Taylor Jensen,
Director, Research and Development,
Sequenom (a LabCorp Company)
Dr. Jensen serves as Director of Research and Development at Sequenom, a wholly owned subsidiary of Laboratory Corporation of America. He joined Sequenom in 2009 and was part of the team that developed and launched the first commercially available noninvasive prenatal test based on circulating cell-free DNA (cfDNA) in the U.S. Since that time, Dr. Jensen has been involved in numerous assay development efforts focused on the detection of genetic and epigenetic changes in cfDNA for use in both the prenatal and oncology fields with the overarching goal of utilizing these aberrations to improve human health. Prior to joining Sequenom, Dr. Jensen received his B.S. degree in biology from Utah State University and completed his PhD in Pharmacology and Toxicology from the University of Arizona.
Low Coverage, Genome-Wide Sequencing of Cell-Free DNA Enables the Monitoring of Response to Immunotherapy in Cancer Patients
Wednesday, 27 March 2019 at 17:30
Add to Calendar ▼2019-03-27 17:30:002019-03-27 18:30:00Europe/LondonLow Coverage, Genome-Wide Sequencing of Cell-Free DNA Enables the Monitoring of Response to Immunotherapy in Cancer PatientsCirculating Biomarkers World Congress 2019 in Coronado Island, CaliforniaCoronado Island, CaliforniaSELECTBIOenquiries@selectbiosciences.com
Inhibitors of the PD-1/PD-L1/CTLA4 immune checkpoint pathway have
revolutionized cancer treatment with a subset of patients showing
durable responses; however, challenges remain in the development of
biomarkers to predict or monitor response to these therapies. The use
of cell-free DNA (cfDNA) isolated from plasma, or liquid biopsy,
provides a promising method for monitoring response. In contrast to
methods that use ultra-deep (>30,000X) targeted sequencing, we will
describe a recently completed a proof-of-concept study using
low-coverage (~0.3X), genome-wide sequencing of cfDNA to detect
tumor-specific copy number alterations. As part of this study, we have
developed a novel metric, the Genome Instability Number (GIN), to
monitor response to these drugs throughout treatment. In a series of
case studies, we will describe how the GIN can be used to discriminate
clinical response from progression, differentiate progression from
pseudoprogression and identify hyperprogressive disease. In addition,
we have utilized this metric to provide evidence for a delayed
pharmacokinetic response for checkpoint inhibitors relative to targeted
therapies.