Boundless Bio Presents Data on the Novel Discovery of the Association Between Extrachromosomal DNA (ecDNA) and Replication Stress at the American Association for Cancer Research Annual Meeting 2022
The study reveals replication stress in ecDNA enabled cancers as a unique vulnerability and therapeutic strategy for treating gene amplified cancers
Excerpt from the Press Release:
SAN DIEGO–(BUSINESS WIRE)–Boundless Bio, a next-generation precision oncology company developing innovative therapeutics directed against extrachromosomal DNA (ecDNA) in oncogene amplified cancers, today will present a new finding at the American Association for Cancer Research (AACR) Annual Meeting 2022, held in New Orleans and virtually from April 8-13, 2022. The poster, Replication stress and the inability to repair damaged DNA, the potential “Achilles’ heel” of ecDNA+ tumor cells, is available to registered attendees online starting today and for in-person presentation on April 11, 2022 at 1:30 PM – 5:00 PM CT.
“Replication stress has long been known to be a driver of genomic instability in cancer,” said Christian Hassig, Ph.D., Chief Scientific Officer of Boundless Bio. “This study demonstrates ecDNA-enabled gene amplified cancers have inherently high replication stress, thereby providing a unique point of intervention for our novel ecDNA-directed therapeutics (ecDTx). This work is an important scientific advancement both in our understanding of gene amplifications on ecDNA and in translating the science into novel therapeutics for patients with gene amplified cancers who currently have few treatment options.”
Boundless Bio previously demonstrated that cancers with oncogenes amplified on ecDNA are associated with poor clinical prognosis1 and generally do not respond to targeted therapies, underscoring the urgent need to identify clinical strategies to treat ecDNA amplified cancers. For the first time, we present data showing a relationship between ecDNA and DNA replication stress, a known form of genomic instability that contributes to oncogenesis and tumor evolution.
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