Bionano Genomics Inc.

08/13/2019 | Press release | Distributed by Public on 08/13/2019 06:36

Preliminary Data Confirm Saphyr's Potential to Replace Traditional Cytogenetics Methods for Detection of Structural Variants in Certain Blood Cancers

Strong concordance with standard of care methods shows how Saphyr can transform cytogenetic workflows and provide an approach that may be faster and more cost-effective and may give better results

SAN DIEGO, Aug. 13, 2019 (GLOBE NEWSWIRE) -- Bionano Genomics, Inc. (NASDAQ: BNGO), a life sciences instrumentation company that develops and markets Saphyr®, a platform for ultra-sensitive and ultra-specific structural variation detection in genome analysis, today announced a summary of results from two key studies presented this week at the 2019 Cancer Genomics Consortium Annual Meeting in Nashville, Tennessee.

In a preliminary read-out of a multi-center clinical validation study using blinded samples, Professor Brynn Levy, Director of Cytogenetics at Columbia University, presented outcomes on the first 11 patient samples analyzed and unblinded. This study compares Saphyr to technologies used in traditional cytogenetics workflows for patient testing in oncology and is being run by a consortium of leading cytogenetics teams at institutions in the United States, including Columbia University, the MD Anderson Cancer Center of the University of Texas, the Mayo Clinic, the University of Washington, Penn State University, Augusta University and the PathGroup. In each of the 11 samples, Saphyr detected all known clinical variants identified by various combinations of karyotype, Fluorescent In-Situ Hybridization (FISH), and Chromosomal MicroArray (CMA), which define the current standard of care in cytogenetics. Some of the variants identified include: in Acute Myeloid Leukemia samples, a large inversion on chromosome 16, which creates a CBFB MYH11 fusion; in one B-Cell Acute Lymphoblastic Leukemia (B-ALL) sample, a BCR-ABL1 translocation, and deletions of tumor suppressor genes IKZF1 and CDK6; and in a separate B-ALL sample, a NF1 deletion, which is a well-known risk factor for childhood leukemia. This detailed characterization of variants allows for a precise treatment tailored to the specific patient's tumor.