• Map3k1 loss cooperates with Braf(V600E) to drive melanomagenesis

      Trucco, Lucas D; Mundra, Piyushkumar A; Garcia-Martinez, Pablo; Hogan, Kate; Baenke, Franziska; Dhomen, Nathalie; Pavet, Valeria R; Marais, Richard; Molecular Oncology Group, Cancer Research UK Manchester Institute, The University of Manchester, Manchester, (2020)
      No abstract available
    • Publisher correction: ultraviolet radiation-induced DNA damage is prognostic for outcome in melanoma

      Trucco, Lucas D; Mundra, Piyushkumar A; Hogan, Kate; Garcia-Martinez, Pablo; Viros, Amaya; Mandal, Amit Kumar; Macagno, N; Gaudy-Marqueste, C; Allan, D; Baenke, Franziska; et al. (2018)
      In the version of this article originally published, Extended Data Fig. 3 was incorrect. A duplicate of Extended Data Fig. 4 was uploaded in place of Extended Data Fig. 3. Extended Data Fig. 3 has now been uploaded. The error has been fixed in the PDF and HTML versions of this article.
    • Resistance to BRAF inhibitors induces glutamine dependency in melanoma cells.

      Baenke, Franziska; Chaneton, B; Smith, Matthew; Van Den Broek, N; Hogan, Kate; Tang, Haoran; Viros, Amaya; Martin, Matthew; Galbraith, L; Girotti, Maria Romina; et al. (2015-08-20)
      BRAF inhibitors can extend progression-free and overall survival in melanoma patients whose tumors harbor mutations in BRAF. However, the majority of patients eventually develop resistance to these drugs. Here we show that BRAF mutant melanoma cells that have developed acquired resistance to BRAF inhibitors display increased oxidative metabolism and increased dependency on mitochondria for survival. Intriguingly, the increased oxidative metabolism is associated with a switch from glucose to glutamine metabolism and an increased dependence on glutamine over glucose for proliferation. We show that the resistant cells are more sensitive to mitochondrial poisons and to inhibitors of glutaminolysis, suggesting that targeting specific metabolic pathways may offer exciting therapeutic opportunities to treat resistant tumors, or to delay emergence of resistance in the first-line setting.
    • Ultraviolet radiation-induced DNA damage is prognostic for outcome in melanoma.

      Trucco, Lucas D; Mundra, Piyushkumar A; Hogan, Kate; Garcia-Martinez, Pablo; Viros, Amaya; Mandal, Amit Kumar; Macagno, N; Gaudy-Marqueste, C; Allan, D; Baenke, Franziska; et al. (2018)
      Erratum in Publisher Correction: Ultraviolet radiation-induced DNA damage is prognostic for outcome in melanoma. [Nat Med. 2018] Abstract The melanoma genome is dominated by ultraviolet radiation (UVR)-induced mutations. Their relevance in disease progression is unknown. Here we classify melanomas by mutation signatures and identify ten recurrently mutated UVR signature genes that predict patient survival. We validate these findings in primary human melanomas; in mice we show that this signature is imprinted by short-wavelength UVR and that four exposures to UVR are sufficient to accelerate melanomagenesis.