Urothelial carcinoma following augmentation cystoplasty: an aggressive variant with distinct clinicopathological characteristics and molecular genetic alterations.
OBJECTIVE
Patients who have undergone intestinal augmentation cystoplasty are at risk for developing latent vesicle malignancy. The aim was to evaluate the histological and immunohistochemical characteristics and molecular genetic alterations in these neoplasms.


RESULTS
Four patients developing urothelial neoplasms after augmentation cystoplasty were included in the current study. The mean age of the patients, including two men and two women, was 37 years. The latency from bladder augmentation to developing malignancy ranged from 17 to 21 years (mean 19 years). All patients died of cancer shortly after diagnosis (mean 5 months). In the morphological evaluation, all tumours were high-grade (grade 3) invasive urothelial carcinoma comprising various architectural patterns with brisk mitoses and tumour necrosis. Three harboured glandular differentiation and the remaining one showed squamous differentiation. All cases revealed abnormal decreasing beta-catenin expression. Two tumours showed nuclear expression of CDX2. On UroVysion fluorescence in situ hybridization (FISH) analysis, all tumours displayed characteristic chromosomal abnormalities. Point mutations of both FGFR3 and p53 genes were identified in one case.


CONCLUSIONS
Urothelial carcinomas developed after augmentation cystoplasty are extremely aggressive and exhibit distinct morphological, immunohistochemical and genetic characteristics. UroVysion FISH analysis may offer a surveillance strategy in patients who undergo augmentation cystoplasty.
Sung
Ming-Tse
MT
Department of Pathology, Chang Gung Memorial Hospital-Kaohsiung Medical Centre, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Zhang
Shaobo
S
Lopez-Beltran
Antonio
A
Montironi
Rodolfo
R
Wang
Mingsheng
M
Davidson
Darrell D
DD
Koch
Michael O
MO
Cain
Mark P
MP
Rink
Richard C
RC
Cheng
Liang
L
D000328:Adult; D000071616:CDX2 Transcription Factor; D002295:Carcinoma, Transitional Cell / Q000235:genetics / Q000473:pathology; D002467:Cell Nucleus / Q000378:metabolism; D002869:Chromosome Aberrations; D003558:Cystoscopy / Q000009:adverse effects*; D005091:Exons; D017809:Fatal Outcome; D005260:Female; D016158:Genes, p53; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence / Q000379:methods; D008297:Male; D008938:Mitosis / Q000235:genetics; D009336:Necrosis / Q000473:pathology; D021141:Nucleic Acid Amplification Techniques; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics*; D012189:Retrospective Studies; D001749:Urinary Bladder Neoplasms / Q000235:genetics / Q000473:pathology; D051176:beta Catenin / Q000235:genetics
D000071616:CDX2 Transcription Factor; C491270:CDX2 protein, human; D018398:Homeodomain Proteins; D051176:beta Catenin; C496365:FGFR3 protein, human; D051498:Receptor, Fibroblast Growth Factor, Type 3