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The concentration of police resources in stable crime hotspots has proven effective in reducing crime, but the extent to which police can disrupt dynamically changing crime hotspots is unknown. Police must be able to anticipate the future location of dynamic hotspots to disrupt them. Here we report results of two randomized controlled trials of near real-time epidemic-type aftershock sequence (ETAS) crime forecasting, one trial within three divisions of the Los Angeles Police Department and the other trial within two divisions of the Kent Police Department (United Kingdom). We investigate the extent to which (i) ETAS models of short-term crime risk outperform existing best practice of hotspot maps produced by dedicated crime analysts, (ii) police officers in the field can dynamically patrol predicted hotspots given limited resources, and (iii) crime can be reduced by predictive policing algorithms under realistic law enforcement resource constraints. While previous hotspot policing experiments fix treatment and control hotspots throughout the experimental period, we use a novel experimental design to allow treatment and control hotspots to change dynamically over the course of the experiment. Our results show that ETAS models predict 1.4–2.2 times as much crime compared to a dedicated crime analyst using existing criminal intelligence and hotspot mapping practice. Police patrols using ETAS forecasts led to an average 7.4% reduction in crime volume as a function of patrol time, whereas patrols based upon analyst predictions showed no significant effect. Dynamic police patrol in response to ETAS crime forecasts can disrupt opportunities for crime and lead to real crime reductions.

The research effort was directed at the development of a reliable scale to measure subcultural tolerance of police corruption among Chicago police officers. The study was also designed to assess the value of a set of individual characteristics in predicting sub-cultural tolerance of police corruption. The data are derived from a random sample survey of 105 active Chicago police officers. The survey instrument was designed to collect data on officers' attitudes toward certain corrupt behavior and contained twelve behavior statements which respondents classified along a five-point scale from “acceptable” to “unacceptable.” The findings indicate that the scale developed is reliable in measuring the level of corruption tolerance present in the sub-culture of the subject agency; that “time-on-the-job” is a significant predictor of tolerance of corruption among Chicago police officers; that “parenthood” is a significant negative predictor of tolerance; that “education” is not predictive of an officer's tolerance of police corruption; and that when considering the most serious forms of corrupt behavior, “youth” is a significant predictor of tolerance. The data analysis also indicates that approximately one-third of the variance in police officer attitudes toward police corruption can be explained by the combined influence of the individual characteristic variables examined.

Fusions between protein-coding genes are common oncogenic drivers across cancers, typically pairing a proto-oncogene with partner that does not independently drive cancer. In all therapeutically actionable fusions, the proto-oncogene is the drug target, the contributions to oncogenicity of the fusion partner have largely been ignored. We studied the role of BRAF fusion partners and found that they are necessary for transformation. In the setting of KIAA1549::BRAF, the most common fusion protein across brain tumors, we found that KIAA1549 is necessary for the oncogenicity of KIAA1549::BRAF and engenders a striking and specific dependency on the protein O-mannosyltransferase complex (POMT1/2). Specifically, we show that genetic silencing or pharmacologic inhibition of the protein O-mannosyltransferase complex (POMT1/2) reverses fusion-induced transformation, thereby representing a novel and MAPK independent therapeutic target. Furthermore, POMT1/2 is required to glycosylate and enable maturation of the K::B fusion protein. These findings represent a proof-of-concept for targeting the partners in oncogenic fusions as a potential cancer therapeutic strategy.