PMID- 10719054
OWN - NLM
STAT- MEDLINE
DCOM- 20000331
LR  - 20201113
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 5
IP  - 4
DP  - 2000 Apr
TI  - The p73 gene is less involved in the development but involved in the progression 
      of neuroblastoma.
PG  - 379-84
AB  - We performed expression, mutation, loss of heterozygosity (LOH) and fluorescence 
      in situ hybridization (FISH) analyses of the p73 gene in neuroblastomas (NBs). 
      Reverse transcription-polymerase chain reaction (RT-PCR) using primers which can 
      detect both the p73alpha and p73beta transcripts was performed on 30 fresh NBs 
      and 22 NB cell lines. Aberrant expression of the p73 gene was found in 4 (25%) of 
      16 primary tumors found by mass screening and in 10 (71.4%) of 14 primary tumors 
      found clinically. The rates of expression in these two types of tumors were 
      significantly different (p=0.026, Fisher's exact test). The incidence of aberrant 
      expression of the p73 gene was significantly higher in stage IV patients than in 
      stages I, II, III plus IVS patients (p=0.0236, Fisher's exact test). No 
      homozygous deletions or rearrangements of the p73 gene were found in any samples 
      examined. In addition to the polymorphism in exon 2, a silent mutation (codon 336 
      GCC/GCT) was found in one primary tumor. LOH of the p73 gene was detected in 5 
      (15%) of 33 primary NBs using PCR-LOH analysis. FISH analysis showed that all 17 
      NB cell lines used in this study revealed allelic loss of the p73 gene, while 
      most of them expressed the p73 gene. These results suggest that the p73 gene is 
      not monoallelically expressed in NB. We conclude that the p73 gene is less 
      involved in the development but involved in the progression of neuroblastoma.
FAU - Yang, H W
AU  - Yang HW
AD  - Department of Pediatrics, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
FAU - Piao, H Y
AU  - Piao HY
FAU - Chen, Y Z
AU  - Chen YZ
FAU - Takita, J
AU  - Takita J
FAU - Kobayashi, M
AU  - Kobayashi M
FAU - Taniwaki, M
AU  - Taniwaki M
FAU - Hashizume, K
AU  - Hashizume K
FAU - Hanada, R
AU  - Hanada R
FAU - Yamamoto, K
AU  - Yamamoto K
FAU - Taki, T
AU  - Taki T
FAU - Bessho, F
AU  - Bessho F
FAU - Yanagisawa, M
AU  - Yanagisawa M
FAU - Hayashi, Y
AU  - Hayashi Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (DNA Primers)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (TP73 protein, human)
RN  - 0 (Tumor Protein p73)
RN  - 0 (Tumor Suppressor Proteins)
SB  - IM
MH  - DNA Primers/chemistry
MH  - DNA, Neoplasm/analysis
MH  - DNA-Binding Proteins/*genetics/metabolism
MH  - Disease Progression
MH  - Gene Expression
MH  - Genes, Tumor Suppressor/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Loss of Heterozygosity
MH  - Neuroblastoma/*genetics/metabolism/pathology
MH  - Nuclear Proteins/*genetics/metabolism
MH  - Point Mutation
MH  - Polymorphism, Genetic
MH  - Polymorphism, Single-Stranded Conformational
MH  - RNA, Messenger/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Cells, Cultured
MH  - Tumor Protein p73
MH  - Tumor Suppressor Proteins
EDAT- 2000/03/17 00:00
MHDA- 2000/03/17 00:01
CRDT- 2000/03/17 00:00
PHST- 2000/03/17 00:00 [pubmed]
PHST- 2000/03/17 00:01 [medline]
PHST- 2000/03/17 00:00 [entrez]
AID - 10.3892/ijmm.5.4.379 [doi]
PST - ppublish
SO  - Int J Mol Med. 2000 Apr;5(4):379-84. doi: 10.3892/ijmm.5.4.379.