th perceptions in shaping driving and passenger behaviours, efforts must be made to disseminate appropriate information regarding cannabis-related driving risks to high school students.
  It is important to have an accurate count of physicians and a measurable understanding of their service provision for physician resource planning. Our objective was to compare 2 methods (income percentiles [IP] and service day activities [SVD]) for calculating the supply of full-time (FT) and part-time (PT) primary care physicians (PCPs) as measures of both physician supply counts and level of provider continuity.
 
  Using an observational study design, we compared 2 methods of calculating the supply of PT and FT PCPs for 2011-2015. For the IP approach, the Canadian Institute for Health Information's method was applied to Alberta Health billing data. The SVD method calculated annual service days for fee-for-service PCPs. A simple descriptive analysis was conducted of the supply of PT and FT PCPs.
 
  The 2 methods agreed on the FT versus PT status of 85.2% of PCPs in 2015 but disagreed on the status of 490 PCPs. A total of 239 PCPs were classified as working FT by the IP method but PT by the SVD method. Two hundred and fifty-one PCPs were classified as working PT according by the IP method but FT by the SVD method. The former group of 239 PCPs worked fewer days per week (3.22 v. 4.1) and fewer weekend days per year (8.6 v. 24.1), billed more per year ($300 327 v. $201 834) and saw more patients per day (26.8 v. 17.8) with less continuity of care (38.0% v. 72.0%) than the latter group of 251 PCPs.
 
  The SVD method provides a valid alternative to calculating GP supply that distinguishes groups of physicians that the standard IP methodology does not. Those groups provide very different service; policy-makers may benefit from distinguishing them.
 The SVD method provides a valid alternative to calculating GP supply that distinguishes groups of physicians that the standard IP methodology does not. Those groups provide very different service; policy-makers may benefit from distinguishing them.The one-year and median overall survival (mOS) rates of advanced gastroesophageal adenocarcinomas (GEA) are ∼50% and less then 12 months, respectively. Baseline spatial and temporal molecular heterogeneity of targetable alterations may be a cause of failure of targeted/immunooncologic therapies. This heterogeneity, coupled with infrequent incidence of some biomarkers, has resulted in stalled therapeutic progress. We hypothesized that a personalized treatment strategy, applied at first diagnosis then serially over up to three treatment lines using monoclonal antibodies combined with optimally sequenced chemotherapy, could contend with these hurdles. This was tested using a novel clinical expansion-platform type II design with a survival primary endpoint. Of 68 patients by intention-to-treat, the one-year survival rate was 66% and mOS was 15.7 months, meeting the primary efficacy endpoint (one-sided P = 0.0024). First-line response rate (74%), disease control rate (99%), and median progression-free survival (8.2 months) were superior to historical controls.  https://www.selleckchem.com/products/catechin-hydrate.html  The PANGEA strategy led to improved outcomes warranting a larger randomized study. SIGNIFICANCE This study highlights excellent outcomes achieved by individually optimizing chemotherapy, biomarker profiling, and matching of targeted therapies at baseline and over time for GEA. Testing a predefined treatment strategy resulted in improved outcomes versus historical controls. Therapeutic resistance observed in correlative analyses suggests that dual targeted inhibition may be beneficial.This article is highlighted in the In This Issue feature, p. 211.Hematopoietic-derived cells are integral components of the tumor microenvironment and serve as critical mediators of tumor-host interactions. Host cells derived from myeloid and lymphoid lineages perform well-established functions linked to cancer development, progression, and response to therapy. It is unclear whether host erythroid cells also contribute to shaping the path that cancer can take, but emerging evidence points to this possibility. Here, we show that tumor-promoting environmental stress and tumor-induced hemodynamic changes trigger renal erythropoietin production and erythropoietin-dependent expansion of splenic erythroid cell populations in mice. These erythroid cells display molecular features indicative of an immature erythroid phenotype, such as the expression of both CD71 and TER119 and the retention of intact nuclei, and express genes encoding immune checkpoint molecules. Nucleated erythroid cells with similar properties are present in mouse and human tumor tissues. Antibody-mediated erythropoietin blockade reduces tumor-responsive erythroid cell induction and tumor growth. These findings reveal the potential of tumor-induced erythropoietin and erythroid cells as targets for cancer treatment. IMPLICATIONS Our study identifies erythropoietin and erythroid cells as novel players in tumor-host interactions and highlights the involvement of multiorgan signaling events in their induction in response to environmental stress and tumor growth.c-MYC (MYC) is deregulated in more than 50% of all cancers. While MYC amplification is the most common MYC-deregulating event, many other alterations can increase MYC activity. We thus systematically investigated MYC pathway activity across different tumor types. Using a logistic regression framework, we established tumor type-specific, transcriptomic-based MYC activity scores that can accurately capture MYC activity. We show that MYC activity scores reflect a variety of MYC-regulating mechanisms, including MYCL and/or MYCN amplification, MYC promoter methylation, MYC mRNA expression, lncRNA PVT1 expression, MYC mutations, and viral integrations near the MYC locus. Our MYC activity score incorporates all of these mechanisms, resulting in better prognostic predictions compared with MYC amplification status, MYC promoter methylation, and MYC mRNA expression in several cancer types. In addition, we show that tumor proliferation and immune evasion are likely contributors to this reduction in survival. Finally, we developed a MYC activity signature for liquid tumors in which MYC translocation is commonly observed, suggesting that our approach can be applied to different types of genomic alterations.