Introduction Pressurized intraperitoneal aerosol chemotherapy (PIPAC) is a novel drug delivery system with superior pharmacological properties for treating peritoneal metastasis (PM). Safety and efficacy results of PIPAC with cisplatin/doxorubicin or oxaliplatin from a registry cohort are presented. Methods IRB-approved registry study. Retrospective analysis. No predefined inclusion criteria, individual therapeutic recommendation by the interdisciplinary tumor board. Safety assessment with CTCAE 4.0. Histological assessment of tumor response by an independent pathologist using the 4-tied peritoneal regression grading system (PRGS). Mean PRGS and ascites volume were assessed at each PIPAC. Results A total of 142 PIPAC procedures were scheduled in 71 consecutive patients with PM from gastric (n = 26), colorectal (n = 17), hepatobiliary/pancreatic (n = 9), ovarian (n = 6), appendiceal (n = 5) origin, pseudomyxoma peritonei (n = 4), and other tumors (n = 3). Mean age was 58 ± 13 years. Patients were heavily pretreated. Mean PCI was 19 ± 13. Laparoscopic nonaccess rate was 11/142 procedures (7.7%). Mean number of PIPAC/patient was 2. All patients were eligible for safety analysis. There was no procedure-related mortality. There were 2.8% intraoperative and 4.9% postoperative complications. 39 patients underwent more than one PIPAC and were eligible for efficacy analysis, and PRGS could be assessed in 36 of them. In 24 patients (67%), PRGS improved or remained unchanged at PIPAC#2, reflecting tumor regression or stable disease. Ascites was present in 24 patients and diminished significantly under therapy. Median survival was 11.8 months (95% CI: 7.45–16.2 months) from PIPAC#1. Conclusion PIPAC is feasible, safe, and well-tolerated and can induce histological regression in a significant proportion of pretreated PM patients. This trial is registered with NCT03210298.

Intravesical instillation of Bi-anti-EGFR monoclonal antibody was well tolerated and showed therapeutic efficacy. Repeated instillation and/or instillation of higher activities of theBi-immunoconjugate might lead to better therapeutic outcomes. A phase I clinical trial is planned.

It has been suggested that chromosome 7q32 contains genes that influence the progression of prostate cancer from latent to invasive disease. In an attempt to confirm this linkage to prostate cancer aggressiveness, 100 German prostate cancer families were genotyped using a panel of eight polymorphic markers on chromosome 7q. We used a multipoint allele sharing method based upon a likelihood ratio test implemented in GENEHUNTERPLUS v1.2 in order to calculate the nonparametric Z lr and the associated LOD scores. We applied the aggressiveness of prostate cancer given by the pathological tumour grade of each individual, and the mean age of onset of a family as covariates, and constructed two weighted models. The first (weight 0 -1 model) puts weights on families with at least two cases of GIII prostate cancer. The second (weight 0 -2 model) also adds weights to families with early and late onset cancer respectively. The unweighted analysis gave no evidence of linkage to chromosome 7q. The Z lr scores increased when including the covariates, to 2.60 (P=0.005) using the weight 0 -1 and to 3.02 (P=0.001) using the weight 0 -2 model for late onset prostate cancer. The associated LOD scores were respectively 1.47 (P=0.009) and 1.98 (P=0.002). The markers that gave most evidence for linkage were exactly in the range of the published prostate cancer aggressiveness region. Our results support a widespread relevance of this locus and suggest that aggressive and late onset prostate cancer is linked to chromosme 7q31-33 in the German population.

BackgroundPrevious investigations on the association of human papillomavirus (HPV) and human bladder cancer have led to conflicting results. The aim of this study was to determine if low and high risk HPV play a role in the etiology of superficial low grade and invasive high grade urothelial carcinoma of the bladder.MethodsWe prospectively collected tumor samples of urothelial carcinoma of the bladder from 109 patients treated with transurethral resection or cystectomy, with bladder tissue from transurethral resection of the prostate serving as control. Unfixed, frozen tumor samples were analyzed for the presence of 14 high risk HPV types using real time PCR. Additionally, all specimens were tested for 35 low risk HPV types with a conventional PCR using degenerate primers located in the L1 region. Six frozen samples of cervical carcinoma served as positive controls.ResultsWe included 109 cases of bladder cancer with 41 superficial (pTa low grade) tumors, 56 invasive (pT1-T4) high grade tumors and 12 others (pTa high grade + pTis). We have not detected HPV-DNA in any sample (95 % Confidence Interval [CI] 0–3.3 %), superficial tumors (95 % CI 0–6.4 %) or in invasive tumors (95 % CI 0–8.6 %) with correct positive controls.ConclusionsUsing a broad, sensitive assay with prospectively collected specimens of a Central European population we could not detect HPV-DNA in any of the cases. Our results suggest that it is unlikely that HPV infections play a major role in the development of urothelial bladder cancer.

AUF results in major hemorrhage and warrants time-efficient diagnosis and treatment. Awareness is key. When AUF is considered, interventional angiography should promptly be performed. Fistula detection can be improved by guidewire manipulation. Pre-interventional CT angiogram may be omitted due to low sensitivity. Endovascular repair with stenting and/or coiling is effective and safe.