Pathologist-Verified Billing: Correction Rates of Miscoded Frozen Section Cases.

Context.—: With the adoption of Epic/Beaker at our institution, surgical pathology specimens are assigned a Current Procedural Terminology (CPT) charge code at the time of accessioning, and pathologists have been made responsible for verifying the accuracy of the code before signing out the case.

Objective.

Complete Pathologic Response to Pembrolizumab and Axitinib in a Patient With Sarcomatoid RCC and Ocrelizumab-Treated Multiple Sclerosis.

Non-clear cell renal cell carcinoma (RCC) is a heterogeneous disease. We report a case of sarcomatoid non-clear cell RCC in a patient with underlying multiple sclerosis (MS) on immunosuppression with a complete pathologic response to pembrolizumab and axitinib. Comprehensive genomic profiling revealed pathogenic mutations in SETD2 and TP53 with high RNA expression levels of immune checkpoint proteins.

Mutations in RABL3 alter KRAS prenylation and are associated with hereditary pancreatic cancer.

Pancreatic ductal adenocarcinoma is an aggressive cancer with limited treatment options. Approximately 10% of cases exhibit familial predisposition, but causative genes are not known in most families. We perform whole-genome sequence analysis in a family with multiple cases of pancreatic ductal adenocarcinoma and identify a germline truncating mutation in the member of the RAS oncogene family-like 3 (RABL3) gene.

Iterative use of nuclear receptor Nr5a2 regulates multiple stages of liver and pancreas development.

The stepwise progression of common endoderm progenitors into differentiated liver and pancreas organs is regulated by a dynamic array of signals that are not well understood. The nuclear receptor subfamily 5, group A, member 2 gene nr5a2, also known as Liver receptor homolog-1 (Lrh-1) is expressed in several tissues including the developing liver and pancreas. Here, we interrogate the role of Nr5a2 at multiple developmental stages using genetic and chemical approaches and uncover novel pleiotropic requirements during zebrafish liver and pancreas development.

Metabolic Responses to Dietary Protein Restriction Require an Increase in FGF21 that Is Delayed by the Absence of GCN2.

FGF21 contributes to the metabolic response to dietary protein restriction, and prior data implicate GCN2 as the amino acid sensor linking protein restriction to FGF21 induction. Here, we demonstrate the persistent and essential role of FGF21 in the metabolic response to protein restriction. We show that Fgf21 KO mice are fully resistant to low protein (LP)-induced changes in food intake, energy expenditure (EE), body weight gain, and metabolic gene expression for 6 months.