and 192 PNs done without clamping (group B). The median tumour size was slightly larger in group B than in group A (3.0 vs 2.8 cm, P = 0.002).• There was no difference in preoperative eGFR ( P = 0.304) or the prevalence of solitary kidney ( P = 0.69).• Median estimated blood loss was 300 mL higher in the unclamped group ( P < 0.001) and was associated with a higher rate of transfusion ( P = 0.001). There was no difference the positive margin rate or rate of recurrence ( P = 0.60).• The median percentage change in eGFR was a 12.3% decrease for group A and a 9.8% decrease for group B at 1 year ( P = 0.037). In the subset of patients with solitary kidneys, the median change in eGFR was a 21% decrease in group A and a 4.4% decrease in group B at 1 year ( P = 0.027).• The rate of complications was similar in groups A and B (11.2 vs 9.9%, P = 0.72). There were no perioperative deaths.

OBJECTIVE To identify changes associated with P‐cadherin expression in bladder cancer and evaluate the potential role of such events in determining the clinical outcome and cell behaviour, as the function of P‐cadherin in normal epithelium is unknown, as is its potential role in neoplastic progression in different cancers. MATERIALS AND METHODS In all, 536 bladder tumour specimens from 408 patients were assembled in seven tissue microarrays. Paraffin sections from each array were processed for immunohistochemistry to assess the expression of P‐cadherin. The expression of P‐cadherin was forced using lipofectin, followed by an assessment of migration and invasion potential using standard in vitro assays. RESULTS The absence of P‐cadherin staining was associated with muscle‐invasive disease, grade 3 (P < 0.001) and nodal disease (P = 0.009). Similar results were obtained when considering cytoplasmic and unrestricted localization of P‐cadherin (P < 0.001), except for nodal involvement. The group with cytoplasmic location of P‐cadherin showed a shorter cancer‐specific survival than the group with membrane location of P‐cadherin (P = 0.03). Forced expression of P‐cadherin in EJ and UM‐UC‐3 cells, that constitutively lack P‐cadherin expression, resulted in modulation of catenin expression and enhanced migration of EJ and UM‐UC‐3/P‐cadherin transfectants (>200%). CONCLUSIONS These results showed that loss of expression, cytoplasmic relocation or unrestricted tissue location of P‐cadherin was associated with a poor clinical outcome and prognosis in bladder cancer. From the in vitro work it is evident that P‐cadherin plays a role in regulating the migration potential of bladder carcinoma cells.

Patients reported to have sigmoid DD were identified and the incidence of sigmoid colon cancer was recorded. Chi squared with Yates correlation statistical analysis was performed with a P value of < 0.05 considered significant.In the 5-year study period, 140 459 BCSP colonoscopies were performed. Sigmoid colon cancers were found in 3.4% of procedures (n = 4738). Sigmoid DD was documented in 27.4% of procedures (n = 38 480). Patients with sigmoid DD were less likely to have coexisting sigmoid colon cancer; 3.99% of those patients without sigmoid DD had sigmoid colon cancer vs 2.23% of those patients with sigmoid colon cancer, P < 0.0001 (Table 1).Based on our preliminary data, an inverse association has been identified between sigmoid colon cancer and sigmoid DD which has not previously been reported. Potential explanations include an increased likelihood of a positive faecal occult blood result (FOBT) with DD, under-reporting of DD when a cancer is detected and missed lesions within the diverticular segment. Alternatively, there may be a true protective effect of DD, which could be related to changes in bacterial flora in the sigmoid diverticular segment. Further studies in non-FOBT populations are warranted. References1 Faucheron JL, Roblin X, Bichard P, Heluwaert F. The prevalence of right-sided colonic diverticulosis and diverticular haemorrhage. Colorectal Dis 2013; 15: e266-70. 2 Stefansson T, Ekbom A, Spar en P, P ahlman L. Increased risk of left side colon cancer in patients with diverticular disease.

Objective To determine the prognostic value of the over-was not linked to recurrence (P=0.5) but was related to worsening histological stage (P<0.01) and increas-expression of p53 protein as determined by immunohistochemistry in recurrent progressive transitional ing grade (P<0.01). Regression analysis showed that overexpression of p53 for the primary tumour was cell carcinomas of the bladder. Patients and methods A total of 222 tumours from 86 not of predictive prognostic value for death from bladder cancer, time to progression or time to recur-patients with recurrent disease, 20 from patients with no evidence of recurrence after resection of initial rence. Tumour grade was the only variable of prognostic value in all the statistical models. Patients with tumour and 11 normal bladder (controls) were investigated. Using a microwave technique to expose overexpression of p53 showed no reduction in overall survival. antigens, formalin-fixed sections were immunohistochemically stained for p53 using a polyclonal anti-Conclusion These findings suggest that overexpression of p53, as determined immunohistochemically, serum. Two independent observers scored the sections for evidence of overexpression of p53.appears to have no predictive prognostic value over stage and grade in bladder tumours. Results Of 86 patients with recurrent disease, 51 demonstrated overexpression of p53 protein, as did six of 20 Keywords p53 overexpression, bladder cancer, p53 immunohistochemistry, prognosis patients with non-recurrent disease. Overexpression lates and switches off replication to allow time for extra