PMID- 11135430
OWN - NLM
STAT- MEDLINE
DCOM- 20010222
LR  - 20191025
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 30
IP  - 2
DP  - 2001 Feb
TI  - Identification of chromosomal loci associated with non-P-glycoprotein-mediated 
      multidrug resistance to topoisomerase II inhibitor in lung adenocarcinoma cell 
      line by comparative genomic hybridization.
PG  - 136-42
AB  - In order to identify genomic changes associated with an etoposide resistance 
      acquisition, we used comparative genomic hybridization (CGH) to compare a human 
      lung adenocarcinoma cell line, A549 wild type, and three sublines, A549-VP1-3, 
      exposed to increasing concentrations of the topoisomerase II inhibitor, VP16. 
      R-banding karyotype, fluorescence in situ hybridization (FISH), and Southern blot 
      for the MLL gene were also performed. The CGH analysis showed that the A549-VP3 
      cell line shared chemoresistance-specific abnormalities (amplification of 
      11q23-qter, loss of chromosome 17, and deletions of 2p14-pter and 2q23-q24). FISH 
      analysis confirmed the loss of one chromosome 17 in the three resistant sublines 
      and revealed an increased fragmentation of chromosome 2 in more than two 
      segments, depending on the etoposide concentration. FISH with an MLL gene probe 
      showed additional signals of MLL (from three in the A549-WT to seven in the 
      A549-VP3 cell line) translocated onto several other chromosomes. Southern blot 
      indicated an amplification of the MLL gene, dependent on the etoposide 
      concentration, without gene rearrangement. The CGH results are suggestive of loci 
      that could be associated with the acquisition of an etoposide-chemoresistant 
      phenotype. Deletion of the 2p region has already been reported, without any 
      candidate gene being identified. The role of MLL in leukemogenesis has previously 
      been demonstrated, but its role in the development of other tumors or its 
      significance in the chemoresistance process remains to be elucidated.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Struski, S
AU  - Struski S
AD  - Laboratory of Hematology, Robert Debre Hospital and Medical Faculty (UPRES EA 
      20-70-IFR 53 Biomolecules), Reims, France.
FAU - Doco-Fenzy, M
AU  - Doco-Fenzy M
FAU - Trussardi, A
AU  - Trussardi A
FAU - Masson, L
AU  - Masson L
FAU - Gruson, N
AU  - Gruson N
FAU - Ulrich, E
AU  - Ulrich E
FAU - Proult, M
AU  - Proult M
FAU - Jardillier, J C
AU  - Jardillier JC
FAU - Potron, G
AU  - Potron G
FAU - Cornillet-Lefebvre, P
AU  - Cornillet-Lefebvre P
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Genetic Markers)
RN  - 0 (Topoisomerase II Inhibitors)
RN  - 6PLQ3CP4P3 (Etoposide)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/physiology
MH  - Adenocarcinoma/drug therapy/enzymology/*genetics
MH  - Blotting, Southern
MH  - Drug Resistance, Multiple/*genetics
MH  - Drug Resistance, Neoplasm/*genetics
MH  - Enzyme Inhibitors/*pharmacology
MH  - Etoposide/*pharmacology
MH  - *Genetic Markers
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Lung Neoplasms/drug therapy/enzymology/*genetics
MH  - Nucleic Acid Hybridization
MH  - *Topoisomerase II Inhibitors
MH  - Tumor Cells, Cultured
EDAT- 2001/01/03 11:00
MHDA- 2001/03/03 10:01
CRDT- 2001/01/03 11:00
PHST- 2001/01/03 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2001/01/03 11:00 [entrez]
AID - 10.1002/1098-2264(200102)30:2<136::AID-GCC1071>3.0.CO;2-S [pii]
AID - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1071>3.0.co;2-t [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2001 Feb;30(2):136-42. doi: 
      10.1002/1098-2264(2000)9999:9999<::aid-gcc1071>3.0.co;2-t.