title: [Multiprobe fluorescence in situ hybridization panel in detection of the common cytogenetic abnormalities of acute myeloid leukemia].
abstract: OBJECTIVE
  To evaluate the value of multiprobe Fluorescence in situ hybridization (FISH) panel in detection of the common cytogenetic abnormalities in acute myeloidleukemia( AML). And to investigate its association with clinical diagnosis, chemotherapy and prognosis.
  
  
  METHODS
  Using the multiprobe AML/MDS panel designed to detect upto eight different FISH probes, which was for AML1/ETO transfusion gene, PML-RARα transfusion gene, CBFβ/MYH11 transfusion gene, MLL breakapart, P53 deletion,Del(5q), Del(7q), Del(20q), 40 cases of AML were investigated. The conventional karyotype analysis and the in-formation about the treatment responses were also used for assessing.
  
  
  RESULTS
  22 of the 40 AML cases were found to carry 7 types of cytogenetic abnormalities by multiprobe FISH panel including AML1/ETO transfusion gene, PML-RARa transfusion gene, MLL breakapart, P53 deletion, Del (5q), Del7q and trisomy 8. However conventional karyotype analysis only discovered 11 cases with the corresponding cytogenetic abnormalities, the positive ratio was 57.5% in multiprobe FISH panel higher than that in karyotype analysis (27.50%). Patiens with AML1/ETO or PML-RARa transfusion gene are easily to reach CR in the first induction chemotherapy, while the Del(7q), MLL breakapart, complex cytogenetic abnormalities may indicate poor prognosis.
  
  
  CONCLUSIONS
  Mutiprobe FISH panel is more rapid, accurate and effective for detecting the common cytogenetic abnormalities in AML, compared with the conventional karyotype analysis and common FISH analysis.
authors.affiliation: Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
authors.forename: Lu-lu
authors.initials: LL
authors.lastname: Xu
authors.forename: Xiao-li
authors.initials: XL
authors.lastname: Liu
authors.forename: Qing-feng
authors.initials: QF
authors.lastname: Du
authors.forename: Lan-lin
authors.initials: LL
authors.lastname: Song
authors.forename: Rui
authors.initials: R
authors.lastname: Cao
authors.forename: Yong-qiang
authors.initials: YQ
authors.lastname: Wei
authors.forename: Na
authors.initials: N
authors.lastname: Xu
authors.forename: Jin-fang
authors.initials: JF
authors.lastname: Zhang
mesh_terms: D000293:Adolescent; D000328:Adult; D002869:Chromosome Aberrations; D002872:Chromosome Deletion; D002898:Chromosomes, Human, Pair 8 / Q000235:genetics; D050676:Core Binding Factor Alpha 2 Subunit / Q000032:analysis; D005260:Female; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D006824:Hybridization, Genetic; D017404:In Situ Hybridization, Fluorescence / Q000379:methods*; D007621:Karyotyping / Q000379:methods; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D051788:Myeloid-Lymphoid Leukemia Protein / Q000032:analysis*; D015514:Oncogene Proteins, Fusion / Q000032:analysis*; D000075142:RUNX1 Translocation Partner 1 Protein; D015203:Reproducibility of Results; D013379:Substrate Specificity; D014314:Trisomy / Q000235:genetics
chemical_list: C107844:AML1-ETO fusion protein, human; C095514:CBFbeta-MYH11 fusion protein; D050676:Core Binding Factor Alpha 2 Subunit; D015514:Oncogene Proteins, Fusion; D000075142:RUNX1 Translocation Partner 1 Protein; C093476:promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; D051788:Myeloid-Lymphoid Leukemia Protein