STK11/TP53 co-mutated Non-Small Cell Lung Cancer (NSCLC) displays a unique tumor microenvironment (TME) and metabolic profile.


Abdul Rafeh Naqash, Charalampos S. Floudas, Asaf Maoz, Joanne Xiu, Yasmine Baca, Jia Zeng, Chul Kim, Julia Judd, Luis E. Raez, Gilberto Lopes, Jorge J. Nieva, Hossein Borghaei, Wolfgang Michael Korn, Naoko Takebe, Stephen V. Liu, Hirva Mamdani

Background: Recent data suggest inferior responses to immune checkpoint inhibitors (ICIs) in STK11-mt NSCLC. TP53 is a critical tumor suppressor gene regulating DNA repair by arresting cells in the G1 phase in response to critical double strand breaks. We hypothesized that accumulated DNA damage from mutations in the TP53 gene might increase immunogenicity and potentially enhance benefit of ICIs in STK11-mt NSCLC.

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