CECAD Microsite

Anna Schmitt´s paper on the role of ATM in NSCLC has just been accepted at Cancer Research


Anna has generated a mouse model for the inactivation of the DNA damage response kinase ATM in Kras-mutant lung adenocarcinoma

Anna's work demonstrates that bi-allelic Atm deletion in mouse models of Kras-mutant lung adenocarcinoma does not affect cisplatin responses but enhances response to the topoisomerase-II poison etoposide. Moreover, Atm-deficient cells and tumors were sensitive to the PARP inhibitor olaparib and to the ATR inhibitor VE-822.  These data strongly suggest that even in lung adenocarcinomas displaying a high-risk mutational constellation, response to targets small molecule drugs is dictated by additional mutations affecting the DNA damage response. These data also implicate that the functional ATM status should be evaluated in human lung adenocarcinomas for which no directly targeted therapeutic approach exists, regardless of the Tp53 status of these tumors.