As you explained, NSCLC is one solid tumor where comprehensive genomic profiling can dramatically alter a precision-based strategy. Can you provide a patient example where you have observed that the detection of a rare insertion altered the treatment choice?
Can you give us an example of a real world patient with a rare or refractory cancer whose treatment course was altered by an NGS-based FoundationOne Report?
What is the problematic aspect for the patient of employing a platform that fails to detect an actionable molecular alteration?
Why are current genomic testing models based on targeted sequencing (“Hot Spot”) less sustainable and less effective than comprehensive NGS-based genomic profiling (CGP) that undergird other diagnostic platforms?
How do we make sense of an NGS-based molecular profile when there appear to be a number of potentially actionable genomic alterations? How might a “molecular tumor board” be helpful?
What are your impressions of the ProfiLER Study and its implications for employing NGS and channeling people into trials driven by early molecular profiling?
How has the landscape of actionable alterations changed over time -- with respect to new fusion configurations in the setting of lung cancer, for example? And how do we approach the more rare cancers?
How has the landscape of actionable alterations changed over time — with respect to new fusion configurations in the setting of lung cancer, for example? And how do we approach the more rare cancers?
Using FoundationOne NGS-based whole exome profiling as a reporting platform, what foundational and clinically actionable information is provided, and how should clinicians apply the report’s findings to the front lines of practice?
In the setting of lung cancer, what is the advantage of using whole exome NGS versus targeted gene testing? Why do you advocate comprehensive molecular profiling?
What is the importance of ROS-1 fusion mutations? What are the therapeutic implications of their detection?
What is the importance of ALK fusion mutations? What are the therapeutic implications of their detection? How effective are the second-generation ALK inhibitors? What does the data show as far as PFS?
What are the most important activating EGFR mutations and what are the specific implications of their detection? And what if these patients relapse on a TKI?