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The demand for radiation therapy services in New Zealand is growing due to an increasing and ageing population. The radiation therapist (RT) workforce is currently in a vulnerable state and this study aimed to understand RT perceptions on intent to remain in both the workplace and profession. Understanding factors that contribute to satisfaction and retention are important for the development of strategies by healthcare leaders to improve workforce sustainability.

All current practising RTs were invited via email link to complete an online survey. Multivariate regression models were used to investigate any impact of demographic, workplace and professional variables on intent to remain in the workplace and intent to leave the profession.

Three hundred and sixty two (91% response rate) RTs completed the survey. Key findings include a) 33% are thinking of leaving their current workplace with 31% of these intending to leave within the next 12 months; b) 35% intend to change careers before they retire; and c) 25% indicated they would leave the profession if they could. Workplace satisfaction, being challenged and a lack of career development opportunities were common factors that influence intention to leave both the workplace and profession.

Strategies to ensure the sustainability of the RT workforce in New Zealand need to focus on developing a robust framework for career development including advanced practice opportunities that challenge RTs and ensuring workplaces create an environment that promote a sense of pride, camaraderie and flexibility in how they operate.

Strategies to ensure the sustainability of the RT workforce in New Zealand need to focus on developing a robust framework for career development including advanced practice opportunities that challenge RTs and ensuring workplaces create an environment that promote a sense of pride, camaraderie and flexibility in how they operate.Cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6i) namely palbociclib, ribociclib and abemaciclib were granted approval by the European Medicines Agency (EMA) between 2017 and 2018. They are currently prescribed in combination with hormone therapy to treat hormone receptor positive, HER2 negative metastatic or locally advanced breast cancer. Their combination with radiotherapy raises safety concerns as preclinical data enlightened their possible synergistic effect. Moreover, data about toxicity when combining CDK4/6i with radiotherapy are scarce. This review of literature focused on the use of CDK4/6i combined with radiotherapy. PLX5622 datasheet It aimed at listing every published data about such combination so as to understand its possible resulting toxicity in metastatic breast cancer.

Stereotactic body radiotherapy (SBRT) is an established ablative treatment for liver tumors with excellent local control rates. Magnetic resonance imaging guided radiotherapy (MRgRT) provides superior soft tissue contrast and may therefore facilitate a marker-less liver SBRT workflow. The goal of the present study was to investigate feasibility, workflow parameters, toxicity and patient acceptance of MRgSBRT on a 1.5T MR-Linac.

Ten consecutive patients with liver metastases treated on a 1.5T MR-Linac were included in this prospective trial. Tumor delineation was performed on four-dimensional computed tomography scans and both exhale triggered and free-breathing T2 MRI scans from the MR-Linac. An internal target volume based approach was applied. Organ at risk constraints were based on the UKSABR guidelines (Version 6.1). Patient acceptance regarding device specific aspects was assessed and toxicity was scored according to the common toxicity criteria of adverse events, version 5.

Nine of ten tumors werepresents a promising new non-invasive marker-free treatment modality based on high image quality, clinically reasonable in-room times and high patient acceptance. Further studies are necessary to assess clinical outcome, to validate advanced motion management and to explore the benefit of online response adaptive liver SBRT.Munc-18 interacting protein 3 (Mint3) is an activator of hypoxia-inducible factor-1 in cancer cells, macrophages, and cancer-associated fibroblasts under pathological conditions. However, exactly which cells highly express Mint3 in vivo and whether Mint3 depletion affects their physiological functions remain unclear. Here, we surveyed mouse tissues for specific expression of Mint3 by comparing Mint3 expression in wild-type and Mint3-knockout mice. Interestingly, immunohistochemical analyses revealed that Mint3 was highly expressed in islet cells of the pancreas, distal tubular epithelia of the kidney, choroid plexus ependymal cells of the cerebrum, medullary cells of the adrenal gland, and epithelial cells of the seminal gland. We also studied whether Mint3 depletion affects the physiological functions of the islets and kidneys. Mint3-knockout mice did not show any abnormalities in glucose-tolerance and urine-biochemical tests, indicating that Mint3 depletion was compensated for in these organs. Thus, loss of Mint3 might be compensated in the islets and kidneys under physiological conditions in mice.Mutation in the transmembrane protein 65 gene (TMEM65) results in mitochondrial dysfunction and a severe mitochondrial encephalomyopathy phenotype. However, neither the function of TMEM65 nor the cellular responses to its depletion have been fully elucidated. Hence, we knocked down TMEM65 in human cultured cells and analyzed the resulting cellular responses. Depletion of TMEM65 led to a mild increase in ROS generation and upregulation of the mRNA levels of oxidative stress suppressors, such as NFE2L2 and SESN3, indicating that TMEM65 knockdown induced an oxidative stress response. A mild induction of apoptosis was also observed upon depletion of TMEM65. Depletion of TMEM65 upregulated protein levels of the mitochondrial chaperone HSPD1 and mitochondrial protease LONP1, indicating that mitochondrial unfolded protein response (UPRmt) was induced in response to TMEM65 depletion. Additionally, we found that the mitochondrial protein import receptor TOMM22 and HSPA9 (mitochondrial Hsp70), were also upregulated in TMEM65-depleted cells.