Alexander Drilon, MD

Alexander Drilon, MD
 

Medical Oncologist
Memorial Sloan Kettering Cancer Center
New York, NY, USA


What are currently the most important actionable drivers, from a mutational perspective, for lung cancer? And what is the emerging importance of RET kinase inhibitors?

What are currently the most important actionable drivers, from a mutational perspective, for lung cancer? And what is the emerging importance of RET kinase inhibitors?

How would you approach a middle-aged female, non-smoker diagnosed with stage 1-B lung adenocarcinoma in which the FoundationOne CGP identified a TRIM33-RET fusion?

How would you approach a middle-aged female, non-smoker is diagnosed with stage 1–B lung adenocarcinoma in which the FoundationOne CGP identified a TRIM33–RET fusion. What would be the “target-focused” treatment and timing implications of this finding?

What is the rationale for referring this patient to a phase II study of cabozantinib or other multi-TKI if she had had surgery and chemotherapy, but shows progression after cytotoxic chemotherapy?

What would be the rationale for referring this patient to a phase II study of cabozantinib or other multi-TKI if she had had surgery and chemotherapy, but shows progression to Stage IV disease after two prior lines of cytotoxic chemotherapy?

Can you provide an overview of the actionable targets--such as EGFR, ALK, and MET--that are relevant for patients with NSCLC, and how to deploy NGS technologies to identify molecular drivers?

Can you provide an overview of the clinically actionable targets—such as EGFR, ALK, and MET—that are relevant for patients with NSCLC, and how to optimally deploy NGS technologies to identify molecular drivers in the clinic setting?

How, in the setting of lung cancer, specifically should oncologists optimally deploy specific NGS technologies, especially those that use hybrid capture to identify molecular drivers of NSCLC in the clinic?

How, in the setting of lung cancer, specifically should oncologists optimally deploy specific NGS technologies, especially those that use hybrid capture to identify molecular drivers of NSCLC in the clinic?

If MET amplification is documented in NSCLC, why is crizotinib considered to have "targeted activity" against this tumor profile? What support suggests high activity in patients with tumors manifesting this genetic alteration?

If MET amplification is documented in NSCLC, why is crizotinib considered by the NCCN to have “targeted activity” against this tumor profile? What clinical study-based support—improvements in PFS and/or OS—suggests high activity of this ...

What is the importance of the gene encoding the ROS1 proto-oncogene receptor tyrosine kinase as a distinct molecular subgroup of NSCLC? In what percentage of patients is ROS1 detected?

What is the importance of the gene encoding the ROS1 proto-oncogene receptor tyrosine kinase (ROS1) as a distinct molecular subgroup of NSCLC? In what percentage of patients is ROS1 detected? What is the role of crizotinib in these patients?

At what stage in the presentation of NSCLC should one consider doing comprehensive NGS with hybrid capture?

At what stage in the presentation of NSCLC should one consider doing comprehensive NGS with hybrid capture?