Epic Sciences launches single-cell microsatellite and chromosomal instability genomic analysis.
New capability identifies sub-clonal tumor microsatellite instability in metastitc cancers to understand patient selectin for PD-1 inhibitors, PARP inhibitors and combination therapies.
Epic Sciences, Inc. adds simultaneous microsatellite instability (MSI) and chromosomal instability (CIN) measurements, also known as genomic scarring analysis, to the single cell next generation sequencing (NGS) workflow for clinical research of immuno-oncology therapies. MSI is currently utilized to identify patients who may respond to PD-1 checkpoint inhibitors across multiple cancer indications. However, the prevalence of patients with high levels of MSI in their cancers, currently identified through invasive tissue biopsy or circulating tumor DNA (ctDNA) analysis, often represents a very minor percent of the patient population in some cancer indications. This significantly reduces the effect of MSI as a biomarker in predicting clinical benefit from immune checkpoint inhibitor therapy.
To illustrate the power of these new single-cell genomic analyses, Epic Sciences analyzed circulating tumor cells (CTCs) from the blood of metastatic prostate cancer patients. The results revealed multiple patients that had sub-clonal high MSI CTCs amongst a predominance of CTCs with low MSI. Some of the CTCs with low MSI had high levels of genomic scarring.
“Patient selection for PD-1 inhibitors and PD-1 combination therapies remains a very large and growing unmet medical need,” said Mark Landers, vice president of translational research at Epic Sciences. “The ability to examine and monitor sub-clonal microsatellite instability, often missed by tissue and ctDNA analysis, in the context of disease heterogeneity, clonality, and PD-L1 expression will rapidly improve our understanding of the biology underlying clinical responses to checkpoint inhibitors.”
Recently, synergistic benefits of combining PD-1 checkpoint inhibitors with DNA damage repair targeted therapies such as ATR and PARP inhibitors have been reported. Markers for response to these therapies individually (MSI and genomic scarring, respectively) are traditionally thought to be mutually exclusive mechanisms of drug response.
“By understanding the prevalence of both MSI and genomic scarring indicative of homologous recombination deficiency in single cells within individual patients, we have a unique view to understand why patients may benefit from PD-1 and PARP inhibitors in combination, but are unlikely to respond to either drug class as single agent therapies,” said Landers. “In the immediate future, we will be applying this new analysis to a number of clinical studies with our academic and biopharma partners to deliver exclusive insights into patient response to PD-1, PARP, and combination therapies.”
About Epic Sciences
At Epic Sciences, we develop clinically proven predictive tests to detect and monitor cancer at the individual cell level. With a proprietary rare-cell detection engine, we provide insights to clinical, biotech, pharmaceutical and academic teams on how cancer emerges, mutates and remits so they can make pivotal decisions at every point in patient treatment with greater certainty. Recognizing the unique nature of each person’s cancer, we offer truly personalized diagnostic tests, while being non-invasive for the patient.
We have developed the first clinically proven predictive test for metastatic castration-resistant prostrate cancer (mCRPC), the Epic AR-V7 test. Using the same rare-cell detection platform and Epic’s biobank of over 30,000 blood samples, each profiled with predictive biomarkers, we partner with leading pharmaceutical and biotechnology companies, major cancer centers, the National Cancer Institute (NCI), and the National Institutes of Health (NIH) to pursue additional predictive tests for breast, ovarian, colon and other cancers and diseases. Our mission is to revolutionize cancer care and therapies to make them as precise, safe and life-sustaining as humanly possible.
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