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The geographical distribution of 15;17 translocation in acute promyelocytic leukemia
LETTERS TO THE EDITOR The Geographical Distribution of 15;17 Translocation m Acute Promyelocytic Leukemia
The translocation between chromosomes 15 and 17, t(15q+;17q-), described by Rowley et al. [1] in acute promyelocytic leukemia (APL) has been confirmed by several subsequent reports [2-7]. This chromosomal abnormality appears to be distinctive for APL, but not all patients with APL show it. Moreover, the incidence of the translocation in patients with APL reported from different centers varies considerably. Whereas the translocation was found in all of 3 patients from Chicago [1] and in 11 of 16 Belgium patients [4], it was not found in any 12 patients from Finland and Sweden. Geographical variation in the incidence of the translocation in APL patients was recently reviewed by the Second International Workshop on Chromosomes in Leukemia [9]. Of 80 patients with APL who were evaluated, 33 patients (41%) carried the 15;17 translocation. The geographical distribution of the patients was again quite unusual. Whereas Belgium and France had many cases with the translocation, it was not found in any patients from Finland, Sweden, Germany, or Italy. Striking differences occurred even within the U.S.A. The tre_n_slocation was found in all of 6 patients examined in Chicago hut in only I of 18 patients examined in Buffalo. In the Pacific area, five patients from Australia did not show the translocation, but it was present in the two Japanese patients studied. Four other Japanese patients with the translocation have been described elsewhere [7]. We have recently reviewed six patients from the Canterbury region of New Zealand who were diagnosed as having APL during the 4 year period 1977-1980. Successful G-banded chromosome preparations were obtained from 5 of the patients at the time of diagnosis or at subsequent relapse. Four of the patients conformed to the FAB criteria for MB acute leukemia and one to the hypogranular M3 variant. [10,11]. All were aged over 50 years, except one 12-year-old girl. Three of the patients, including the M3 variant and the young girl, showed the 15;17 translocation, two of them in direct bone marrow preparations. A bone marrow was not obtained from the third patient, the M3 variant, but the tra~n~location was present in cultured blood cells. Excellent banded preparations were obtained from the other 2 patients and they clearly did not carry the tra_nslocation in bone marrow cells prepared directly and cultured for 24 hr. The total numbers of banded cells examined from the patients were 68 and 28. We confirm that the chromosomal abnormality found in APL appears to be a reciprocal translocation between chromosomes 15q and 17q. The precise break points are not easily determined but appear to be at either 15q24 and 17(121-22 or at 15q21-22 and about the region of 17qll or 12.
273 © Elsevier North Holland, Inc.. 1981 52 Vanderbilt Ave.. New York, NY 10017
Cancer Genetics and Cytogenetics 3, 273-274 (1981) 0165-4608/@1/032730252.50
274
Letter to the Editor To our knowledge this is the first report of the 15;17 translocation from a country in the South Pacific region, and in a population of largely British orion. A full report of these findings will be published elsewhere. It has been suggested that the geographical distribution of the 15;17 translocation in patients with APL may reflect ethnic or environmental backgrounds that are relevant to the development of the disease [8,9]. There is a need to examine more cases to determine if this apparent uneven geographical distribution is real or whether it is an artifact, possibly of technical procedures. P.H. FITZGERALD JAN FRASER M.E.J. BEARD
Cancer Society of New Zealand Cytogenetics Unit and Department of Hematology Christchurch Hospital Christchurch, New Zealand
REFERENCES 1. Rowley JD, Golomb HM, Dougherty C (1977}: 15/17 translocation; a consistent chromosomal change in acute promyelocyttc |eukaemia. Lancet 1, 549-550. 2. KanekoY, Sakurai M (1977}: 15/17 translocation in acute promyelocytic leukaemia. Lancet 7, 961. 3. Scheres JMJC, Hustinx TWJ, de Vaan GAM, Ruttea FJ (1978): 15/17 translocetion in acute promyelocytic leukaemia. Hum Genet 43, 115-117. 4. Van Den Berghe H, Louwagie A, Broeckaert-Van Orshoven A, David G, Verwilghen R, Michaux JL, Sokal G (1979}: Chromosome abnormalities in acute promyelocytic leukemia (APL). Cancer 43, 558- 562. 5. Testa JR, Colomb HM, Rowley JD, Vardiman JW, Sweet DL (1978): Hypergranular promyelocytic leukemia (APL}:cytogenetic and ultrastructural specificity. Blood 52,272-280. 6. Golomb HM, Testa JR, Vardiman JW, Butler AE, Rowley JD (1979): Cytogenetic and ultrastructural features of de novo acute promyelocytic leukemia; the University of Chicago F,x. perience (1973-1978). Cancer Genet Cytogenet 1, 69-78. 7. Kondo K, Sasaki M (1979): Cytogenetic studies in four cases of acute promyelocytic leukemia (APL). Cancer Genet Cytogenet 1,131-138. 8. Teerenhovi L, Borgstrom GH, Mitelman F, Brandt L, Vuopio P, Timonen T, Almqvist A, de la Chapelle A (1978): Uneven geographical distribution of 15;17-translocation in acute promuelocytic leukaemia. Lancet 2, 797. 9. Second International Workshop on Chromosomes in Leukemia (1980): Chromosomes in aoJte promyelocytic leukemia. Cancer Gent Cytogenet 2,103 - 107. 10. Bennett )M, Catovsky D, Daniel M-T, Flandrin G, Galton DAG, Gralnick HR, Sultan C (1976}: Proposals for the classification of the acute leukaemias. French-American-British (FAB) Co-operative Group. Br J Haematol 33, 451-458. 11. Bennett JM, Catovsky D, Daniel M-T, Flandrin G, Galton DAG, Gralnick HR, St~ltan C (1960): A variant form of hypergranular promyelocytic leukaemia (M3). Br J Haemato144, 169-170. Received October 21, 1980; accepted November 10, 1980.
The translocation between chromosomes 15 and 17, t(15q+;17q-), described by Rowley et al. [1] in acute promyelocytic leukemia (APL) has been confirmed by several subsequent reports [2-7]. This chromosomal abnormality appears to be distinctive for APL, but not all patients with APL show it. Moreover, the incidence of the translocation in patients with APL reported from different centers varies considerably. Whereas the translocation was found in all of 3 patients from Chicago [1] and in 11 of 16 Belgium patients [4], it was not found in any 12 patients from Finland and Sweden. Geographical variation in the incidence of the translocation in APL patients was recently reviewed by the Second International Workshop on Chromosomes in Leukemia [9]. Of 80 patients with APL who were evaluated, 33 patients (41%) carried the 15;17 translocation. The geographical distribution of the patients was again quite unusual. Whereas Belgium and France had many cases with the translocation, it was not found in any patients from Finland, Sweden, Germany, or Italy. Striking differences occurred even within the U.S.A. The tre_n_slocation was found in all of 6 patients examined in Chicago hut in only I of 18 patients examined in Buffalo. In the Pacific area, five patients from Australia did not show the translocation, but it was present in the two Japanese patients studied. Four other Japanese patients with the translocation have been described elsewhere [7]. We have recently reviewed six patients from the Canterbury region of New Zealand who were diagnosed as having APL during the 4 year period 1977-1980. Successful G-banded chromosome preparations were obtained from 5 of the patients at the time of diagnosis or at subsequent relapse. Four of the patients conformed to the FAB criteria for MB acute leukemia and one to the hypogranular M3 variant. [10,11]. All were aged over 50 years, except one 12-year-old girl. Three of the patients, including the M3 variant and the young girl, showed the 15;17 translocation, two of them in direct bone marrow preparations. A bone marrow was not obtained from the third patient, the M3 variant, but the tra~n~location was present in cultured blood cells. Excellent banded preparations were obtained from the other 2 patients and they clearly did not carry the tra_nslocation in bone marrow cells prepared directly and cultured for 24 hr. The total numbers of banded cells examined from the patients were 68 and 28. We confirm that the chromosomal abnormality found in APL appears to be a reciprocal translocation between chromosomes 15q and 17q. The precise break points are not easily determined but appear to be at either 15q24 and 17(121-22 or at 15q21-22 and about the region of 17qll or 12.
273 © Elsevier North Holland, Inc.. 1981 52 Vanderbilt Ave.. New York, NY 10017
Cancer Genetics and Cytogenetics 3, 273-274 (1981) 0165-4608/@1/032730252.50
274
Letter to the Editor To our knowledge this is the first report of the 15;17 translocation from a country in the South Pacific region, and in a population of largely British orion. A full report of these findings will be published elsewhere. It has been suggested that the geographical distribution of the 15;17 translocation in patients with APL may reflect ethnic or environmental backgrounds that are relevant to the development of the disease [8,9]. There is a need to examine more cases to determine if this apparent uneven geographical distribution is real or whether it is an artifact, possibly of technical procedures. P.H. FITZGERALD JAN FRASER M.E.J. BEARD
Cancer Society of New Zealand Cytogenetics Unit and Department of Hematology Christchurch Hospital Christchurch, New Zealand
REFERENCES 1. Rowley JD, Golomb HM, Dougherty C (1977}: 15/17 translocation; a consistent chromosomal change in acute promyelocyttc |eukaemia. Lancet 1, 549-550. 2. KanekoY, Sakurai M (1977}: 15/17 translocation in acute promyelocytic leukaemia. Lancet 7, 961. 3. Scheres JMJC, Hustinx TWJ, de Vaan GAM, Ruttea FJ (1978): 15/17 translocetion in acute promyelocytic leukaemia. Hum Genet 43, 115-117. 4. Van Den Berghe H, Louwagie A, Broeckaert-Van Orshoven A, David G, Verwilghen R, Michaux JL, Sokal G (1979}: Chromosome abnormalities in acute promyelocytic leukemia (APL). Cancer 43, 558- 562. 5. Testa JR, Colomb HM, Rowley JD, Vardiman JW, Sweet DL (1978): Hypergranular promyelocytic leukemia (APL}:cytogenetic and ultrastructural specificity. Blood 52,272-280. 6. Golomb HM, Testa JR, Vardiman JW, Butler AE, Rowley JD (1979): Cytogenetic and ultrastructural features of de novo acute promyelocytic leukemia; the University of Chicago F,x. perience (1973-1978). Cancer Genet Cytogenet 1, 69-78. 7. Kondo K, Sasaki M (1979): Cytogenetic studies in four cases of acute promyelocytic leukemia (APL). Cancer Genet Cytogenet 1,131-138. 8. Teerenhovi L, Borgstrom GH, Mitelman F, Brandt L, Vuopio P, Timonen T, Almqvist A, de la Chapelle A (1978): Uneven geographical distribution of 15;17-translocation in acute promuelocytic leukaemia. Lancet 2, 797. 9. Second International Workshop on Chromosomes in Leukemia (1980): Chromosomes in aoJte promyelocytic leukemia. Cancer Gent Cytogenet 2,103 - 107. 10. Bennett )M, Catovsky D, Daniel M-T, Flandrin G, Galton DAG, Gralnick HR, Sultan C (1976}: Proposals for the classification of the acute leukaemias. French-American-British (FAB) Co-operative Group. Br J Haematol 33, 451-458. 11. Bennett JM, Catovsky D, Daniel M-T, Flandrin G, Galton DAG, Gralnick HR, St~ltan C (1960): A variant form of hypergranular promyelocytic leukaemia (M3). Br J Haemato144, 169-170. Received October 21, 1980; accepted November 10, 1980.