The abnormal eosinophils are part of the leukemic cell population in acute myelomonocytic leukemia with abnormal eosinophils (AML M4Eo) and carry the pericentric inversion 16: A combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridization

被引:63
|
作者
Haferlach, T
Winkemann, M
Loffler, H
Schoch, R
Gassmann, W
Fonatsch, C
Schoch, C
Poetsch, M
WeberMatthiesen, K
Schlegelberger, B
机构
[1] CHRISTIAN ALBRECHTS UNIV KIEL,INST HUMAN GENET,D-24116 KIEL,GERMANY
[2] UNIV LUBECK,INST HUMAN GENET,COOPERAT GRP TUMOR CYTOGENET,W-2400 LUBECK,GERMANY
关键词
D O I
10.1182/blood.V87.6.2459.bloodjournal8762459
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The French-American-British subtype acute myelomonocytic leukemia with abnormal eosinophils (FAB AML M4Eo) with pericentric inversion of chromosome 16 is cytomorphologically defined by a myelomonoblastic blast population and abnormal eosinophils. Until now, it remained an open question whether these abnormal eosinophils are part of the malignant clone or an epiphenomenon. We analyzed five cases of AML M4Eo with inv(16) and combined May-Grunwald-Giemsa staining with fluorescence in situ hybridization using yeast artificial chromosome clone 854E2, which spans the inv(le) breakpoint on 16p. In the case of inv(16), three instead of the normal two hybridization signals can be observed both on metaphase spreads and in interphase cells. With this approach, we were able to show inversion 16 in abnormal eosinophils and, therefore, identified them as a part of the leukemic cell population. (C) 1996 by The American Society of Hematology.
引用
收藏
页码:2459 / 2463
页数:5
相关论文
共 6 条
  • [1] Abnormal eosinophils in AML M4Eo carry the inversion 16(p13q22)
    Winkemann, M
    Haferlach, T
    Loffler, H
    Schoch, R
    Schoch, C
    Fonatsch, C
    WeberMatthiesen, K
    Schlegelberger, B
    BLOOD, 1995, 86 (10) : 2976 - 2976
  • [2] Cell lineage specific involvement in acute promyelocytic leukemia (APL) using a combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridization techniques for the detection of the translocation t(15;17).
    Haferlach, T
    Loffler, H
    Nickenig, C
    RammPetersen, L
    Meeder, M
    Schoch, R
    Schlegelberger, B
    Schnittger, S
    Schoch, C
    Hiddemann, W
    BLOOD, 1997, 90 (10) : 291 - 291
  • [3] The detection of the translocation (9;22) in single cells of Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL) using a combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridization (FISH).
    Winkemann, M
    Haferlach, T
    Meeder, M
    RammPetersen, L
    Schafhausen, P
    Nickelsen, M
    WeberMatthiesen, K
    Schlegelberger, B
    Loffler, H
    BLOOD, 1996, 88 (10) : 304 - 304
  • [4] New insights into the biology of Philadelphia-chromosome-positive acute lymphoblastic leukaemia using a combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridization techniques at the single cell level
    Haferlach, T
    Winkemann, M
    RammPetersen, L
    Meeder, M
    Schoch, R
    WeberMatthiesen, K
    Schlegelberger, B
    Schoch, C
    Ludwig, WD
    Hiddemann, W
    Loffler, H
    BRITISH JOURNAL OF HAEMATOLOGY, 1997, 99 (02) : 452 - 459
  • [5] Spectral karyotyping and fluorescence in situ hybridization analyses identified a novel three-way translocation involving inversion 16 in therapy-related acute myeloid leukemia M4eo
    Ohsaka, Akimichi
    Otsubo, Kaori
    Yokota, Harushige
    Hisa, Tomoko
    Saito, Hajime
    Kozaki, Takazumi
    CANCER GENETICS AND CYTOGENETICS, 2008, 184 (02) : 113 - 118
  • [6] Cell lineage specific involvement in acute promyelocytic leukaemia (APL) using a combination of May-Grunwald-Giemsa staining and fluorescence in situ hybridization techniques for the detection of the translocation t(15;17)(q22;q12)
    Haferlach, T
    Löffler, H
    Nickenig, C
    Ramm-Petersen, L
    Meeder, M
    Schoch, R
    Schlegelberger, B
    Schnittger, S
    Schoch, C
    Hiddemann, W
    BRITISH JOURNAL OF HAEMATOLOGY, 1998, 103 (01) : 93 - 99