PMID- 25059482
OWN - NLM
STAT- MEDLINE
DCOM- 20150721
LR  - 20211203
IS  - 1098-2264 (Electronic)
IS  - 1045-2257 (Linking)
VI  - 53
IP  - 11
DP  - 2014 Nov
TI  - Different TP53 mutations are associated with specific chromosomal rearrangements, 
      telomere length changes, and remodeling of the nuclear architecture of telomeres.
PG  - 934-50
LID - 10.1002/gcc.22205 [doi]
AB  - TP53 mutations are the most common mutations in human cancers, and TP53-R175H and 
      TP53-R273H are the most frequent. The impact of these mutations on genomic 
      instability after tumor initiation is still uncovered. To gain insight into this, 
      we studied the effects of three specific TP53 mutants (TP53-V143A, TP53-R175H, 
      and TP53-R273H) on genomic instability using four isogenic lines of LoVo cells. 
      Multicolor fluorescence in situ hybridization (FISH), three-dimensional (3D) 
      quantitative FISH (Q-FISH) on interphase and Q-FISH on metaphases were used to 
      investigate genomic instability. We found that LoVo cells expressing mutant 
      TP53-R175H displayed the highest level of chromosomal instability among the LoVo 
      cell lines. Furthermore, we observed that mutant TP53-R175H and TP53-V143A showed 
      more alterations in their 3D nuclear architecture of telomeres than the mutant 
      TP53-R273H and the wild type. Moreover, we noted an association between some 
      chromosomal abnormalities and telomere elongation in the mutant TP53-R175H. Taken 
      together, our results indicate that the mutation TP53-R175H is more likely to 
      cause higher levels of genomic instability than the other TP53 mutations. We 
      proposed that the type of TP53 mutations and the genetic background of a cancer 
      cell are major determinants of the TP53-dependent genomic instability.
CI  - (c) 2014 Wiley Periodicals, Inc.
FAU - Samassekou, Oumar
AU  - Samassekou O
AD  - Division of Genetics, Department of Pediatrics, Faculty of Medicine and Health 
      Sciences, Universite de Sherbrooke, Sherbrooke, QC, Canada; Manitoba Institute of 
      Cell Biology, CancerCare Manitoba, Department of Physiology, Faculty of Medicine, 
      University of Manitoba, Winnipeg, MB, Canada.
FAU - Bastien, Nathalie
AU  - Bastien N
FAU - Lichtensztejn, Daniel
AU  - Lichtensztejn D
FAU - Yan, Ju
AU  - Yan J
FAU - Mai, Sabine
AU  - Mai S
FAU - Drouin, Regen
AU  - Drouin R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140725
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (Shelterin Complex)
RN  - 0 (TP53 protein, human)
RN  - 0 (Telomere-Binding Proteins)
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - Cell Line, Tumor
MH  - Cell Nucleus/*metabolism/ultrastructure
MH  - Cell Proliferation
MH  - *Chromosomal Instability
MH  - Colonic Neoplasms
MH  - Humans
MH  - Mutation
MH  - Shelterin Complex
MH  - Telomere/*ultrastructure
MH  - Telomere-Binding Proteins/genetics/metabolism
MH  - Transcriptome
MH  - Tumor Suppressor Protein p53/*genetics
EDAT- 2014/07/26 06:00
MHDA- 2015/07/22 06:00
CRDT- 2014/07/26 06:00
PHST- 2014/06/11 00:00 [received]
PHST- 2014/07/02 00:00 [accepted]
PHST- 2014/07/26 06:00 [entrez]
PHST- 2014/07/26 06:00 [pubmed]
PHST- 2015/07/22 06:00 [medline]
AID - 10.1002/gcc.22205 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2014 Nov;53(11):934-50. doi: 10.1002/gcc.22205. Epub 
      2014 Jul 25.