On May 17, 2021 Boundless Bio, a next-generation precision oncology company developing innovative therapeutics directed against extrachromosomal DNA (ecDNA) in aggressive cancers, reported that scientific founders, Paul Mischel, M.D., Roel Verhaak, Ph.D., and Howard Chang, M.D., Ph.D., will participate in an educational session at the 2021 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting (Press release, Boundless Bio, MAY 17, 2021, View Source [SID1234580164]). The scientists will deliver a series of presentations on Extrachromosomal DNA in Cancer. The session is available to registered conference attendees.
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The session details are as follows:
Session Title: Extrachromosomal DNA in Cancer
Chairperson: Paul Mischel, M.D.
Session Category: ED004
Date and Time: May 21, 2021, 1:45 p.m. – 3:15 p.m. ET
Title: Introduction: Where things are matters: The role of extrachromosomal DNA (ecDNA) in cancer
Presenter: Paul Mischel, M.D., Professor and Vice Chair of Research for the Department of Pathology and Institute Scholar of ChEM-H at Stanford University
Title: Uneven segregation and clustering of extrachromosomal DNA elements
Presenter: Roel Verhaak, Ph.D., Professor and Associate Director of Computational Biology at The Jackson Laboratory
Title: Control of cancer genes beyond chromosomes
Presenter: Howard Chang, M.D., Ph.D., Virginia and D.K. Ludwig Professor of Cancer Genomics and Genetics at Stanford University and Howard Hughes Medical Institute Investigator
Title: Plasticity of extrachromosomal and intrachromosomal BRAF amplifications in mediating targeted therapy dosage challenges
Presenter: Thomas Graeber, Ph.D., Professor of Molecular and Medical Pharmacology and Director of the Metabolomics Center at UCLA
About ecDNA
Extrachromosomal DNA, or ecDNA, are distinct circular units of DNA lacking centromeres but containing functional genes, including oncogenes, that are separated from tumor cell chromosomes. ecDNA replicate within cancer cells and can be passed to daughter cells asymmetrically during cell division, thereby constituting a primary driver of focal gene amplification and copy number heterogeneity in cancer. By leveraging the plasticity afforded by ecDNA, cancer has the ability to increase or decrease copy number of select oncogenes located on ecDNA to enable survival under selective pressures, including chemotherapy, targeted therapy, immunotherapy, or radiation, making ecDNA one of cancer cells’ primary mechanisms of recurrence and treatment resistance. ecDNA are not found in healthy cells but are present in many solid tumor cancers. They are a key driver of the most aggressive and difficult-to-treat cancers, specifically those characterized by high copy number amplification of oncogenes.