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What categories of genomic alterations are identified by the method of genomic profiling you are familiar with? Do they include all classes of alterations, i.e. base substitutions, insertions/deletions, copy number alterations and rearrangements? ...
What kind of clinical samples are required to implement next generation sequencing (NGS)? Can NGS be applied to samples other than FFPE?
Exactly what does it mean that a tumor sample has a mutation or rearrangement? Exactly what is being measured? Is the presence of a mutation on an NGS panel an “all-or–none” phenomenon or are there additional quantitative levels of characterization ...
What is the importance of NGS for 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 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?
In what kind of solid tumors, specifically NSCLC, can comprehensive genomic profiling/NGS make a difference in identifying patients with EGFR and other mutations—ALK, MET, ROS-1—that may be missed by hotspot tests?
Based on published clinical data and FDA approvals, why do NCCN guidelines for NSCLC recommend erlotinib and gefitinib as recommended (category 1) first-line systemic therapy in patients with sensitizing EGFR mutations?
What genomic alterations (i.e. driver events) does the NCCN identify for non-small cell lung cancer (NSCLC)? And what targeted agents does the NCCN recommend for these specific driver events?
What is the current and emerging role of liquid biopsies?
What is the current and emerging role of liquid biopsies?
Why are current genomic testing models based on targeted sequencing (“Hot Spot”) unsustainable given what we know about genomically-targeted therapy; and why have comprehensive genomic profiling (CGP) NGS platforms, such as those developed ...
Which of the four classes of genomic alterations—base substitutions, insertions and deletions, copy number alterations, and rearrangements can a typical multi-gene “Hot Spot” test detect? Which alterations does it fail to detect and why is NGS preferable?
What do the evolutionary studies of tumor progression—and heterogeneity—teach us about timing, longitudinal sampling, serial biopsies, and sampling sites for NGS-based genomic testing in patients with metastatic cancer?