FEATURED AUTHORITIES ON Precision oncology
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Can you discuss the critical information reported in the genomics alteration section of the FoundationOne Report, the targeted therapies that may be relevant, and the interpretive statement for each genomic alteration, and the biologic/therapeutic ...
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 ...
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 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?
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.
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?
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?
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 current status of molecular profiling in the context of NSCL?
What is the current status of molecular profiling in the context of NSCL?
What is the role of liquid biopsies and hybrid capture NGS in the face of our understanding that there is sub-clonal evolution in many solid tumors?
What other gene rearrangements (ie, gene fusions) have recently been identified (such as ROS1, BRAF, RET) that are susceptible to targeted therapies? What are the current clinical implications for testing?
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?