PMID- 10383132
OWN - NLM
STAT- MEDLINE
DCOM- 19990719
LR  - 20161124
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 59
IP  - 12
DP  - 1999 Jun 15
TI  - Elevated and biallelic expression of p73 is associated withprogression of human
      bladder cancer.
PG  - 2791-3
AB  - p73, a member of the p53 family at 1p36.3, has been demonstrated to be expressed 
      monoallelically and induce apoptosis or G1 arrest of the cell cycle. To explore
      the candidacy of p73 as a suppressor in bladder tumorigenesis, we examined
      expression level, allelic origin, and mutation of p73 mRNA in 45 primary bladder 
      carcinomas. Quantitative PCR analysis showed no allelic loss of the gene but
      showed various levels of mRNA expression in both carcinoma and noncancerous
      tissues. Elevated expression of p73 was frequently observed in carcinoma tissues 
      [18 (40.0%) of 45] and showed a strong correlation with tumor stage or grade.
      Allotyping analysis using a StyI polymorphism detected biallelic expression in 12
      (52.2%) of 23 heterozygous carcinomas but none in 4 noncancerous tissues.
      Tumor-specific biallelic expression was also identified from one matched set. In 
      addition, 8 (66.7%) of these 12 expressed high levels of p73 mRNA, whereas only 2
      (18.2%) of 11 monoallelic expressors showed high expression, which suggests that 
      the increased expression of p73 might be caused by the transcriptional activation
      of a silent allele in carcinomas. Single-strand conformational polymorphism
      analysis of the entire coding region of p73 revealed no mutation, whereas 12
      (26.7%) of the same set showed p53 alterations. No relationship between
      expression of p73 and p53 mutation or expression of p21Waf1 or MDM2 was
      identified. Taken together, our data argue that p73 does not play a role as a
      tumor suppressor in bladder carcinogenesis and suggest that the activation of a
      silent allele may contribute to the progression of bladder tumors.
FAU - Chi, S G
AU  - Chi SG
AD  - Department of Pathology and Kohwang Medical Research Institute, School of
      Medicine, Kyung Hee University, Seoul, Republic of Korea. chi6302@nuri.net
FAU - Chang, S G
AU  - Chang SG
FAU - Lee, S J
AU  - Lee SJ
FAU - Lee, C H
AU  - Lee CH
FAU - Kim, J I
AU  - Kim JI
FAU - Park, J H
AU  - Park JH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (CDKN1A protein, human)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Cyclins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Protein p73)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 0 (p73 protein, human)
SB  - IM
MH  - Alleles
MH  - Cyclin-Dependent Kinase Inhibitor p21
MH  - Cyclins/genetics
MH  - DNA-Binding Proteins/*biosynthesis/genetics
MH  - Disease Progression
MH  - Gene Expression
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor
MH  - Humans
MH  - Mutation
MH  - Nuclear Proteins/*biosynthesis/genetics
MH  - RNA, Messenger/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Cells, Cultured
MH  - Tumor Protein p73
MH  - Tumor Suppressor Protein p53/genetics
MH  - Tumor Suppressor Proteins
MH  - Urinary Bladder/metabolism
MH  - Urinary Bladder Neoplasms/genetics/*metabolism
EDAT- 1999/06/26 00:00
MHDA- 1999/06/26 00:01
CRDT- 1999/06/26 00:00
PHST- 1999/06/26 00:00 [pubmed]
PHST- 1999/06/26 00:01 [medline]
PHST- 1999/06/26 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1999 Jun 15;59(12):2791-3.