Oncologia Experimental

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Staff Scientists

  • Matthias Drosten
  • Raquel García
  • Carmen Guerra
  • Monica Musteanu

Post-Doctoral Fellows

  • Sara García
  • Carolina Navas
  • Guillem Paniagua

Graduate Students

  • Laura De Esteban
  • Fernando Fernández
  • Jing Li
  • Vasiliki Liaki
  • Lucía Morales
  • Marina Salmón
  • Manuel Sanclemente


  • Irene de Diego
  • Mª Carmen González
  • Patricia Teresa Guerra
  • Silvia Jiménez
  • Anna Köck
  • Marta San Román
  • Raquel Villar

KRAS oncogenes have been identified in at least one fifth of all human cancers. In spite of recent successes with checkpoint inhibitors, most KRAS mutant tumours, including lung adenocarcinomas, are still treated with cytotoxic compounds approved over 2 decades ago. Moreover, attempts to block KRAS oncogenic activity with selective inhibitors of the MEK kinase, a downstream effector, have turned out to be major failures. Two MEK inhibitors, Trametinib and Selumetinib, have failed to show significant anti-tumour activity in large phase III clinical trials due to unacceptable toxicities. In our laboratory, we have continued our quest to validate therapeutic targets using a new generation of genetically engineered mouse tumour models that allow us to evaluate their anti-tumour properties as well as their potential toxic effects in tumour- bearing mice. These studies have allowed the identification of c-RAF as a target capable of inducing significant tumour regressions in advanced KRAS/TRP53 mutant lung tumours without inducing major toxicities. These observations suggest that forthcoming c-RAF inhibitors may provide significant therapeutic benefits in the clinic.