Descriptions and Changes in Charge Master Pricings of US Children's Hospitals From 2019 to 2021.

BACKGROUND AND OBJECTIVES: A lack of price transparency may contribute to high healthcare costs. US hospitals were mandated to post their charge masters online in 2019. To compare changes in charge master prices of 3 common tests (complete blood count, complete metabolic panel, and chest radiograph) at US children's hospitals between 2019 and 2021. METHODS: Online search for charge master was conducted from July to December 2019 and October to December 2021. Descriptive statistics were reported for each test. Prices between years were adjusted for inflation and compared with paired t test. City-level variation was evaluated by comparing the coefficient of variation in 6 metropolitan areas: Baltimore, California Bay Area, Chicago, Dallas-Fort Worth, Los Angeles, and New York City. RESULTS: Of 847 hospitals, charge masters were found in 747 (88%) in 2021 and 728 (86%) in 2019. Complete blood count prices ranged from $5 to $1037 in 2019 and $5 to $1085 in 2021, with no difference between the 2 years (P = .17). Complete metabolic panel prices ranged from $10 to $2440 in 2019 and $6 to $2746 in 2021, with no difference in prices (P = .75). Chest radiograph prices ranged from $20 to $1900 in 2019 compared with $30 to $5800 in 2021. Prices were higher compared with 2019 ($392 vs. $365, P < .0006). City-level changes in the coefficient of variation showed only 2 cities with reduced coefficients of variation in all 3 tests. CONCLUSIONS: Two years after mandating hospitals post charge masters online, there continues to be tremendous variability in prices of common tests across US children's hospitals.

Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma.

Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma. Here, we identify KMT2D as a potent tumor suppressor in melanoma through an in vivo epigenome-focused pooled RNAi screen and confirm the finding by using a genetically engineered mouse model (GEMM) based on conditional and melanocyte-specific deletion of KMT2D. KMT2D-deficient tumors show substantial reprogramming of key metabolic pathways, including glycolysis. KMT2D deficiency aberrantly upregulates glycolysis enzymes, intermediate metabolites, and glucose consumption rates. Mechanistically, KMT2D loss causes genome-wide reduction of H3K4me1-marked active enhancer chromatin states. Enhancer loss and subsequent repression of IGFBP5 activates IGF1R-AKT to increase glycolysis in KMT2D-deficient cells. Pharmacological inhibition of glycolysis and insulin growth factor (IGF) signaling reduce proliferation and tumorigenesis preferentially in KMT2D-deficient cells. We conclude that KMT2D loss promotes tumorigenesis by facilitating an increased use of the glycolysis pathway for enhanced biomass needs via enhancer reprogramming, thus presenting an opportunity for therapeutic intervention through glycolysis or IGF pathway inhibitors.