssDNA is considered a contributing factor to tumor heterogeneity and drug resistance in a number of human cancers. Despite its clinical impact, little is known about A3B ssDNA substrate ...
    • Suboptimal T-cell Therapy Drives a Tumor Cell Mutator Phenotype That Promotes Escape from First-Line Treatment. 

      Evgin, L; Huff, AL; Kottke, T; Thompson, J; Molan, AM; Driscoll, CB; Schuelke, M; Shim, KG; Wongthida, P; Ilett, EJ; Smith, KK; Harris, RS; Coffey, M; Pulido, JS; Pandha, H; Selby, PJ; Harrington, KJ; Melcher, A; Vile, RG (2019-05)
      Antitumor T-cell responses raised by first-line therapies such as chemotherapy, radiation, tumor cell vaccines, and viroimmunotherapy tend to be weak, both quantitatively (low frequency) and qualitatively (low affinity). ...
    • Transcriptome-wide association study of multiple myeloma identifies candidate susceptibility genes. 

      Went, M; Kinnersley, B; Sud, A; Johnson, DC; Weinhold, N; Försti, A; van Duin, M; Orlando, G; Mitchell, JS; Kuiper, R; Walker, BA; Gregory, WM; Hoffmann, P; Jackson, GH; Nöthen, MM; da Silva Filho, MI; Thomsen, H; Broyl, A; Davies, FE; Thorsteinsdottir, U; Hansson, M; Kaiser, M; Sonneveld, P; Goldschmidt, H; Stefansson, K; Hemminki, K; Nilsson, B; Morgan, GJ; Houlston, RS (2019-08-20)
      <h4>Background</h4>While genome-wide association studies (GWAS) of multiple myeloma (MM) have identified variants at 23 regions influencing risk, the genes underlying these associations are largely unknown. To identify ...