Cellular acidity, capacity for net acid extrusion, and expression of acid-base transporters in human breast carcinomas independently predict variation in proliferative activity, lymph node metastasis, and patient survival.
In this ideal example of pharmacogenomics, individuals with a common variant in a gene encoding for an inflammatory lipid mediator benefit selectively from standard-of-care anti-inflammatory treatment used for tuberculous meningitis.
The percentage of a tumor’s genome with alterations in copy number is correlated with increased mortality across a range of tumor types and can be measured using a clinically approved sequencing assay.
Faithful models of RMC require SMARCB1 loss for survival, and genetic and small-molecule screens identify inhibition of the ubiquitin-proteasome system (UPS) as a potential therapeutic approach for SMARCB1 deficient cancers.
Genomic associations with lifespan principally reflect heart disease/smoking/dementia but not other cancers, and distinguish lifespan differences of five years between top/bottom deciles of a score derived from DNA alone.
Radiomics allows automated quantification of the radiographic phenotype of a tumor across diverse patient cohorts and is connected to the underlying molecular pathway activities, which together determine the clinical outcome.