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PTEN mutant non-small cell lung cancer require ATM to suppress pro-apoptotic signalling and evade radiotherapy.

Thomas FischerOliver HartmannMichaela ReisslandCristian Prieto-GarciaKevin KlannNikolett PahorChristina Schülein-VölkApoorva BaluapuriBülent PolatArya AbazariElena Gerhard-HartmannHans-Georg KoppFrank EssmannMathias RosenfeldtChristian MünchMichael FlentjeMarkus Elmar Diefenbacher
Published in: Cell & bioscience (2022)
PTEN tumors are addicted to ATM to detect and repair radiation induced DNA damage. This creates an exploitable bottleneck. At least in cellulo and ex vivo we show that low concentration of ATM inhibitor is able to synergise with IR to treat PTEN-deficient tumors in genetically well-defined IR resistant lung cancer models.
Keyphrases
  • dna damage
  • radiation induced
  • dna repair
  • pi k akt
  • cell proliferation
  • radiation therapy
  • oxidative stress
  • dna damage response
  • anti inflammatory
  • cell death
  • signaling pathway
  • early stage
  • wild type
  • locally advanced