A multi-institutional team has reported in their recent paper that oncogenes, i.e. cancer-promoting genes on DNA’s extrachromosomal pieces often drive tumor progression. Genomic alterations were tracked by the researchers at the time when they had been identified in patient samples after and before treatment, in patient-derived xenograft (PDX) mouse models, and during tumor cell evolution. Glioblastoma (GBM) tumors bearing underlying processes responsible for cell-to-cell differences have been said to be better understood with the help of the research. This is considered to be a crucial finding as such differences are expected to give their contribution to therapy resistance.
Development of Sequencing-based Protocols to Identify ecDNA More Efficiently
The ultimate aim of the research study is said to determine pathways that could be targeted for the purpose of blocking glioma progression. Published in Nature Genetics, the study was led by Hermelin Brain Tumor Center’s Assistant Professor in Detroit, MI, Ana C. deCarvalho, Ph.D. and The Jackson Laboratory’s (JAX) Professor, Roel Verhaak, Ph.D.
According to the researchers, extrachromosomal (ec) DNA is relatively turned a blind eye to because of the difficulty to identify it with the help of standard sequencing methods. These methods don’t really separate it from chromosomal DNA or identify it accurately. However, ecDNA is now attracting attention and with the advancement of researches, the difficulty to treat GBM and other cancers and rapid evolution of therapy resistance could be explained.
As per Verhaak, if researchers could only learn why and how ecDNA elements form and block the mechanisms, we will have a way to perhaps prevent the formation and evolution of several cancers.