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Mutated Kras spins a molecular loop that launches pancreatic cancer
Date:1/26/2012

lated inflammatory genes were present in high levels in mice with mutated Kras and active IKK2/ but only found at lower levels in mice with IKK2/ knocked out.
  • In human pancreatic tumors, high expression of the same inflammatory genes in the mutated Kras mice were associated with positive lymph node status, high-risk, late tumor stage and poor survival.
  • Expression of several genes regulated by NF-κB progressed from low levels in normal pancreases to higher levels in precancerous lesions and tumors, including IL-α.
  • IL-1α was known to be both a target of and an inducer of NF-κB, but its expression had not previously been connected to mutated Kras. The team found that downstream targets of Kras, including IL-1, are interrupted when IKK2/β is inactivated.
  • Analysis of 14 human pancreatic cancer tumor samples showed that overexpression of IL-1α, the presence of Kras mutation and the activation of NF-κB are correlated and are associated with poor survival.
  • Continued activation of NF-κB and its gene transcription activity are sustained by IL-1α and p62.


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  • Contact: Scott Merville
    smerville@mdanderson.org
    713-792-0661
    University of Texas M. D. Anderson Cancer Center
    Source:Eurekalert  

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