Paul Mitchell, MD

Paul Mitchell, BHB, MBChB, FRACP, MD
 

Associate Professor
Senior Specialist
Austin Health Cancer Services
Director, North Eastern Metropolitan Integrated Cancer Services (NEMICS)
Melbourne, Australia



With respect to EGFR mutations in NSCLC, what validations support routine target profiling using hybrid capture-based NGS platforms, and what target-drug alignments have improved PFS?

With respect to EGFR mutations in NSCLC, what clinical validations exist to support routine molecular target profiling using hybrid capture-based NGS platforms, and what target-drug alignments have been shown to improve PFS outcomes?

What is the importance of finding EGFR sensitizing mutations such as exon 19 or exon 21 in NSCLC? What is their relationship to sensitivity to TKIs, such as erlotinib, gefitinib, and afatinib?

What is the importance of finding EGFR sensitizing mutations such as exon 19 or exon 21 in NSCLC? What is their relationship to sensitivity to TKIs, such as erlotinib, gefitinib, and afatinib?

From a patient outcomes perspective, how well-defined are the predictive effects of the drug-sensitive EGFR mutations-- Exon19 and 21 deletions and L858R--in patients with NSCLC?

From a patient outcomes perspective, how well-defined are the predictive effects of the drug-sensitive EGFR mutations— Exon19 and 21 deletions and L858R—in patients with NSCLC?

PFS is improved with use of a TKI in patients with sensitizing EGFR mutations when compared with standard chemotherapy, although OS is not statistically different. Please summarize clinical results.

PFS is improved with use of a TKI in patients with sensitizing EGFR mutations when compared with standard chemotherapy, although overall survival is not statistically different? Please summarize clinical results.

If HER2 rearrangements are documented in NSCLC, why are such agents as trastuzimab and afatninib considered by the NCCN to have “targeted activity” against this tumor profile?

If HER2 rearrangements are documented in NSCLC, why are such agents as trastuzimab and afatninib considered by the NCCN to have “targeted activity” against this tumor profile?

If BRAF V600E mutations are documented in NSCLC, why are such agents as vemurafenib and dabrafenib considered by the NCCN to have "targeted activity" against this tumor profile?

If BRAF V600E mutations are documented in NSCLC, why are such agents as vemurafenib and dabrafenib considered by the NCCN to have “targeted activity” against this tumor profile?

If MET amplification is documented in NSCLC, why is crizotinib considered by the NCCN to have "targeted activity" against this tumor profile? What high activity in patients with 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 ...