On September 22, 2021 Boundless Bio, a next-generation precision oncology company developing innovative therapeutics directed against extrachromosomal DNA (ecDNA) in aggressive cancers, reported plans to present at the AACR (Free AACR Whitepaper)-NCI-EORTC Virtual AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper), held virtually from October 7-10, 2021 (Press release, Boundless Bio, SEP 22, 2021, View Source [SID1234590139]).
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Boundless Bio, in collaboration with the Dana Farber Cancer Institute and Mirati Therapeutics, will share in vivo results from a colorectal cancer xenograft model revealing ecDNA as a key mediator of resistance to adagrasib and sotorasib, clinical-stage and FDA approved KRASG12C inhibitors respectively. These findings support previous Boundless Bio published work that ecDNA is an important underlying cause of cancer resistance and reinforces the critical need for novel therapeutic strategies to address ecDNA enabled cancers. The poster presentation will be available on-demand throughout the conference, details are below:
Title: Detection of KRAS amplification on extrachromosomal DNA (ecDNA) upon acquired resistance to KRASG12C inhibitors
Presenter: Ryan J. Hansen, Ph.D.
Poster Number: LBA005
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.