Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-1-24
pubmed:abstractText
Cyclin D1 contributes to regulate G1 progression by forming a complex with different cyclin-dependent kinases. It has oncogenic properties and is frequently overexpressed in several human tumor types. In our study, expression of cyclin D1 and Ki67, a proliferation marker, was evaluated by immunohistochemistry in human papillary superficial (pTa-pT1) bladder cancers and was correlated with p27(Kip1), p21(Waf1) and c-erbB-2 expression, with p53 gene status and protein expression, ploidy and cancer progression. Cyclin D1 expression was neither associated with tumor stage nor with tumor grade but high cyclin D1 expression (> or =25% positive nuclei) was significantly associated with p53 gene mutation (p = 0.012), low p21(Waf1) (p = 0.015) and high p27(Kip1) (p = 0.016) protein expression. Ki67 expression was not associated with tumor stage but a high proliferation index (> or =10% positive nuclei) was significantly associated with high tumor grade (p = 0.001) and with DNA aneuploidy (p = 0.005). There was no significant difference in proliferative activity between high and low cyclin D1 expressor tumors. Patients whose tumors showed high expression of cyclin D1 displayed a significantly longer disease-free survival (p < 0.001 by log-rank test). Increased Ki67 expression was significantly associated with shorter disease-free survival (p = 0.003). Both cyclin D1 (p = 0.027; RR = 1.898) and Ki67 (p = 0.047; RR = 1.932) protein expressions were independent predictors of reduced disease-free survival on a multivariate analysis that also included p27(Kip1) expression and tumor stage. The simultaneous presence of low cyclin D1, low p27(Kip1) and high Ki67 expression defined a "high-risk" group of patients who displayed a significantly increased risk of recurrence (p < 0.0001). These results suggest that evaluation of cell cycle-associated markers can help to identify high-risk patients and may affect the management of patients with papillary superficial bladder cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
671-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11807796-Adult, pubmed-meshheading:11807796-Aged, pubmed-meshheading:11807796-Aged, 80 and over, pubmed-meshheading:11807796-Carcinoma, Papillary, pubmed-meshheading:11807796-Cell Cycle Proteins, pubmed-meshheading:11807796-Cell Division, pubmed-meshheading:11807796-Cohort Studies, pubmed-meshheading:11807796-Cyclin D1, pubmed-meshheading:11807796-Cyclin-Dependent Kinase Inhibitor p27, pubmed-meshheading:11807796-Disease Progression, pubmed-meshheading:11807796-Disease-Free Survival, pubmed-meshheading:11807796-Female, pubmed-meshheading:11807796-Follow-Up Studies, pubmed-meshheading:11807796-Humans, pubmed-meshheading:11807796-Immunohistochemistry, pubmed-meshheading:11807796-Ki-67 Antigen, pubmed-meshheading:11807796-Male, pubmed-meshheading:11807796-Middle Aged, pubmed-meshheading:11807796-Ploidies, pubmed-meshheading:11807796-Predictive Value of Tests, pubmed-meshheading:11807796-Prognosis, pubmed-meshheading:11807796-Receptor, erbB-2, pubmed-meshheading:11807796-Risk Assessment, pubmed-meshheading:11807796-Tumor Markers, Biological, pubmed-meshheading:11807796-Tumor Suppressor Proteins, pubmed-meshheading:11807796-Urinary Bladder Neoplasms
pubmed:year
2002
pubmed:articleTitle
Cyclin D1 expression in papillary superficial bladder cancer: its association with other cell cycle-associated proteins, cell proliferation and clinical outcome.
pubmed:affiliation
Centro di Ricerche Oncologiche "Giovanni XXIII," Istituto di Patologia Generale, Catholic University, Rome, Italy. asgambato@rm.unicatt.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't