Hidenobu Yamamoto

Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene

Loss of ABO blood group antigen expression has been reported in transitional cell carcinoma (TCC) of the bladder. Synthesis of the ABO blood group antigen was genetically determined by allelic variants of the ABO gene assigned on 9q34.1. We analyzed loss of heterozygosity (LOH) and promoter hypermethylation of the ABO gene in TCC and compared them with alterations of A antigen expression in TCC, dysplasia and normal urothelium. A total of 81 samples of TCC of the bladder obtained from transurethral resection (TUR) (n=44) and radical cystectomy (n=37) were examined. Expression of the A antigen was evaluated by immunohistochemical staining (IHC) using anti-A antigen monoclonal antibody. LOH of the ABO gene locus was examined by blunt-end single-strand DNA conformational polymorphism (SSCP) analysis using flouresence-based auto sequencer. Promoter hypermethylation of the ABO gene were examined by bisulfite PCR-SSCP (BiPS) analysis and/or methylation-specific PCR (MSP). Loss of A allele and/or hypermethylation were significantly associated with abnormal expression of the A antigen in cases undergoing TUR (P=0.02) and radical cystectomy (P=0.0005). For the analysis of the concomitant dysplasia in 23 cases with TCC of the bladder, the expression of the A antigen was maintained, regardless of the A allelic loss or methylation status in the tumor. In conclusion, A allelic loss and hypermethylation in the promoter region of the ABO gene showed significant correlation with reduction of A antigen expression in TCC, while the expression of the A antigen is maintained in concomitant dysplasia or normal urothelium, suggesting that loss of the ABO gene and/or its promoter hypermethylation is a specific marker for TCC.

Multilocular cystic renal cell carcinoma: a clinicopathological, immuno- and lectin histochemical study of nine cases

Multilocular cystic renal cell carcinoma (MCRCC) is an uncommon variant of renal neoplasm and its histogenesis is unclear. The aim of this study was to use immuno‐ and lectin histochemistry to delineate histochemical patterns which might indicate the histogenetic origin of MCRCC from a particular part or parts of the nephron. We present our experience with nine cases of MCRCC. Fifteen cases of renal cell carcinoma with cystic degeneration (RCC‐CD) were selected for comparison with MCRCC. We carried out clinicopathological and immunohistochemical examinations of the MCRCC cases. Clinically, the prognosis of the patients was quite good, in that all nine patients are alive and without recurrence at the time of this report. The MCRCCs reacted strongly in a higher proportion of cases with the distal nephron markers, such as peanut agglutinin (PNA, 88.9%) and MUC1–core antibody (MUC1, 100%), but none reacted preferentially with proximal nephron markers such as vimentin, Leu M1 and Lotus tetragonolobus (LTA). The RCC‐CD tumours reacted with vimentin (40%), Leu M1 (66.7%) and LTA (86.7%). Except for two cases, the RCC‐CD tumours did not react with PNA or MUC1 core antibody. These results illustrate the different patterns of expression of MCRCC and RCC‐CD and suggest that MCRCC originates from the distal nephron. Therefore, MCRCC should be differentiated from other types of renal cell carcinoma on the basis of the histogenesis of the tumour and the clinicopathological findings.

Erratum: Loss of blood group A antigen expression in bladder cancer caused by allelic loss and/or methylation of the ABO gene (Laboratory Investigation (2005) 85 (895-907) DOI: 10.1038/sj.labinvest.3700268))

Correction to: Laboratory Investigation (2005) 85, 895–907. doi:10.1038/sj.labinvest.3700268 Following the publication of the above paper, the author has identified an error in the affiliation of Dr Setsuo Hirohashi. The correct affiliation for Dr Hirohashi is shown above.

A modified procedure for construction of a Kock continent ileal urinary reservoir: Nonafferent limb procedure

SummaryA modified technique for the construction of a Kock continent ileal urinary reservoir (Koch pouch) is reported. Our procedure avoids the afferent limb mechanism by direct uretero-pouch anastomosis using the Le Duc-Camey procedure; the nipple valve of the efferent limb is fixed directly to the pouch wall by the King procedure. This modified procedure was used in five patients with invasive bladder cancer, and the postoperative condition of the urinary tracts were periodically evaluated by image diagnostic techniques. Neither hydronephrosis nor hydroureter was observed during the study period. Pouchography and pouchometry were done in all cases studied; no pouch-ureteral reflux was observed, and both day-and night-time continence were maintained in all cases. No patient has thus far had problems with selfcatheterization. This modified technique could be a promising operative approach for the construction of a continent ileal urinary reservoir.