Dissecting the role of YAP/WWTR1-mediated drug resistance signaling in lung adenocarcinoma

Lung cancer shows the highest incidence and mortality of all cancer types worldwide and causes about 18% of all cancer-related deaths. Even though therapies targeting driver mutations have improved therapeutic options for lung cancer patients, drug resistance and subsequent tumor relapse is virtually inevitable. Emerging evidence indicates an important role of two Hippo pathway effectors (YAP and WWTR1) in resistance to targeted therapy of lung adenocarcinoma.
In my research, I seek to examine the molecular mechanisms of YAP- and WWTR1-mediated drug resistance in lung adenocarcinoma in a comparative approach. However, I do not exclusively pursue the goal to contribute to the unveiling of YAP and WWTR1 biology. Rather, I strive to translate my findings into potential therapeutic approaches. Therefore, I seek to identify promising drug targets and will further assess combinations of EGFR or KRAS inhibition and pharmacological inhibition of identified resistance-mediating YAP and WWTR1 effectors.
The goal my research is to translate my results into proof-of-concept in vivo models to pave the way for a clinical application of my findings to foster personalized treatment strategies for lung cancer patients.