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A new mouse model to explore the initiation, progression, and therapy of BRAFV600E-induced lung tumors.

Mutationally activated BRAF(V600E) (BRAF(VE)) is detected in approximately 6% of human malignancies and promotes sustained MEK1/2-ERK1/2 pathway activation. We have designed BRaf(CA) mice to express normal BRaf prior to Cre-mediated recombination after which BRaf(VE) is expressed at physiological levels. BRaf(CA) mice infected with an Adenovirus expressing Cre recombinase developed benign lung tumors that only rarely progressed to adenocarcinoma. Moreover, BRaf(VE)-induced lung tumors were prevented by pharmacological inhibition of MEK1/2. BRaf(VE) expression initially induced proliferation that was followed by growth arrest bearing certain hallmarks of senescence. Consistent with Ink4a/Arf and TP53 tumor suppressor function, BRaf(VE) expression combined with mutation of either locus led to cancer progression.

Pubmed ID: 17299132


  • Dankort D
  • Filenova E
  • Collado M
  • Serrano M
  • Jones K
  • McMahon M


Genes & development

Publication Data

February 15, 2007

Associated Grants

  • Agency: NCI NIH HHS, Id: CA84244

Mesh Terms

  • Adenocarcinoma
  • Animals
  • Cell Cycle
  • Cell Proliferation
  • Cyclin-Dependent Kinase Inhibitor p16
  • Disease Models, Animal
  • Disease Progression
  • Lung
  • Lung Neoplasms
  • MAP Kinase Kinase 1
  • MAP Kinase Kinase 2
  • Mice
  • Mice, Mutant Strains
  • Mutation
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins B-raf
  • Tumor Suppressor Protein p53