LETTER TO THE EDITOR

15/17 Chromosome Translocation in Acute Promyelocytic Leukemia

The t(15q+ ;17q-) chromosome rearrangement frequently found in acute promye- locytic leukemia (APL) [1] has an uneven geographical distribution. For example, in Chicago (United States) six out of six (6/6) patients with APL have the translo- cation, in Buffalo (United States) 1/18, in Belgium 16/18, and in Finland 0/9 [2]. In England, chromosome analysis of only one patient with APL has been reported, and in this case the translocation was not present [2]. The reasons for this distri- bution are unclear, and methodological factors in chromosome preparations and culture conditions have been suggested as playing a role [2].

We report here the first case of APL (M3 variant) [3] in England in which the 15/17 translocation was demonstrated. The patient is a 57-year-old Caucasian fe- male, with a previous history of bladder cancer, treated with radical radiation therapy in 1978. At the time of referral, in July 1980, her peripheral blood count showed a hemoglobin level of 7.7 g/dl, a white cell count of 2.9 × 10~/liter (with 58% hypogranular blasts and promyelocytes), and a platelet count of 18 x 10~/ liter. Disseminated intravascular coagulation was present. Bone marrow cells were separated on Ficoll-Isopaque and analyzed with the following immunological markers [4]: sheep E rosettes (<1.0%), anti-immunoglobulin (anti-Ig) (<1.0%), monoclonal anti-common acute lymphoblastic leukemia (anti-cALL) (<1.0%), monomorphic anti-HLA-DR (DA-2) (<1.0%), and anti-terminal deoxynucleotidyl- transferase (TdT) (<1.0%). Lack of reactivity with markers that are lymphoid lin- eage-directed (E rosettes, anti-cALL, anti-Ig, TdT) is to be expected; the absence of staining with anti-HLA-DR accords with the diagnosis of APL rather than an- other variant of acute myeloblastic leukemia (AML) [4]. The patient was treated with adriamycin, cytosine arabinoside, and 6-thioguanine. Complete remission was achieved after two cycles, and four further cycles of consolidation treatment were given. The patient was discharged in January 1981, well and with a recover- ing blood count.

Chromosome spreads were prepared by standard methods from unstimulated pe- ripheral blood at diagnosis. The culture medium consisted of RPMI 1640, 10% fetal calf serum, L-glutamine (0.03%), and heparin (20 U/ml). Cultures were harvested after 19 and 22 hr. G-Banding [5] revealed a 15/17 translocation in 28 out of 30 spreads examined. A partial karyotype showing this rearrangement is shown in Fig. 1. The other chromosomes were normal. The translocation chromosomes appear identical to those previously described [1]. We interpret the break in chromosome No. 15 to be in band 15q25 or 15q26, and in chromosome No. 17 to be in band 17q22. It appears that the 17q22-17qter region has been translocated to the distal portion of 15q; it is difficult to say with certainty, however, whether the translo-

© Elsevier Science Publishing Co., Inc., 1982 52 Vanderbilt Ave., New York, NY 10017

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Cancer Genetics and Cytogenetics 5, 353-354 (1962) 0165-460S/82/040353-0252.75

354 D. Sheer et al.

I ! 15 15q ÷ 17 17q-

Figure 1 Partial karyotype showing t(15q+;17q-}.

cation is reciprocal. APL with t(15q + ; 1 7 q - ) is therefore to be found in England, but its overall incidence remains to be established. The reasons for its apparently peculiar geographical distribution may become evident with more consistent con- ditions for cytological analysis.

D. SHEER E. SOLOMON M.F. GREAVES

T.A. LISTER

Imperial Cancer Research Fund Lincoln's Inn Fields

London and

ICRF Medical Oncology Unit St. Bartholomew's Hospital

London

REFERENCES

1. Rowley JD, Golomb HM, Vardiman J, Fukuhara S, Dougherty S, Potter D (1977): Further evidence for a non-random chromosomal abnormality in acute promyelocytic leukemia. Int J Cancer 20, 869-872.

2. Second International Workshop on Chromosomes in Leukemia (1980): Chromosomes in acute promyelocytic leukaemia. Cancer Genet Cytogenet 2, 103-107.

3. Bennett JM, Catovsky D, Daniel MT, Flandrin G, Galton DAG, Gralnick HR, Sultan C (1980): A variant form of hypergranular promyelocytic leukaemia (M3). Br J Haematol 44, 169-170.

4. Boss MA, Delia D, Robinson JB, Greaves MF (1980): Differentiation-linked expression of cell surface markers on HL-60 leukaemic cells. Blood 56, 910-916.

5. Seabright M (1972): The use of proteolytic enzymes for the mapping of structural rearrange- ments in the chromosomes of man. Chromosoma (Berlin) 36, 204-210.

Received June 19, 1981; accepted August 3, 1981.