Gad Getz

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.

TL;DR: A streamlined approach for the prediction and validation of neoantigens derived from individual tumors and presented by patient-specific HLA alleles is implemented, suggesting that neoantIGens are frequent in most tumors.

TL;DR: The approach identifies salient T2D genetically anchored and physiologically informed pathways, and supports the use of genetics to deconstruct T1D heterogeneity.

TL;DR: Mutations in TP53, TET2, or DNMT3A identify patients with MDS with shorter OS after HSCT, and these mutations were associated with decreased OS in univariable and multivariable analyses.

TL;DR: This study used whole-genome sequencing and whole-exome sequencing of multiple sectors from primary and paired recurrent GBM tumors to reconstruct the genomic profile of residual, therapy resistant tumor initiating cells and found that genetic alteration of the p53 pathway is a primary molecular event predictive of a high number of subclonal mutations in glioblastoma.