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not available at time of publication. Abstract not available at time of publication. Retrospective studies on male breast cancer (MBC) have suff ered from small numbers of cases available from any one centre; thus a signifi cant problem in eff ectively studying this disease is accruing suffi ciently large numbers to allow comparative analysis of biomarkers associated with response. Using a coordinated multicentre approach, we present the fi rst large-scale study to address the relevance of the expression of hormone receptors in MBC and female breast cancer (FBC) using immunohistochemistry combined with a novel bioinformatics approach. Following ethical approval, 523 archival blocks (260 MBCs and 263 matched FBCs) were obtained retrospectively. Tissue microarrays were constructed and sections stained for ERα, ERβ1, ERβ2, ERβ5, total PR, PRA, PRB and AR and typed using CK5/6, CK14, CK18 and CK19 by immunohistochemistry. Following scoring, a range of ordination techniques were conducted on the datasets including hierarchical clustering and principal component analysis (PCA) + ) were infrequent in both. Hierarchical clustering revealed common clusters between MBC and FBC including total PR-PRA-PRB and ERβ1/2 clusters. ERα occurred on distinct clusters between males and females. AR, ERβ1, ERβ2 and ERβ5 all existed on the same cluster but with a diff erent substructure, particularly around the positioning of AR. ERα associated with this cluster in the male but not the female group. PCA confi rmed that in both groups strong infl uences came from PR-PRA-PRB. In MBC strong infl uences additionally came from AR and ERβ1, ERβ2 and ERβ5, whereas in FBC strong infl uences came from ERα alone. Our data support the hypothesis that breast cancer is biologically diff erent in male and females, which could have implications for therapy. Introduction The response rarely sustains long among the responders for Herceptin (trastuzumab) monotherapy treatment. It is still poorly understood how Herceptin exerts its mechanism of action and how the acquired resistance to this drug occurs. Materials and methods We used a multidisciplinary approach including fl uorescence resonance energy transfer and biochemical methods to assess the eff ects of Herceptin on various signalling pathways and to determine the acquired resistance mechanisms of Herceptin in various HER2-positive breast cell lines and a BT474 xenograft model. Results We have shown that Herceptin does not decrease HER2 phosphorylation despite the eff ect on HER2 receptor downregulation. HER2 phosphorylation is maintained by the activation of EGFR, HER3 and HER4 via their dimerisation with HER2 in breast cancer cells. The activation of EGFR, HER3 and HER4 is induced by HER ligand release, including heregulin and betacellulin. The release of HER ligands is mediated by ADAM proteases including ADAM17/TACE. Furthermore, we demonstrated that the feedback loop involving HER ligands and ADAM proteases is activated due to a decrease in PKB phosphorylation induced by Herceptin t...

Transplantation is the preferred treatment option for end-stage renal disease as it offers superior results and patient reported outcomes in comparison to dialysis. Patients treated with a transplant live longer, healthier and more independent lives. Transplantation is also more cost-effective, reducing the overall burden of renal disease. Despite the rising incidence of renal failure, the uptake of living donor kidney transplantation has been static across the UK for several years. Among transplantation, living donation offers a number of advantages compared with deceased donor transplantation. The procedure is more likely to be performed pre-dialysis and the elective nature allows for better perioperative planning. Awareness for living donation processes among healthcare professionals, patients and the public appears to be poor. Sharing information regarding the process will help educate colleagues, dispel myths and, crucially, allow patients the opportunity to talk about this treatment option with their hospital doctor.

1961recombinant interferon aA (Hoffmann-La Roche), receiving 9 MU daily intramuscularly for eight days followed by 3 MU daily for a week. At this stage the nodules on the chest wall were observed to be regressing. She developed malaise and headache, so during the third and fourth weeks of treatment the dose of interferon was reduced to 3 MU thrice weekly. By this time the nodules had completely regressed. After a week's break in treatment interferon 3 MU three times weekly was resumed for a further six weeks. The nodules had appeared again by week 9, and an excision biopsy of one showed epithelioid granulomas as before ( figure). The The morbidity that is associated with immunosuppressive treatment given for the rejection of a renal transplant makes the accurate identification and exclusion of non-immunological causes of deteriorating function essential. We report a case in which a ureteric calculus originating in the donor kidney (apparently unrecognised at transplantation) produced the clinical signs of acute rejection in the recipient. Case reportA 24 year old man with end stage renal failure received a cadaveric renal transplant, which functioned immediately. During the first month after transplantation two episodes of deteriorating renal function (with normal isotope renograms and abdominal ultrasound) were diagnosed and treated as acute rejection. One month later he presented with deteriorating renal function and this time the transplanted kidney was enlarged. An abdominal ultrasound examination showed a dilated ureter and an intravenous urogram showed a calculus 0-6 cm in diameter in the lower ureter (see figure). Attempts to remove the calculus by Dormia extraction failed and the stone was removed by ureterolithotomy. The patient's recovery from the operation was uneventful, his renal function remained stable with a creatinine concentration of less than 200 itmol/l for a year, and the bone biochemistry remained normal throughout. The calculus contained calcium and phosphate.

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