Registry data entered by each individual surgeon's team (self-reported) on all 6042 nephrectomy surgeries reported to BAUS during 2012 were analysed to identify all NU surgery. Parameters for analysis included demographics, indication, type of surgery, histopathology and complications (Clavien system) of surgery. Data did not include tumour location or multiplicity, preoperative diagnostic evaluation or details of minimally invasive surgery (MIS) undertaken. Before analysis for this report a central process of 'datacleansing' was undertaken by a BAUS group to address any discrepancy between the listed surgery and the preoperative indication. ResultsIn all, 863 NU surgeries were included, performed by 220 consultant surgeons in 119 centres, and the median (range) number of NU per surgeon and unit was 3 (1-20) and 6 (1-29), respectively. The most common age group was 71-80 years (40%), most were male (64%), and haematuria was the most common presentation (74%). The dominant pathology was upper tract urothelial cancer (89%, 735), with final stage ≥pT2 in 47% (367), and the grade was 1, 2 or 3 in 6% (38), 36% (228) and 58% (362) respectively. Operative technique included MIS in 85% (720) and total reported operative complication rate (any Clavien) was 15% (128), of which Clavien ≥3 was reported in 4% (36), and perioperative death was reported in nine patients (1%). Advantages in favour of MIS included reduced hospital stay (median 5 vs 8 days), reduced major blood loss (3% vs 14%) and reduced transfusion requirement (6% vs 24%). In all, 76 cases (8%) were excluded from analysis based on benign pathology leading to reassignment to the 'simple nephrectomy' category. ConclusionsNU is currently a low-volume operation (median 3 cases/ year) within the remit of the nephrectomy surgeon, but is a safe procedure with a relatively low complication rate. Most NU surgery in the UK is now performed with laparoscopic assistance, with advantages including reduced major blood loss, reduced transfusion requirement and shorter hospital stay.
BACKGROUND Numerous epidemiological studies have highlighted the protective role of immunoglobulin E-mediated allergic diseases on glioblastoma (GBM) susceptibility and prognosis. However, the mechanistic explanations behind these phenomena remain unexplored. Our objective was to set up a preclinical model and investigate the mechanisms underlying such protection to improve our understanding of the crosstalk between immune system and brain tumor development. MATERIAL AND METHODS A mouse model of allergic airway inflammation (AAI) induced by repeated nasal instillation of House Dust Mite extract was initiated before intracranial implantation of GL261 glioma cells, in both immunocompetent (C57BL/6) and immunodeficient (RAG-KO) mice. Tumor take and tumor growth were monitored by MRI. Central (microglia) and peripheral (spleen, bone marrow) immune cells were characterized by flow cytometry. The response of microglia was further assessed by RNA sequencing. Impact of candidate genes on patient survival was characterized by Cox regression analysis using data from TCGA and CGGA. RESULTS Following AAI induction in C57BL/6 mice, engraftment of GL261 cells in the brain was delayed and tumor growth rate was reduced. This correlated with an increase in survival of the mice and was accompanied by increased effector memory T-cells in the circulation. Of note, the survival benefit was lost in RAG-KO mice devoid of adaptive immunity. At the level of the brain, we observed enhanced secretion of TNFα and IL6 in microglia ex vivo. AAI induced a transcriptional reprogramming of microglia towards a pro-inflammatory-like state. We identified an allergy-related microglia gene signature that is associated with improved prognosis of glioma patients. CONCLUSION Our results demonstrate that AAI limits both tumor take and GBM progression in mice, providing a preclinical model to study the role of allergic inflammation in GBM susceptibility and prognosis, respectively. At the functional level, we identify a potentiation of microglial and adaptive anti-tumoral immunity. Further investigations are warranted to shed light on the reciprocal crosstalk between microglial reprogramming and peripheral immunity in the context of allergies and brain tumors.
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