P. Nagesh Rao

TL;DR: It is found that drug resistance is associated with the reactivation of BCR-ABL signal transduction in all cases examined and a strategy for identifying inhibitors of STI-571 resistance is suggested.

TL;DR: Coexpression of EGFRvIII and PTEN by glioblastoma cells is associated with responsiveness to EGFR kinase inhibitors, and effects of the molecular abnormalities in vitro are identified.

TL;DR: It is shown that ecDNA was found in nearly half of human cancers; its frequency varied by tumour type, but it was almost never found in normal cells, and the results suggest that ec DNA contributes to accelerated evolution in cancer.

TL;DR: Single-cell analyses of patient-derived models and clinical samples from glioblastoma patients treated with EGFR tyrosine kinase inhibitors demonstrate that tumor cells reversibly up-regulate or suppress mutant EGFR expression, conferring distinct cellular phenotypes to reach an optimal equilibrium for growth.

TL;DR: The results suggest extracellular missense mutations as a novel mechanism for oncogenic EGFR activation and may help identify patients who can benefit from EGFR kinase inhibitors for treatment of glioblastoma.