PMID- 8616034
OWN - NLM
STAT- MEDLINE
DCOM- 19960610
LR  - 20190816
IS  - 0007-1048 (Print)
IS  - 0007-1048 (Linking)
VI  - 92
IP  - 3
DP  - 1996 Mar
TI  - Secondary acute leukaemias with 11q23 rearrangement: clinical, cytogenetic, FISH 
      and FICTION studies.
PG  - 673-80
AB  - Three patients with secondary acute leukaemia after treatment with topoisomerase 
      II inhibitor agents are described. Two patients had acute myeloid leukaemia 
      (AML). FAB M5a, one had pro-B-acute lymphoblastic leukaemia (ALL). The interval 
      between initiation of chemotherapy and the onset of secondary acute leukaemia was 
      19-20 months. 11q23 rearrangements were detected in all cases. They were due to 
      translocations t(11;19) (q23;p13.3), t(11;16)(q23;p13) and t(4;11)(q21;q23), 
      respectively. Fluorescence in situ hybridization (FISH) with Yeast Artificial 
      Chromosome (YAC) probe 13HH4 spanning the ALL-1 gene on 11q23 confirmed that in 
      each case the ALL-1 gene had been disrupted by the translocations. The study 
      underlined the relationship between the development of secondary acute leukaemias 
      with 11q23 rearrangement and previous chemotherapy with topisomerase II inhibitor 
      agents. So far, however, only six adult patients with secondary ALL with t(4;11) 
      after treatment with topoisomerase II inhibitor agents have been reported. All 
      with t(4;11) mostly occurs in infants or young children. Our patient received 
      epirubicin continuously for >19 months. This indicates that both myeloid and 
      lymphoid leukaemias with involvement of the ALL-1 gene can be induced by 
      exogenous agents, especially topoisomerase II inhibitors. Thus they may have a 
      common biological background. This hypothesis was substantiated by means of 
      combined immunophenotyping and FISH (FICTION). In the case of AML M5a with 
      t(11;19), the tumour cells with ALL-1 rearrangement expressed CD34. Moreover, the 
      pro-B-ALL with t(4;11) was CD34 positive. These findings suggest that the cell of 
      origin of secondary AML and ALL with 11q23 rearrangement is an immature 
      haemopoietic progenitor cell.
FAU - Zhang, Y
AU  - Zhang Y
AD  - Department of Human Genetics, University of Kiel, Germany.
FAU - Poetsch, M
AU  - Poetsch M
FAU - Weber-Matthiesen, K
AU  - Weber-Matthiesen K
FAU - Rohde, K
AU  - Rohde K
FAU - Winkemann, M
AU  - Winkemann M
FAU - Haferlach, T
AU  - Haferlach T
FAU - Gassmann, W
AU  - Gassmann W
FAU - Ludwig, W D
AU  - Ludwig WD
FAU - Grote, W
AU  - Grote W
FAU - Loffler, H
AU  - Loffler H
FAU - Schlegelberger, B
AU  - Schlegelberger B
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Haematol
JT  - British journal of haematology
JID - 0372544
RN  - 0 (Antineoplastic Agents)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (KMT2A protein, human)
RN  - 0 (Topoisomerase II Inhibitors)
RN  - 0 (Transcription Factors)
RN  - 149025-06-9 (Myeloid-Lymphoid Leukemia Protein)
RN  - EC 2.1.1.43 (Histone-Lysine N-Methyltransferase)
SB  - IM
MH  - Acute Disease
MH  - Adult
MH  - Aged
MH  - Antineoplastic Agents/adverse effects
MH  - *Chromosomes, Human, Pair 11
MH  - *Chromosomes, Human, Pair 4
MH  - DNA-Binding Proteins/*genetics
MH  - Enzyme Inhibitors/adverse effects
MH  - Female
MH  - Gene Rearrangement
MH  - Histone-Lysine N-Methyltransferase
MH  - Humans
MH  - Immunophenotyping
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Leukemia/chemically induced/*genetics
MH  - Male
MH  - Middle Aged
MH  - Myeloid-Lymphoid Leukemia Protein
MH  - Neoplasms, Second Primary/*chemically induced
MH  - *Proto-Oncogenes
MH  - Topoisomerase II Inhibitors
MH  - *Transcription Factors
MH  - *Translocation, Genetic
EDAT- 1996/03/01 00:00
MHDA- 1996/03/01 00:01
CRDT- 1996/03/01 00:00
PHST- 1996/03/01 00:00 [pubmed]
PHST- 1996/03/01 00:01 [medline]
PHST- 1996/03/01 00:00 [entrez]
AID - 10.1046/j.1365-2141.1996.00399.x [doi]
PST - ppublish
SO  - Br J Haematol. 1996 Mar;92(3):673-80. doi: 10.1046/j.1365-2141.1996.00399.x.