PMID- 9491326
OWN - NLM
STAT- MEDLINE
DCOM- 19980319
LR  - 20171116
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 21
IP  - 2
DP  - 1998 Feb
TI  - Pre-clinical evaluation of probes to detect t(8;21) AML minimal residual disease 
      by fluorescence in situ hybridization.
PG  - 144-51
AB  - The 8;21 translocation in acute myeloid leukemia (AML) results in a consistent 
      fusion transcript, AML1/ETO. Long-term clinical remission occurs in some patients 
      despite incomplete eradication of AML1/ETO as demonstrated by RT-PCR, thus 
      limiting the usefulness of this assay. An important future goal will be to 
      determine if there is a level of minimal residual disease (MRD) in patients below 
      which relapse is unlikely. For the detection of MRD, we have developed reagents 
      for fluorescence in situ hybridization (FISH) that identify both derivative 8 and 
      21 chromosomes with a high analytical sensitivity. In t(8;21) AML cells, two 
      fused signals were detected in addition to the normal 8 and 21 alleles. The 
      sensitivity and specificity of this probe mixture were analyzed in cell lines and 
      patient bone marrows. One and two randomly juxtaposed signals were observed in 
      2.4 and 0.04% of normal cells, respectively. However, these were easily 
      differentiated from t(8;21) cells by the absence of signals from the normal 
      alleles. Using as criteria the presence of two fused signals plus the normal 
      alleles, we observed no false positives among 5,000 normal cells. The probe 
      correctly identified 20/20 patients with t(8;21) AML and 10/10 non-t(8;21) 
      patients. In cell dilution experiments, the analytical sensitivity of this 
      reagent was equal to that of the X chromosome and Y chromosome alpha-satellite 
      probes. These optimized probes should facilitate the quantitative assessment and 
      study of MRD in t(8;21) AML.
FAU - Paskulin, G A
AU  - Paskulin GA
AD  - University of Colorado Health Sciences Center, Medical Oncology Division, Denver, 
      USA.
FAU - Philips, G
AU  - Philips G
FAU - Morgan, R
AU  - Morgan R
FAU - Sandberg, A
AU  - Sandberg A
FAU - Richkind, K
AU  - Richkind K
FAU - Borovik, C
AU  - Borovik C
FAU - McGavran, L
AU  - McGavran L
FAU - Rabinovich, N
AU  - Rabinovich N
FAU - Dietz-Band, J
AU  - Dietz-Band J
FAU - Erickson, P
AU  - Erickson P
FAU - Drabkin, H
AU  - Drabkin H
FAU - Varella-Garcia, M
AU  - Varella-Garcia M
LA  - eng
GR  - CA46934/CA/NCI NIH HHS/United States
GR  - P01HDO17449/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (AML1-ETO fusion protein, human)
RN  - 0 (Core Binding Factor Alpha 2 Subunit)
RN  - 0 (DNA Probes)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (RUNX1 Translocation Partner 1 Protein)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Bone Marrow Cells/pathology
MH  - Chromosome Mapping
MH  - Chromosomes, Human, Pair 21/*genetics
MH  - Chromosomes, Human, Pair 8/*genetics
MH  - Core Binding Factor Alpha 2 Subunit
MH  - *DNA Probes
MH  - *Fluorescent Dyes
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Leukemia, Myeloid, Acute/diagnosis/*genetics
MH  - Neoplasm, Residual/diagnosis/*genetics
MH  - *Oncogene Proteins, Fusion
MH  - RUNX1 Translocation Partner 1 Protein
MH  - Recombinant Fusion Proteins/analysis/genetics
MH  - Sensitivity and Specificity
MH  - Transcription Factors/analysis/genetics
MH  - *Translocation, Genetic
EDAT- 1998/03/10 03:03
MHDA- 2000/06/20 09:00
CRDT- 1998/03/10 03:03
PHST- 1998/03/10 03:03 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/03/10 03:03 [entrez]
AID - 10.1002/(SICI)1098-2264(199802)21:2<144::AID-GCC10>3.0.CO;2-R [pii]
PST - ppublish
SO  - Genes Chromosomes Cancer. 1998 Feb;21(2):144-51.