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Why are current genomic testing models based on targeted sequencing (“Hot Spot”) unsustainable and less effective than comprehensive genomic profiling (GGP) developed by FoundationOne?
What is the evidence supporting the observation that a systematic and comprehensive NGS-generated profiling of actionable alterations in genes associated with solid tumors should or can inform therapeutic decision-making?
For what specific solid tumors and hematologic malignancies has NGS genomic profiling shown to be most valuable for identifying disease alleles which can reliably guide the use of molecularly targeted therapy?
What is the evidence that more personalized, gene-directed cancer therapy, in which specific molecular drivers of a patient’s disease are aligned with specific therapy, will improve patient outcomes? To what extent are they improved with ...
What guidance can you give in those cases in which the F1M CGP profile reveals multiple actionable mutations? On what basis would you select targeted therapies when multiple significant genomic alterations or rearrangements co-exist?
What common mutations and rearrangements—among them EGFR, ALK, HER2, BRAF, RAS, MET, RET and ROS— present in tumors represent the best molecular targets for cancer therapy? Are some more predictive of success with targeted therapy than others? Why?
How well do other non-F1M methods for NGS assessment work? Are they as effective? Why or why not? Highly aggressive or resistant tumors? Cancers of unknown primary? Cancers with limited tissue samples? Please explain.
How does the FoundationOne CGP improve the power of its test to detect an alteration that is present in only some, but not all, of the tumor cells?
How do you select patients with solid tumors that are appropriate for NGS? Is it useful just for patients with cancer at time of presentation? Can it be used for patients under treatment? For assessment of tumors in patients who have relapsed?
What is the overall accuracy and reproducibility rate for cancer genomic profiling based on massively parallel DNA sequencing? And at what point in the cancer disease process should CGP be employed?
Why are current genomic testing models based on targeted sequencing (“Hot Spot”) unsustainable and less effective than comprehensive genomic profiling (CGP) developed by FoundationOne?
The current FoundationOne assay examines about 315 genes known to be somatically altered in human solid tumors, as well as 28 translocations. How were these genes determined? What makes them significant?