Application Of Multi-Molecular Protein Markers And Chromosome Anomaly Detection In Diagnosis And Differential Diagnosis Of Bladder Urothelial Tumors

【AIM】 In the different types of bladder urothelial tumors, multi-molecular proteinmarkers (including CK20, P63, P53, CK7, Ki67) were detected by immunohistochemistry(IHC), and chromosomes3、7、17and gene P16were analysised by fluorescence in situhybridization（FISH）, which were to analyse its clinical significance for diagnosis anddifferential diagnosis of bladder urothelial tumors.【METHODS】1. The first section: CK20, P63, P53, CK7, Ki67protein were examined by EliVision TMplus IHC in the180bladder urothelial lesions (including normal mucosa, glandular cystitis,inverted papilloma, low malignant potential of papillary urothelial tumors, non invasiveurothelial carcinoma, infiltrating urothelial carcinoma, which were divided into6groups(A, B,C, D, E, F), and each group was30cases), which collected from Fuzhou general hospital ofNanjing Military Command between2004and2010, and analyse its clinical significance fordiagnosis and differential diagnosis of bladder urothelial tumors.2. The second part: chromosome3、7、17and P16genes were analyse by FISH in the eachgroup of180bladder urothelial lesions, and reaserch its sensitivity and specificity forurothelial malignant tumor.【RESULTS】1. The overexpression rates of CK7were100.0%(30/30) in all of groups; Theoverexpression rates of P63were80.0%(24/30),93.3%(28/30),86.7%(26/30),93.3%(28/30) in A, B, C, D groups respectively, and100.0%positive in E，F groups; CK20showednegative in the groups of A,B,C,D，while the overexpression rates in E,F group was as high as16.7%(5/30) and40.0%(12/30) respectively, and which was arising along with the increased severity of the lesions.,The positive rates of tumor cells for P53showed a raising trend in eachgroup,which were3.3%(1/30),6.7%(2/30),26.7%(8/30),26.7%(8/30),40.0%(12/30) and80.0%(24/30) in A, B, C, D, E, F groups respectively, the positive rates of tumor cells forKi67also were gradually raised, which showed≤1%in the A, B, C groups, and3%-10%,8%-15%,≥20%in D, E, F groups.2. According to the FISH analysis, chromosome3was normal in A, B and C groups, and theamplification rates were3.3%(1/30),10.0%(3/30) and80.0%(24/30) in D,E,F groups; Therewas no abnormal of chromosome7observed in A, B and E groups, the amplification rateswere3.3%(1/30),6.7%(2/30) and86.7%(26/30) in C, D, F group; Chromosome17wasnormal in A, B and C groups, and the amplification rate were3.3%(1/30),3.3%(1/30) and73.3%(22/30) in D, E, F groups; There was no abnormal of P16genes observed in A andB groups, and the amplification rate were0%(0/30),0%(0/30),3.3%(1/30),40.0%(12/30),the gene missing rate were3.3%(1/30),3.3%(1/30),6.7%(2/30),60.0%(18/30) respectivelyin C, D, E, F group; The rates of≥2indexes abnormality in each groups were0%、0%、3.3%、6.7%、10.0%、100.0%. According to the FISH analysis, It was normal in A and Bgroups, and the sensitivities were3.3%、6.7%、10.0%、100.0%and specificities were2.8%、5.6%、8.3%、83.3%in C、D、E、F groups respectively。【CONCLUSION】 CK7and P53can be used as a good protein markers for urothelial tumors;CK20may become to be a very good reference index for the diagnosis of malignant bladderurothelial tumors, and Ki67also can provide a convenience for the diagnosis and differentialdiagnosis of benign and malignant bladder urothelial tumors; P63overexpression has noclinical significance for bladder tumor.Different types of bladder papillary urothelial lesions showed different degrees anddifferent chromosomes abnormality and P16genes amplification and loss, however, thecomplexity degree of aneuploid diversity and signal style were low in all of the benign tumorsand urothelial non-invasive carcinoma; Almost all dense signal were observed in invasiveurothelial carcinoma.The examination of multi-molecular protein markers by IHC and chromosomes3、7、17and P16abnormality analysed by FISH were important means for diagnosis and differential diagnosis of bladder urothelial tumors, and which also provide a certain significance forpredicting the progress and prognosis of BUT.