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9% (95% CI 27.5% to 28.2%) versus 27.9% (95% CI 27.5% to 28.2%)), when death is considered as a competing event. In the adjusted cause-specific Cox proportional hazards model, ESAS assessment was associated with a 6% increase in palliative care services (HR 1.06, 95% CI 1.04 to 1.08).

We have demonstrated that patients exposed to ESAS were more likely to receive palliative care services compared with patients who were not exposed. This observation provides real-world data of the impact of routine assessment with a patient-reported outcome.

We have demonstrated that patients exposed to ESAS were more likely to receive palliative care services compared with patients who were not exposed. This observation provides real-world data of the impact of routine assessment with a patient-reported outcome.Exercise is a well-established factor which improves outcomes of oncological patients during curative treatment as well as in cancer survivors. However, the role of physical activity in metastatic disease, due to the deficiency of high-level evidence from prospective clinical trials, remains a partially unexplored field of research. Additionally, no specific guidelines related to exercise for persons with advanced cancer have been developed so far. Unfortunately, this research deficit may effectively prevent physicians from prescribing adequate and safe recommendations on physical activity to their patients. In an attempt to fill this gap in clinical practice, we present here an up-to-date review of potential benefits of exercise interventions in relation to the survival, quality of life and supportive care for patients with metastatic cancer. We also review the data on the safety of physical activity with special emphasis on elderly populations or individuals with bone metastases. Finally, we discuss the most relevant clinical factors that should be considered during exercise qualification. In conclusion, physical activity is an important tool for improving the outcomes of people undergoing anticancer therapy for metastatic disease. However, the training should be tailored individually to the patient’s functional status, comorbidities and preferences. Physical activity should become a standard component of every metastatic cancer care plan.

Patients with gastrointestinal (GI) cancers experience a high symptom burden due to the effects of both cancer and treatment. As such, trials assessing symptom burden and supportive interventions are crucial. Here, we characterise the landscape of phase III GI cancer clinical trials and explore study outcomes centred on the patient’s quality of life (QoL).

We searched ClinicalTrials.gov for phase III randomised controlled trials (RCTs) registered between 2000 and 2017 that are assessing a therapeutic intervention in adult patients with cancer and grouped trials by GI disease sites.

Overall, we identified 76 phase III trials specific to GI cancers that enrolled a total of 53 725 patients. When analysing the primary outcomes measured, the vast majority of studies (n=71, 86%) measured disease-related endpoints such as progression-free survival or overall survival. All trials had a secondary endpoint that measured adverse events, but only 30 trials (39%) included QoL measures as secondary endpoints. Of the 30 trials that included QoL secondary endpoints, only 16 (53%) reported these results. Only five trials (7%) assessed interventions aimed at supportive measures impacting disease-related or treatment-related toxicity. read more None of the supportive trials included QoL as a primary endpoint and only two of these trials (40%) included QoL as a secondary endpoint.

Most GI cancer trials failed to incorporate patient-centred outcomes or QoL measures when studying new interventions. These findings call for greater integration of patient-reported metrics, which may lead to better care and outcomes for patients with GI malignancies.

Most GI cancer trials failed to incorporate patient-centred outcomes or QoL measures when studying new interventions. These findings call for greater integration of patient-reported metrics, which may lead to better care and outcomes for patients with GI malignancies.Iron-sulfur (Fe-S) clusters are inorganic cofactors that are present in all kingdoms of life as part of a large number of proteins involved in several cellular processes, including DNA replication and metabolism. In this work, we demonstrate an additional role for two Fe-S cluster genes in biotic stress responses in plants. Eleven Fe-S cluster genes, including the NITROGEN FIXATION S-LIKE1 (NFS1) and its interactor FRATAXIN (FH), when silenced in Nicotiana benthamiana, compromised nonhost resistance to Pseudomonas syringae pv. tomato T1. NbNFS1 expression was induced by pathogens and salicylic acid. Arabidopsis (Arabidopsis thaliana) atnfs and atfh mutants, with reduced AtNFS1 or AtFH gene expression, respectively, showed increased susceptibility to both host and nonhost pathogen infection. Arabidopsis AtNFS1 and AtFH overexpressor lines displayed decreased susceptibility to infection by host pathogen Psyringae pv. tomato DC3000. The AtNFS1 overexpression line exhibited constitutive upregulation of several defense-related genes and enrichment of gene ontology terms related to immunity and salicylic acid responses. Our results demonstrate that NFS1 and its interactor FH are involved not only in nonhost resistance but also in basal resistance, suggesting a new role of the Fe-S cluster pathway in plant immunity.Wood formation is a complex process that involves cell differentiation, cell expansion, secondary wall deposition, and programmed cell death. We constructed a four-layer wood formation transcriptional regulatory network (TRN) in Populus trichocarpa (black cottonwood) that has four Secondary wall-associated NAC-Domain1 (PtrSND1) transcription factor (TF) family members as the top-layer regulators. We characterized the function of a MYB (PtrMYB161) TF in this PtrSND1-TRN, using transgenic Ptrichocarpa cells and whole plants. PtrMYB161 is a third-layer regulator that directly transactivates five wood formation genes. Overexpression of PtrMYB161 in P. trichocarpa (OE-PtrMYB161) led to reduced wood, altered cell type proportions, and inhibited growth. Integrative analysis of wood cell-based chromatin-binding assays with OE-PtrMYB161 transcriptomics revealed a feedback regulation system in the PtrSND1-TRN, where PtrMYB161 represses all four top-layer regulators and one second-layer regulator, PtrMYB021, possibly affecting many downstream TFs in, and likely beyond, the TRN, to generate the observed phenotypic changes.