MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeuticallyMore about Open Access at the Crick
Authors listEnkhtsetseg Munkhbaatar Michelle Dietzen Deepti Agrawal Martina Anton Moritz Jesinghaus Melanie Boxberg Nicole Pfarr Pidassa Bidola Sebastian Uhrig Ulrike Höckendorf Anna-Lena Meinhardt Adam Wahida Irina Heid Rickmer Braren Ritu Mishra Arne Warth Thomas Muley Patrina SP Poh Xin Wang Stefan Fröhling Katja Steiger Julia Slotta-Huspenina Martijn van Griensven Franz Pfeiffer Sebastian Lange Roland Rad Magda Spella Georgios T Stathopoulos Jürgen Ruland Florian Bassermann Wilko Weichert Andreas Strasser Caterina Branca Mathias Heikenwalder Charles Swanton Nicholas McGranahan Philipp J Jost
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Evasion of programmed cell death represents a critical form of oncogene addiction in cancer cells. Understanding the molecular mechanisms underpinning cancer cell survival despite the oncogenic stress could provide a molecular basis for potential therapeutic interventions. Here we explore the role of pro-survival genes in cancer cell integrity during clonal evolution in non-small cell lung cancer (NSCLC). We identify gains of MCL-1 at high frequency in multiple independent NSCLC cohorts, occurring both clonally and subclonally. Clonal loss of functional TP53 is significantly associated with subclonal gains of MCL-1. In mice, tumour progression is delayed upon pharmacologic or genetic inhibition of MCL-1. These findings reveal that MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically.
Journal Nature Communications
Issue number 1