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Numeric Aberration of Chromosome 17 Is Strongly Correlated with p53 Overexpression, Tumor Proliferation and Histopathology in Human Bladder Cancer
Author(s) -
Li Benyi,
Kanamaru Hiroshi,
Noriki Sakon,
Fukuda Masaru,
Okada Kenichiro
Publication year - 1998
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.1998.tb00358.x
Subject(s) - polysomy , proliferating cell nuclear antigen , pathology , immunohistochemistry , chromosome , histopathology , bladder cancer , urinary bladder , biology , transitional cell carcinoma , medicine , cancer , microbiology and biotechnology , fluorescence in situ hybridization , gene , genetics
Background This study investigated the relationships between the numeric aberrations of chromosome 17 and p53 expression, the proliferating cell nuclear antigen labeling index (PCNA‐LI) and histopathology, to determine their prognostic significance in bladder cancer. Methods Using in situ hybridization (1SH) with a biotin‐labeled chromosome‐specific DNA probe, the copy number of pericentromeric sequences in chromosome 17 were detected within interphase nuclei in formalin‐fixed paraffin‐embedded sections from 59 nonmetastasized transitional cell carcinomas (TCCs) of the urinary bladder. Expression of p53 and PCNA‐LI were determined in serial sections by an immunohistochemical method. Results The percentage of hyperdiploid cells for chromosome 17 correlated with p53 overexpression (P< 0.002), PCNA‐LI (P< 0.002), increasing tumor grade (P< 0.002) and advanced pathologic stage (P< 0.002). The average percentage of hyperdiploid cells was lower in tumors with negative p53 expression than in tumors with p53 overexpression (P< 0.002). Also, more polysomic TCCs were found in muscle‐invasive than in superficial cases (P< 0.01), and there was a difference in both p53 overexpression or PCNA‐LI between disomic and polysomic TCCs (P<0.01). Patients with chromosome 17 disomic tumors showed less frequent tumor progression than patients with polysomic tumors (P< 0.05). However, chromosome 17 polysomy was an independent prognostic indicator only for patient survival (P< 0.05). Conclusion The occurrence and extent of numeric aberrations of chromosome 17 may be associated with the evolution of aggressive growth in TCC and may be a useful indicator for survival.

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