Counterevidence of crime-reduction effects from federal grants of military equipment to local police.

In 2017, the Trump Administration restored local law enforcement agencies' access to military weapons and some other types of surplus military equipment (SME) that had been prohibited by the Obama Administration. The Justice Department background paper used to justify this decision cited two papers published by the American Economic Association. These papers used SME data collected with a 2014 Freedom of Information Act request and concluded that SME, supplied to local law enforcement by the federal government via the 1033 Program, reduces crime. Here we show that the findings of these studies are not credible due to problems with the data. Using more detailed audit data on 1033 SME, we show that the 2014 data are flawed and that the more recent data provide no evidence that 1033 SME reduces crime.

Protein S drives oral squamous cell carcinoma tumorigenicity through regulation of AXL.

The TAM family of proto-oncogenic receptor protein tyrosine kinases, comprising of TYRO3, AXL, and MERTK, is implicated in many human cancers. Their activation leads to cancer cell proliferation, enhanced migration, invasion, and drug resistance; however how TAMs are activated in cancers is less understood. We previously showed that Protein S (PROS1) is a ligand of the TAM receptors. Here we identify PROS1 as a mediator of Oral Squamous Cell Carcinoma (OSCC) in proliferation, cell survival and migration. We demonstrate that excess PROS1 induces OSCC proliferation and migration. Conversely, blocking endogenous PROS1 expression using shRNA significantly inhibits cell proliferation and migration in culture. This inhibition was rescued by the addition of purified PROS1. Moreover, PROS1 knockdown reduced anchorage-independent growth in-vitro, reduced tumor xenograft growth in nude mice and altered their differentiation profile. Mechanistically, we identify the downregulation of AXL transcripts and protein following PROS1 knockdown. Re-introducing PROS1 rescues AXL expression both at the protein and transcriptional levels. The anti-proliferative effect of the AXL inhibitor R428 was significantly reduced following PROS1 inhibition, indicating the functional significance of PROS1-mediated regulation of AXL in OSCC. Taken together, we identify PROS1 as a driver of OSCC tumor growth and a modulator of AXL expression. Our results point to PROS1 as a potential novel anti-cancer therapeutic target.