Background: 30-day mortality might be a useful indicator of avoidable harm to patients from systemic anticancer treatments, but data for this indicator are limited. The Systemic Anti-Cancer Therapy (SACT) dataset collated by Public Health England allows the assessment of factors affecting 30-day mortality in a national patient population. The aim of this first study based on the SACT dataset was to establish national 30-day mortality benchmarks for breast and lung cancer patients receiving SACT in England, and to start to identify where patient care could be improved.
View Article and Find Full Text PDFBMJ Open
July 2016
Objectives: This paper describes the methods used in the International Cancer Benchmarking Partnership Module 4 Survey (ICBPM4) which examines time intervals and routes to cancer diagnosis in 10 jurisdictions. We present the study design with defining and measuring time intervals, identifying patients with cancer, questionnaire development, data management and analyses.
Design And Setting: Recruitment of participants to the ICBPM4 survey is based on cancer registries in each jurisdiction.
The International Cancer Benchmarking Partnership (ICBP) was initiated by the Department of Health in England to study international variation in cancer survival, and to inform policy to improve cancer survival. It is a research collaboration between twelve jurisdictions in six countries: Australia (New South Wales, Victoria), Canada (Alberta, British Columbia, Manitoba, Ontario), Denmark, Norway, Sweden, and the United Kingdom (England, Northern Ireland, Wales). Leadership is provided by policymakers, with academics, clinicians and cancer registries forming an international network to conduct the research.
View Article and Find Full Text PDFDeciphering the role of lymphocyte membrane proteins depends on dissecting the role of a protein in the steady state and on engagement with its ligand. We show that expression of CD6 in T cells limits their responsiveness but that engagement by the physiological ligand CD166 gives costimulation. This costimulatory effect of CD6 is mediated through phosphorylation-dependent binding of a specific tyrosine residue, 662Y, in its cytoplasmic region to the adaptor SLP-76.
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