Mesenteric Fibromatosis Mimicking Tumor Recurrence Following Radical Cystectomy and Bladder Replacement.

We report an unusual case of benign tumor mimicking tumor recurrence following radical cystectomy and bladder replacement for high grade urothelial carcinoma.

The isolation and characterization of renal cancer initiating cells from human Wilms' tumour xenografts unveils new therapeutic targets.

There are considerable differences in tumour biology between adult and paediatric cancers. The existence of cancer initiating cells/cancer stem cells (CIC/CSC) in paediatric solid tumours is currently unclear. Here, we show the successful propagation of primary human Wilms' tumour (WT), a common paediatric renal malignancy, in immunodeficient mice, demonstrating the presence of a population of highly proliferative CIC/CSCs capable of serial xenograft initiation. Cell sorting and limiting dilution transplantation analysis of xenograft cells identified WT CSCs that harbour a primitive undifferentiated-NCAM1 expressing-"blastema" phenotype, including a capacity to expand and differentiate into the mature renal-like cell types observed in the primary tumour. WT CSCs, which can be further enriched by aldehyde dehydrogenase activity, overexpressed renal stemness and genes linked to poor patient prognosis, showed preferential protein expression of phosphorylated PKB/Akt and strong reduction of the miR-200 family. Complete eradication of WT in multiple xenograft models was achieved with a human NCAM antibody drug conjugate. The existence of CIC/CSCs in WT provides new therapeutic targets.

Does RNA editing play a role in the development of urinary bladder cancer?

PURPOSE: A-to-I RNA editing is essential for the development of normal cells and is involved in a wide variety of biological pathways. Currently, limited information suggests linkage between changes in RNA editing levels and the development of cancer. We aimed to explore the possible linkage between altered RNA editing levels and the development of human urinary bladder neoplasms. MATERIALS AND METHODS: Thirty-two patients underwent transurethral resection of bladder tumor. Normal and tumoral urinary bladder tissues were obtained from each patient during surgery. Total RNA was extracted from tissue cells and converted by RT-PCR reaction to cDNA molecules for further analysis. We explored known editing sites in RNA encoding for proteins (BLCAP, Cyfip2, FLNA, GluB Q/R) as well as in RNA transcribed from Alu elements in noncoding regions of the genes encoding for CARD11, FANCC, MDM4, BRCA1, and RBBP9 proteins. Editing levels were determined using Sequenom MassARRAY Compact Analyzer. RESULTS: Eleven tumoral tissues obtained were low grade TCC, 14 high grade TCC, 1 CIS, and another 5 inflammation. One sample contained only normal tissue. We got a total number of 30 normal bladder tissue samples and overall 29 paired samples (i.e., normal and tumoral tissues obtained from the same patient). Statistical analysis revealed no significant changes in editing levels between normal and tumoral tissues. CONCLUSIONS: Relying on the results obtained for 9 different editing sites, it can be determined that RNA editing is an epigenetic mechanism that does not participate in the evolution of urinary bladder cancer.

AKT1 E17 K pleckstrin homology domain mutation in urothelial carcinoma.

The PI3K/AKT pathway is frequently activated in human cancer. Recently, a G to A point mutation (E17K) was found in the pleckstrin homology domain of AKT1. We aimed to explore this mutation in cases of urothelial carcinoma. Using chip-based matrix-assisted laser desorption-time-of-flight (MALDI-TOF) mass spectrometer, AKT1 E17K mutation was searched in 26 total RNA samples obtained from 26 patients known to have urothelial carcinoma. Mutation was found in one out of 26 (3.8%) patients - a 46 year old female with a low grade transitional cell carcinoma located to the lamina propria (Ta disease). Our finding is in line with previous studies showing AKT1 E17K mutation to be rare. Yet, further studies are required to determine whether this mutation is indeed related to less aggressive disease and carries better prognosis.

Isolated testicular polyarteritis nodosa mimicking testicular neoplasm-long-term follow-up.

Polyarteritis nodosa is a systemic vasculitis characterized by segmental necrotizing lesions of medium and small-size arteries. Rarely, the inflammatory process is isolated and involves a single organ without systemic manifestations. We describe a patient with isolated polyarteritis nodosa of the testis who presented with a testicular mass mimicking primary testicular tumor. The postoperative laboratory evaluation was negative. Long-term follow-up, without systemic treatment, showed no evidence of recurrence in the remainder of the testis or development of systemic vasculitis.