November 15


Biodesign Auditorium
727 E. Tyler St. Tempe
AZ 85287

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Lung cancer, and more specifically non-small cell lung cancer (NSCLC), is the primary contributor to cancer related mortalities within the United States and accounts for the majority of lung cancers compared to the other subtypes. Due to limited choices in treatment (surgical resection, chemotherapy and radiation), significant work has identified unique genetic alterations within NSCLC tumors in hopes of utilizing this information to develop improved treatment modalities. Genetic inactivation of the tumor suppressor gene, LKB1/STK11, is frequent in NSCLC and contributes to NSCLC disease progression. The unique regulatory functions of LKB1, combined with the increased frequency of inactivation in NSCLC, have resulted in considerable interest in developing therapies targeted towards LKB1 null NSCLC. In this talk, I will discuss the current understanding of LKB1’s regulatory functions and contribution of LKB1 loss to NSCLC progression, as well as our and others attempts to tailor treatments towards LKB1 null NSCLC.