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t(6;9)(p22;q34) associated with acute myeloblastic leukemia (M1)
LETTERS TO THE EDITOR t(6;9)(p22;q34) Associated with Acute Myeloblastic Leukemia (M1)
A nonrandom association between t(6;9)(p22;q34) and acute myeloblastic leukemia (AML) has been described. Because patients with this abnormality often have an increased proportion of basophilic cells in the bone marrow (BM), a strong but not absolute association apparently exists between t(6;9)(p22;q34) and an excess of basophils [1]. Approximately 27 cases of malignant myeloproliferative disorders have been reported with t(6;9) as the only cytogenetic abnormality noted at diagnosis [2]. Most have been classified as M2 or M4, and only four cases have been classified as M1 [1]. We report a fifth patient with AML (M1) who had a translocation between 6p22 and 9q34. A 29-year-old man was diagnosed with AML (M1) in March 1990. The initial hematologic analyses showed the following data: white blood cell (WBC) count 5.4 x 109/L (with 80% blast cells), hemoglobin level 5.7 g/dl, and platelet count 30 x 109/L. No hepatomegaly, splenomegaly, or lymphadenopathies were noted. No infectious focus was evident. BM aspirate showed increased cellullarity, with more than 90% blasts cells without maturation (small and intermediate size, high nuclear:cytoplasmic ratio, and scarce granulation with basophilic cytoplasm); no basophils were evident. The peroxidase was positive ( + + + + in 36% blast cells) and periodic-acid Schiff (PAS) test was negative (French-American-British criteria = AML - M1). Immunologic data from BM cells showed CD13, 80%; CD7, 30%; and HLA-DR, 83%. CD33, CD14, CD9, CD71, CD41, CD19, CD3, CD24, CD10, and they were glycophorin and IgM negative. Cytogenetic investigations of BM cells
Figure 1
showed a 46,XY,t(6;9)(p22;q34) karyotype (Fig. 1). The patient received chemotherapy (BF-9 modification, Royal Marsden Hospital: ara-C (10 mg/kg) days 1 and 10, daunoblastine (1.5 mg/kg) days 3 and 12, 6-thioguanine (100 mg/m 2) days 2, 3, 11, and 12 and, finally, mitoxantrone (12 mg/m 2) days 4 and 13). A febrile episode was treated with antibiotics (ceftazidine, amikacin, and vancomicin) and with amphotericin-B. All microbiologic studies were negative. A partial remission was obtained in April 1990. An intensification course with high-dose ara-C and VP-16 (2 g/ m2/12 h and 100 mg/m2/24 h for 4 days) was given on April 24, 1990. The treatment was well tolerated, and the patient showed a full hematologic recovery in the peripheral blood. BM aspirate and bilateral biopsies showed complete remission (May 21, 1990). A relapse occurred in October 1990. At this time, immunologic data from BM cells showed CD45, 70%, HLA-DR, 55%, CD13, 93%, CD14, 24%, CD7, CD3, CD9, CD19, CD33, CD61, and they were glycophorin negative. The patient died in November 1990. Patients with t(6;9) have been reported with an average age of 33 years and a median age of 38 years [1]. Our patient, who was aged 29 years, was relatively young. Our case lacked marrow basophilia. Marrow basophilia has been specifically sought in at least 22 patients with AML and t(6;9). Whereas five of nine patients with M2 had an excess of basophils in their BM, only one of five patients with M1 and one of eight with M4 showed this finding [3]. Thus, the association between t(6;9) and basophilia may be restricted to M2, with only an occasional finding of M1 and M4.
t(6;9)(p;22;q34) in a patient with acute myeloblastic leukemia (M1).
76 Cancer Genet Cytogenet63:76-77 (1992) 0165-4608/92/$05.00
© 1992 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010
t(6;9)(p22;q34) in AML(M1)
A. PLAJA
J. M. PUEYO X. LABRAI~A D. GARCIA R.-A. DE LA CHICA F. SOLE S. WOESSNER
77
U n i d a d de Gen6tica Hospital Maternal Valle Hebr6n Paseo Valle Hebr6n s/n 08035 Barcelona, Spain Reference Laboratory Barcelona, Spain
Laboratori de Citologia Hematologica Servei d'Hematologia i Oncologia Hospital Central L'Alian~a Barcelona, Spain
R. MATAIX T. MOLERO E. OJEDA
Servicio de Hematologia Hospital N. Sra del Pino Las Palmas de Gran Canaria, Spain
REFERENCES
1. Heim S, Mitelman F (1987): Cancer Cytogenetics. Alan R. Liss, New York. 2. Fonatsch C, Stollmann B, Holldack J, Engert A (1987): Translocation (6;9)(p23;q34) in smoldering leukemia and acute nonlymphocytic leukemia. Cancer Genet Cytogenet 26:363368. 3. Sandberg A (1990): The Chromosomes in Human Cancer and Leukemia. 2nd Ed. Elsevier, New York.
A nonrandom association between t(6;9)(p22;q34) and acute myeloblastic leukemia (AML) has been described. Because patients with this abnormality often have an increased proportion of basophilic cells in the bone marrow (BM), a strong but not absolute association apparently exists between t(6;9)(p22;q34) and an excess of basophils [1]. Approximately 27 cases of malignant myeloproliferative disorders have been reported with t(6;9) as the only cytogenetic abnormality noted at diagnosis [2]. Most have been classified as M2 or M4, and only four cases have been classified as M1 [1]. We report a fifth patient with AML (M1) who had a translocation between 6p22 and 9q34. A 29-year-old man was diagnosed with AML (M1) in March 1990. The initial hematologic analyses showed the following data: white blood cell (WBC) count 5.4 x 109/L (with 80% blast cells), hemoglobin level 5.7 g/dl, and platelet count 30 x 109/L. No hepatomegaly, splenomegaly, or lymphadenopathies were noted. No infectious focus was evident. BM aspirate showed increased cellullarity, with more than 90% blasts cells without maturation (small and intermediate size, high nuclear:cytoplasmic ratio, and scarce granulation with basophilic cytoplasm); no basophils were evident. The peroxidase was positive ( + + + + in 36% blast cells) and periodic-acid Schiff (PAS) test was negative (French-American-British criteria = AML - M1). Immunologic data from BM cells showed CD13, 80%; CD7, 30%; and HLA-DR, 83%. CD33, CD14, CD9, CD71, CD41, CD19, CD3, CD24, CD10, and they were glycophorin and IgM negative. Cytogenetic investigations of BM cells
Figure 1
showed a 46,XY,t(6;9)(p22;q34) karyotype (Fig. 1). The patient received chemotherapy (BF-9 modification, Royal Marsden Hospital: ara-C (10 mg/kg) days 1 and 10, daunoblastine (1.5 mg/kg) days 3 and 12, 6-thioguanine (100 mg/m 2) days 2, 3, 11, and 12 and, finally, mitoxantrone (12 mg/m 2) days 4 and 13). A febrile episode was treated with antibiotics (ceftazidine, amikacin, and vancomicin) and with amphotericin-B. All microbiologic studies were negative. A partial remission was obtained in April 1990. An intensification course with high-dose ara-C and VP-16 (2 g/ m2/12 h and 100 mg/m2/24 h for 4 days) was given on April 24, 1990. The treatment was well tolerated, and the patient showed a full hematologic recovery in the peripheral blood. BM aspirate and bilateral biopsies showed complete remission (May 21, 1990). A relapse occurred in October 1990. At this time, immunologic data from BM cells showed CD45, 70%, HLA-DR, 55%, CD13, 93%, CD14, 24%, CD7, CD3, CD9, CD19, CD33, CD61, and they were glycophorin negative. The patient died in November 1990. Patients with t(6;9) have been reported with an average age of 33 years and a median age of 38 years [1]. Our patient, who was aged 29 years, was relatively young. Our case lacked marrow basophilia. Marrow basophilia has been specifically sought in at least 22 patients with AML and t(6;9). Whereas five of nine patients with M2 had an excess of basophils in their BM, only one of five patients with M1 and one of eight with M4 showed this finding [3]. Thus, the association between t(6;9) and basophilia may be restricted to M2, with only an occasional finding of M1 and M4.
t(6;9)(p;22;q34) in a patient with acute myeloblastic leukemia (M1).
76 Cancer Genet Cytogenet63:76-77 (1992) 0165-4608/92/$05.00
© 1992 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010
t(6;9)(p22;q34) in AML(M1)
A. PLAJA
J. M. PUEYO X. LABRAI~A D. GARCIA R.-A. DE LA CHICA F. SOLE S. WOESSNER
77
U n i d a d de Gen6tica Hospital Maternal Valle Hebr6n Paseo Valle Hebr6n s/n 08035 Barcelona, Spain Reference Laboratory Barcelona, Spain
Laboratori de Citologia Hematologica Servei d'Hematologia i Oncologia Hospital Central L'Alian~a Barcelona, Spain
R. MATAIX T. MOLERO E. OJEDA
Servicio de Hematologia Hospital N. Sra del Pino Las Palmas de Gran Canaria, Spain
REFERENCES
1. Heim S, Mitelman F (1987): Cancer Cytogenetics. Alan R. Liss, New York. 2. Fonatsch C, Stollmann B, Holldack J, Engert A (1987): Translocation (6;9)(p23;q34) in smoldering leukemia and acute nonlymphocytic leukemia. Cancer Genet Cytogenet 26:363368. 3. Sandberg A (1990): The Chromosomes in Human Cancer and Leukemia. 2nd Ed. Elsevier, New York.