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From the Institute for Pathology and Urologic Clinics,*
University of Basel, Basel, Switzerland; the Cancer Genetics
Branch,
National Human Genome Research
Institute, National Institutes of Health, Bethesda, Maryland; the
Institute for Pathology
and Urologic
Clinics,§
Cantonal Hospital St. Gallen, St.
Gallen, Switzerland; the Institute for Pathology
¶
and Urologic Clinics,||
City Hospital Triemli,
Zürich, Switzerland; the Urologic
Clinics,**
Limmattal Hospital, Schlieren,
Switzerland; the Clara Hospital,
Basel, Switzerland; Vysis
Incorporated,
Downers Grove,
Illinois; the Institute for
Pathology§§
and Urologic
Clinics,¶¶
Cantonal Hospital Baden,
Baden, Switzerland; the Institute for
Pathology||
||
and Urologic
Clinics,***
Cantonal Hospital
Münsterlingen, Münsterlingen, Switzerland; the Institute
for Pathology
and Urologic
Clinics,
Cantonal
Hospital Winterthur, Winterthur, Switzerland; and the Urologic
Clinics,§§
§
Cantonal
Hospital Schaffhausen, Schaffhausen, Switzerland
Studies by comparative genomic hybridization revealed that the 19q13 chromosomal region is frequently amplified in bladder cancer. The cyclin E gene (CCNE), coding for a regulatory subunit of cyclin-dependent kinase 2, has been mapped to 19q13. To investigate the role of cyclin E alterations in bladder cancer, a tissue microarray of 2,317 specimens from 1,842 bladder cancer patients was constructed and analyzed for CCNE amplification by fluorescence in situ hybridization and for cyclin-E protein overexpression by immunohistochemistry. Fluorescence in situ hybridization analysis showed amplification in only 30 of the 1,561 evaluable tumors (1.9%). Amplification was significantly associated with stage and grade (P < 0.0005 each). Immunohistochemically detectable cyclin E expression was strong in 233 (12.4%), weak in 354 (18.9%), and negative in 1,286 of the 1,873 interpretable tumors. The majority (62.1%) of CCNE-amplified tumors were strongly immunohistochemistry-positive (P < 0.0001). The frequency of protein expression increased from stage pTa (22.2%) to pT1 (45.5%; P < 0.0001) but then decreased for stage pT2-4 (29.4%; P < 0.0001 for pT1 versus pT2-4). Low cyclin E expression was associated with poor overall survival in all patients (P < 0.0001), but had no prognostic impact independent of stage. It is concluded that cyclin E overexpression is characteristic to a subset of bladder carcinomas, especially at the stage of early invasion. This analysis of the prognostic impact of CCNE gene amplification and protein expression in >1,500 arrayed bladder cancers was accomplished in a period of 2 weeks, illustrating how the tissue microarray technology remarkably facilitates the evaluation of the clinical relevance of molecular alterations in cancer.
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