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Poster display

750 - Dissecting the roles of Fra proteins in lung adenocarcinoma


10 Oct 2016


Poster display


Albanderi Alfraidi


Annals of Oncology (2016) 27 (6): 1-14. 10.1093/annonc/mdw362


A. Alfraidi1, L. Bakiri1, A. Ucero1, M. Musteanu2, M. Barbacid2, E. Wagner1

Author affiliations

  • 1 Genes, Development And Disease, CNIO- Spanish National Cancer Center, 28029 - Madrid/ES
  • 2 Molecular Oncology, CNIO- Spanish National Cancer Center, 28029 - Madrid/ES


Abstract 750


Lung cancer is a life-threatening disease with increased incidence worldwide. Most patients are diagnosed with advanced disease, and as a result, the 5 year survival rate is among the lowest in cancer. Among all lung cancer, 85% are non small lung cancer (NSCLC) subtype, which can be subdivided in lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). K-Ras mutation is the most common in NSCLC, but no drugs that target K-Ras directly or indirectly have yet been discovered. Therefore, there is a need to find a druggable target that can help in the treatment of lung cancer patients. Fos-related antigen 2 (Fra-2), a member of AP-1 transcription factors, has been shown to be activated by K-Ras signalling, as well as deregulated in many cancer types.


Prognosis value of Fra-2 mRNA expression level was assessed in transcriptomic data from 1928 NSCLC patients through an online survival analysis software. We generated a genetic engineered mouse model (GEMM) for Fra-2 inactivation in an experimental model of lung ADC induced by K-Ras mutation (G12V) and p53 inactivation. Fra-2 and p53 inactivation, and mutant K-Ras expression, are induced simultaneously by infection with a Cre-expressing Adenovirus delivered intra-nasally. Development of lung tumours was longitudinally monitored by micro-CT.


Fra-2 mRNA high expression was found to be significantly correlated to poor outcome in this ADC patient cohort. Genetic inactivation of Fra-2 in this lung cancer model prolongs the survival of the mice compared with heterozygous Fra-2 by decreasing tumor incidence, number and volume.


Our results identify a new potential therapeutic target in K-Ras mutated lung ADC.

Clinical trial identification

Legal entity responsible for the study

A. Alfraidi


World Wide Cancer Research formerly AICR


All authors have declared no conflicts of interest.

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