Intratumoral heterogeneity of EGFR abnormalities linked to clonal evolution in glioblastoma by single nucleus sequencing

摘要

Numerous studies have now documented the extensive molecular heterogeneity characterizing glioblastoma, both on an intertumoral and intratumoral basis. Regarding the latter, recent work has shown that a variety of distinct pathogenic alterations in receptor tyrosine kinases (RTK) such as EGFR are frequently co-existent in a single tumor. Such findings are reminiscent of other studies documenting distinct RTK amplification events characterizing non-overlapping cellular subclones within an individual neoplasm. This sort of heterogeneity has obvious clinical implications, particularly with regard to targeted therapeutics and latent resistance mechanisms.