PMID- 19188704
OWN - NLM
STAT- MEDLINE
DCOM- 20090311
LR  - 20211020
IS  - 1424-859X (Electronic)
IS  - 1424-8581 (Print)
IS  - 1424-8581 (Linking)
VI  - 122
IP  - 3-4
DP  - 2008
TI  - Increased genomic alteration complexity and telomere shortening in B-CLL cells 
      resistant to radiation-induced apoptosis.
PG  - 343-9
LID - 10.1159/000167821 [doi]
AB  - B-cell chronic lymphocytic leukemia (B-CLL) results in an accumulation of mature 
      CD5(+)/CD23(+) B cells due to an uncharacterized defect in apoptotic cell death. 
      B-CLL is not characterized by a unique recurrent genomic alteration but rather by 
      genomic instability giving rise frequently to several chromosomal aberrations. 
      Besides we reported that approximately 15% of B-CLL patients present malignant 
      B-cells resistant to irradiation-induced apoptosis, contrary to approximately 85% 
      of patients and normal human lymphocytes. Telomere length shortening is observed 
      in radioresistant B-CLL cells. Using fluorescence in situ hybridization (FISH) 
      and multicolour FISH, we tested whether specific chromosomal aberrations might be 
      associated with the radioresistance of a subset of B-CLL cells and whether they 
      are correlated with telomere shortening. In a cohort of 30 B-CLL patients, all of 
      the radioresistant B-CLL cell samples exhibited homozygous or heterozygous 
      deletion of 13q14.3 in contrast to 52% of the radiosensitive samples. In addition 
      to the 13q14.3 deletion, ten out of the 11 radioresistant B-cell samples had 
      another clonal genomic alteration such as trisomy 12, deletion 17p13.1, mutation 
      of the p53 gene or translocations in contrast to only three out of 19 
      radiosensitive samples. Telomere fusions and non-reciprocal translocations, 
      hallmarks of telomere dysfunction, are not increased in radioresistant B-CLL 
      cells. These findings suggest (i) that the 13q14.3 deletion accompanied by 
      another chromosomal aberration is associated with radioresistance of B-CLL cells 
      and (ii) that telomere shortening is not causative of increased clonal 
      chromosomal aberrations in radioresistant B-CLL cells.
CI  - Copyright 2008 S. Karger AG, Basel.
FAU - Salin, H
AU  - Salin H
AD  - Laboratoire de Radiobiologie et d'Oncologie, CEA, DSV/iRCM, Fontenay-aux-Roses, 
      France.
FAU - Ricoul, M
AU  - Ricoul M
FAU - Morat, L
AU  - Morat L
FAU - Sabatier, L
AU  - Sabatier L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090130
PL  - Switzerland
TA  - Cytogenet Genome Res
JT  - Cytogenetic and genome research
JID - 101142708
RN  - EC 2.7.7.49 (Telomerase)
SB  - IM
MH  - Apoptosis/radiation effects
MH  - B-Lymphocytes/pathology
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 13/genetics/radiation effects
MH  - Genomic Instability
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/enzymology/*genetics/pathology
MH  - Metaphase
MH  - Sequence Deletion/radiation effects
MH  - Telomerase/metabolism
MH  - Telomere/*genetics/ultrastructure
PMC - PMC2813806
EDAT- 2009/02/04 09:00
MHDA- 2009/03/12 09:00
PMCR- 2009/02/01
CRDT- 2009/02/04 09:00
PHST- 2008/09/25 00:00 [accepted]
PHST- 2009/02/04 09:00 [entrez]
PHST- 2009/02/04 09:00 [pubmed]
PHST- 2009/03/12 09:00 [medline]
PHST- 2009/02/01 00:00 [pmc-release]
AID - 000167821 [pii]
AID - cgr0122-0343 [pii]
AID - 10.1159/000167821 [doi]
PST - ppublish
SO  - Cytogenet Genome Res. 2008;122(3-4):343-9. doi: 10.1159/000167821. Epub 2009 Jan 
      30.