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Genetic alterations as clonal markers for bladder cancer detection in urine
Author(s) -
Mao Li
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(1996)25+<191::aid-jcb27>3.0.co;2-q
Subject(s) - bladder cancer , loss of heterozygosity , retinoblastoma , biology , cancer , allele , cancer research , genetic marker , tumor suppressor gene , genetics , gene , pathology , medicine , carcinogenesis
Bladder cancer is the result of a clonal expansion of cancer cells in which multiple genetic alterations have accumulated. Point mutations of the p53 gene are frequently observed in bladder cancer. Loss of a retinoblastoma ( Rb ) allele is also common in bladder cancer. Recent data have shown frequent loss of heterozygosity (LOH) and homozygous deletion of 9p21, including the region of p16 INK4A , a putative tumor suppressor gene, in bladder cancer. LOH is also observed frequently at several other chromosome regions in bladder cancer. These genetic changes have proved useful as clonal markers in the detection of cancer cells in urine. Because of their complexity, most molecular diagnostic approaches are not considered promising cancer screening tools in patients or high‐risk populations. However, a new molecular approach, the examination of microsatellite alterations in bladder cancer and urine specimens, is a promising screening tool for the disease. The common genetic alterations in bladder cancer and their use as clonal markers in screening or diagnosis strategies will be discussed. J. Cell. Biochem. 25S: 191–196. © 1997 Wiley‐Liss, Inc.