Rajcani J, Kajo K, Adamkov M, Moravekova E, Lauko L, Felcanova D, Bencat M
Alpha Medical, Martin, Slovakia.
Bratisl Lek Listy. 2013;114(8):431-8. doi: 10.4149/bll_2013_091.
From the archive of BB Biocyt company, 32 urinary bladder carcinomas (urothelium carcinomas, UC) and 7 cases of chronic cystitis were selected and examined in semiserial sections for the following antigens: 1) cell proliferation marker Ki-67 (expressed in the nuclei), 2) cell cycle regulator p16/INK4a polypeptide (expressed in the cytoplasm and nuclei), 3) urothelium marker p63 (expressed in the nuclei), 4) cytokeratin 7 (CK7). 5) cytokeratin 20 (CK20) and 6) high molecular weight cytokeratin (HMWCK). Invasive urothelium carcinomas showing a high grade dysplasia (invasive HG UC) comprised over the half (20 out of 32) of the investigated tumours. Microinvasion to lamina propria (seen in three HG papillary carcinomas) was regarded as an early infiltration even when the position of muscular layer could not be determined. Classical invasion across the urinary bladder wall and/or to surrounding tissues was found in 17 cases of low-differentiated HG UCs. The rest (9 out of 32 neoplasms) were either non-invasive papillary carcinomas of high (non-invasive HG UC, 5 cases) or low malignant potential (noninvasive LG UC, 4 cases). Finally, 3 cases were papillary urothelium neoplasms of low malignant potential (PUNLMP). HMWCK was present in all invasive tumours, whereas the frequency of other urothelium markers ranged from 65 to 88 %. Nevertheless, at least two markers were expressed in each invasive tumour. Staining for Ki-67 antigen was positive in over 50 % of the nuclei of HG UCs, while in the LG UCs, the frequency of positive Ki-67 staining did not exceed 25 %. In PUNLMP, the positive rate of Ki-67 stained dysplastic cells was below 10 %. The staining for p16 antigen did not correlate with the degree of dysplasia within urothelium tumours. For routine diagnostic, we recommend to combine the Ki-67 staining with detection of HMWCK. In cases of chronic cystitis, which developed urothelial hyperplasia and/or squamous metaplasia, the presence of p63 antigen was a relevant marker confirming the urothelial origin of the altered transitional cells (Tab. 6, Fig. 4, Ref. 69).
从BB生物细胞公司的存档中，选取了32例膀胱癌（尿路上皮癌，UC）和7例慢性膀胱炎病例，并对其半连续切片进行以下抗原检测：1）细胞增殖标志物Ki-67（在细胞核中表达），2）细胞周期调节因子p16/INK4a多肽（在细胞质和细胞核中表达），3）尿路上皮标志物p63（在细胞核中表达），4）细胞角蛋白7（CK7），5）细胞角蛋白20（CK20），6）高分子量细胞角蛋白（HMWCK）。显示高级别发育异常的浸润性尿路上皮癌（浸润性HG UC）占所研究肿瘤的一半以上（32例中的20例）。即使无法确定肌层位置，向固有层的微浸润（在3例HG乳头状癌中可见）也被视为早期浸润。在17例低分化HG UC中发现了穿过膀胱壁和/或向周围组织的典型浸润。其余（32例肿瘤中的9例）为高恶性潜能（非浸润性HG UC，5例）或低恶性潜能（非浸润性LG UC，4例）的非浸润性乳头状癌。最后，3例为低恶性潜能的乳头状尿路上皮肿瘤（PUNLMP）。HMWCK在所有浸润性肿瘤中均有表达，而其他尿路上皮标志物的表达频率在65%至88%之间。然而，每个浸润性肿瘤中至少有两种标志物表达。HG UC细胞核中超过50%的Ki-67抗原染色呈阳性，而在LG UC中，Ki-67染色阳性频率不超过25%。在PUNLMP中，Ki-67染色的发育异常细胞阳性率低于10%。p16抗原染色与尿路上皮肿瘤内的发育异常程度无关。对于常规诊断，我们建议将Ki-67染色与HMWCK检测相结合。在发生尿路上皮增生和/或鳞状化生的慢性膀胱炎病例中，p63抗原的存在是确认改变的移行细胞尿路上皮起源的相关标志物（表6，图4，参考文献69）。
