Pharmacists are the third largest group of healthcare professionals worldwide, but are underused in the delivery of diabetes care. The aim of this narrative was to describe how integration of community pharmacy services into existing healthcare models may improve diabetes care. Relevant literature exploring pharmacy-led interventions for diabetes were identified from a search of Medline, Embase and Cinahl online databases. This review highlights that community pharmacists are accessible, experts in medicine management, trusted by the public and able to achieve financial savings. They are poorly integrated into existing healthcare models, and commissioning arrangements can be poorly perceived by the public and those working in primary care.  https://www.selleckchem.com/products/GDC-0980-RG7422.html  Community pharmacy interventions in type 2 diabetes have similar, if not greater effects compared to those delivered by other healthcare professionals. It was concluded that community pharmacy interventions in diabetes are feasible, acceptable and deliver improved health outcomes. Future work should build public recognition of pharmacists and improve communication between them and other healthcare professionals. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.Clinical trials are considered the gold-standard method for the evaluation of healthcare interventions. However, randomised control trials are complex to perform and many researchers, especially those in the early stages of their career, can find it challenging to know where to start set up, contribute to or lead a trial. This guide provides an introduction to trials and also practical advice to help potential investigators complete their clinical trial to time and to budget by signposting the pathway through the complex regulatory landscape. The authors draw on their own recent experiences of running clinical trials and provide tips and tricks for troubleshooting common problems encountered including trial design and documentation. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.To identify, evaluate and refine a journal club (JC) format that increases faculty and resident engagement. An initial needs assessment followed by a trial of three JC formats traditional single presenter, debate style and facilitated small group discussion was piloted over 6 months. Anonymous feedback was collected. The facilitated small group format was chosen. Narrative and quantitative feedback were collected from residents and faculty at 6-month intervals for the next 24 months. Changes to the format were made using feedback. Fourteen residents (n=20, 70%) and 10 faculty (n=20, 50%) completed baseline surveys. We initially observed low resident (8/14, 57%) interest in JCs. Additionally, 9/14 (64%) of residents and 1/15 (7%) of faculty reported low confidence presenting articles publicly. After implementation of the new JC format, resident reported enjoyment, on a scale of 1-5, improved from 3.6 to 4.4 (p less then 0.01). We observed improvement in resident confidence in the ability to critique a paper (2.7 to 4.1, p less then 0.01) and in confidence speaking in front of both peers (3.8 to 4.6, p less then 0.01) and faculty (3.0 to 3.8, p=0.04). Faculty confidence with literature critique decreased (from 4.2 to 3.8), but enjoyment remained stable (4.3 to 4.2). A facilitated small group JC format was preferred in our programme. We observed measurable improvements in both resident interest and confidence, as well as sustained faculty interest in JCs. We fostered an environment of inquiry and identified areas of continued professional development. © Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.TACC3, a TACC family member, is frequently upregulated in a broad spectrum of cancers, including breast cancer. It plays critical roles in protecting microtubule stability and centrosome integrity that is often dysregulated in cancers; therefore, making TACC3 a highly attractive therapeutic target. Here, we identified a new TACC3-targeting chemotype, BO-264, through the screening of in-house compound collection. Direct interaction between BO-264 and TACC3 was validated by using several biochemical methods, including drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA) and isothermal titration calorimetry (ITC). BO-264 demonstrated superior anti-proliferative activity to the two currently reported TACC3 inhibitors, especially in aggressive breast cancer subtypes, basal and HER2+, via spindle assembly checkpoint (SAC)-dependent mitotic arrest, DNA damage and apoptosis, while the cytotoxicity against normal breast cells was negligible. Furthermore, BO-264 significantly decreased centrosomal TACC3 during both mitosis and interphase. BO-264 displayed potent anti-proliferative activity (~90% have less than 1 μM GI50 value) in the NCI-60 cell line panel compromising nine different cancer types. Noteworthy, BO-264 significantly inhibited the growth of cells harboring FGFR3-TACC3 fusion, an oncogenic driver in diverse malignancies. Importantly, its oral administration significantly impaired tumor growth in immunocompromised and immunocompetent breast and colon cancer mouse models, and increased survival without any major toxicity. Finally, TACC3 expression has been identified as strong independent prognostic factor in breast cancer and strongly prognostic in several different cancers. Overall, we identified a novel and highly potent TACC3 inhibitor as a novel potential anti-cancer agent, inducing spindle abnormalities and mitotic cell death. Copyright ©2020, American Association for Cancer Research.Alectinib is used as a first-line treatment for anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer (NSCLC). Whereas other ALK inhibitors have been reported to be involved in resistance to ATP binding cassette (ABC) transporters, no data are available regarding the association between resistance to alectinib and ABC transporters. To investigate whether ABC transporters contribute to alectinib resistance, ABC transporter expression in alectinib-resistant cell lines derived from a patient with ALK-rearranged NSCLC and from H2228 lung cancer cells was evaluated and compared with that in each parent cell type. ATP-binding cassette subfamily C member 11 (ABCC11) expression was significantly increased in alectinib-resistant cell lines compared to that in alectinib-sensitive lines. ABCC11 inhibition increased sensitivity to alectinib in vitro. ABCC11-overexpressing cells were established by transfection of an ABCC11 expression vector into H2228 cells, while control cells were established by transfecting H2228 cells with an empty vector.