Samuel Klempner, MD

Samuel Klempner, MD
 

Director of Precision Medicine
The Angeles Clinic and Research Institute
Cedars-Sinai Medical Center
Los Angeles, CA


What are the actionable interfaces between NGS-based whole exome profiling and immunotherapy, focusing on new data on tumor mutational burden, microsatellite instability (MSI), and related signatures?

What are the current actionable interfaces between NGS-based whole exome profiling and immunotherapy, focusing on new data related to tumor mutational burden, microsatellite instability (MSI), and related signatures?

Since assessing tumor mutational burden requires whole exome NGS profiling, how do you decide which tumor subtypes and patients, are appropriate for comprehensive genomic profiling?

Since assessing tumor mutational burden requires whole exome NGS profiling, and given the emerging pervasiveness of immunotherapy for many tumor types, how do you decide which tumor subtypes and patients, especially those with advanced ...

What is your guidance about when to integrate tests for circulating tumor DNA (ctDNA) into protocols for precision cancer medicine? How does this test compare to tissue-based NGS?

What is your current guidance about whether and/or how and when to integrate tests for circulating tumor DNA (ctDNA) into protocols for precision cancer medicine? And how does this test compare to tissue-based NGS? Which patients will benefit most?

How should we integrate and incorporate ctDNA profiling with tissue-based whole exome NGS, including longitudinal biopsies? When are these two tests potentially complementary?

Based on the evidence available, how should we be integrating and incorporating ctDNA profiling with tissue-based whole exome NGS, including longitudinal biopsies? In what settings, patients, and situations are these two tests potentially ...

How would you integrate all the currently available tests — NGS-based mutational profiles and burden and IHC biomarkers — to stratify patients into cohorts likely to be responsive to PD-1 checkpoint inhibitors?

How would you integrate all the currently available tests — NGS-based mutational profiles and burden and IHC biomarkers — to stratify patients into cohorts likely to be responsive to PD-1 checkpoint inhibitors?