Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer

C. Gamell, T. Gulati, B. Solomon, S. Haupt, Y. Haupt

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6 Citations (Scopus)


A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC.

Original languageEnglish
Article numbere1299273
Number of pages3
JournalMolecular and Cellular Oncology
Issue number5
Publication statusPublished - 3 Sept 2017


  • CDC6
  • E6AP
  • INK4/ARF
  • p16
  • tumor suppression

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