Sauter G, Deng G, Moch H, Kerschmann R, Matsumura K, De Vries S, George T, Fuentes J, Carroll P, Mihatsch M J
Department of Laboratory Medicine, University of California, San Francisco.
Am J Pathol. 1994 Apr;144(4):756-66.
To understand better the role of physical p53 deletion in bladder cancer, 106 formalin-fixed and 45 unfixed bladder tumors were examined using fluorescence in situ hybridization. Probes for centromere 17 and the p53 locus were hybridized simultaneously to interphase tumor cells to analyze p53 and chromosome 17 copy number on a cell by cell basis. 17p deletion was found in four of 43 pTa tumors, 18 of 43 pT1 tumors and 29 of 58 pT2-4 tumors (P = 0.0001). 17p deletion was also highly correlated with grade (P = 0.0001) and with p53 immunostaining (P = 0.0005). Chromosome 17 polysomy was associated with stage, grade, 17p deletions, and p53 immunostaining (P = 0.0001). The strong difference in centromere 17 copy number and 17p deletions between pTa and pT1 tumors supports a relevant biological distinction between pTa and pT1 tumors.
为了更好地理解p53基因物理性缺失在膀胱癌中的作用,我们使用荧光原位杂交技术检测了106例福尔马林固定的和45例未固定的膀胱肿瘤。将17号染色体着丝粒和p53基因座的探针同时与肿瘤间期细胞杂交,以便逐个细胞地分析p53和17号染色体的拷贝数。在43例pTa肿瘤中有4例发现17p缺失,43例pT1肿瘤中有18例,58例pT2 - 4肿瘤中有29例(P = 0.0001)。17p缺失也与肿瘤分级高度相关(P = 0.0001)以及与p53免疫染色相关(P = 0.0005)。17号染色体多体性与肿瘤分期、分级、17p缺失以及p53免疫染色相关(P = 0.0001)。pTa和pT1肿瘤之间17号染色体着丝粒拷贝数和17p缺失的显著差异支持了pTa和pT1肿瘤之间存在相关生物学差异的观点。