Cancer Genetics recently presented two studies on diffuse large B-cell lymphoma (DLBCL), looking at various biomarkers and pathways that mark the disease and might predict patient response to treatment. The presentations took place at the 58th ASH Annual Meeting & Exposition (Dec. 3-6) in San Diego.
According to a press release, the first presentation, “PD-L1 Expression Identifies High Risk Diffuse Large B-Cell Lymphoma and is Associated with Several Genomic Markers,” described a study conducted with the Keck School of Medicine, at the University of Southern California (USC), that used Cancer Genetics next generation sequencing (NGS) panel, called Focus::Lymphoma. This panel enables the targeted sequencing of 220 genes that are commonly mutated in lymphomas, providing information that may help determine treatment options.
The study used the panel to detect biomarkers that may help doctors choose which DLBCL patients will benefit from checkpoint inhibitor therapies, improving patient management.
In addition, this study looked at PD-L1 expression and the specificity and sensitivity of three anti-PD-L1 antibodies in 52 patients with primary DLBCL. PD-1 is a checkpoint protein on T-cells that acts as a type of “off switch” to keep T-cells from attacking tumor cells.
“PD-L1 expression reflects the biology of aggressive subsets of DLBCLs, which are also characterized by high risk cytogenetic and molecular biomarkers,” the researchers wrote. “PD-L1 expression can be measured by several antibody clones, which have different performance characteristics but show positive correlation.”
The company believes this work is important in developing durable and reliable immune biomarkers that help to determine which lymphoma patients are more likely to benefit from immune-checkpoint therapies.
The second presentation, “AICDA Introduces Epigenetic Plasticity in Germinal Center-Derived Lymphomas and Accelerates Lymphomagenesis,” described a study that evaluated the contribution of activation-induced cytidine deaminase (AICDA) DNA methylation in DLBCL patients. When B-cells mature in the lymph nodes, AICDA causes mutations that produce antibody diversity, but that same mutation process can lead to B-cell lymphoma.
The study, conducted in collaboration with Weill Cornell Medical College, demonstrated that AICDA changes the methylation status of germinal center B cell-derived lymphomas. Such epigenetic changes lead to alterations in gene expression that contribute to the formation of different tumor clones within one single tumor, contributing to a higher adaptability of the tumor to environment changes and treatment approaches.
Cancer Genetics believes that a better comprehension of these pathways will be essential for the development of new treatments for patients with DLBCL, as well as to better distinguishing groups of patients likely to respond differently to different therapies.
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