inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects. On the other hand, t(5;17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML). We treated a 29-year-old woman with the first reported case of de novo AMML Eo with inv(16)(p13q22) in addition to t(5;17)(q13;q11). Although she attained complete remission (CR) immediately after induction therapy, the disease recurred 1 year after the completion of consolidation therapies. She underwent HLA-matched unrelated allogeneic bone marrow transplantation (UBMT), together with a myeloablative conditioning regimen, after achieving a second CR and has survived without a recurrence for more than 24 months since UBMT. In general, certain secondary chromosomal abnormalities are associated with the phenotype of the disease, which retains its essential biologic characteristics established by the primary abnormality.Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22). We believe this report is the first of de novo AMML Eo with t(5;17)(q13;q11) showing as a secondary chromosomal aberration with inv(16)(p13q22).
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Misawa S, Lee E, Schiffer CA, Liu Z8, Testa JR. Association of the translocation (15;17) with the malignant proliferation of promye-locytes in acute leukemia and chronic myelogenous leukemia at blast crisis. Blood. 1986;67:270–274.
Scolnik MP, Paracios M, Acevedo SH, et al. Promyelocytic blast crisis of chronic myelogenous leukaemia with translocations (9;22) and (15;17). Leuk Lymphoma. 1998;31:231–236.
Enright H, Weisdorf D, Peterson L, Rydell RE, Kaplan ME, Arthur DC. Inversion of chromosome 16 and dysplastic eosinophils in accelerated phase of chronic myeloid leukemia. Leukemia. 1992;6:381–384.
Asou N, Sanada I, Tanaka K, et al. Inversion of chromosome 16 and bone marrow eosinophilia in a myelomonocytic transformation of chronic myeloid leukemia. Cancer Genet Cytogenet. 1992;61:197–200.
Heim S, Christensen BE, Fioretos T, Sorensen AG, Pedersen NT. Acute myelomonocytic leukemia with inv(16)(p13q22) complicating Philadelphia chromosome positive chronic myeloid leukemia. Cancer Genet Cytogenet. 1992;59:35–38.
Grimwade D, Walker H, Oliver F, et al, on behalf of the Medical Research Council Adult and Children’s Leukaemia Working Parties. The importance of diagnostic cytogenetics on outcome in AML: analysis of 1,612 patients entered into the MRC AML 10 trial. Blood. 1998;92:2322–2333.
Roulston D, Espinosa R 3rd, Stoffel M, Bell GI, Le Beau MM. Molecular genetics of myeloid leukemia: identification of the commonly deleted segment of chromosome 20. Blood. 1993;82:3424–3429.
Soenen V, Preudhomme C, Roumier C, Daudignon A, Lai JL, Fenaux P. 17p deletion in acute myeloid leukemia and myelodysplastic syndrome: analysis of breakpoints and deleted segments by fluorescence in situ. Blood. 1998;91:1008–1015.
Mamuris Z, Dumont J, Dutrillaux B, Aurias A. Chromosomal differences between acute nonlymphocytic leukemia inpatients with prior solid tumors and prior hematologic malignancies: a study of 14 cases with prior breast cancer. Cancer Genet Cytogenet. 1989;42:43–50.
Miyawaki S, Sakamaki H, Ohtake S, et al, and the Japan Adult Leukemia Study Group. A randomized, postremission comparison of four courses of standard-dose consolidation therapy without maintenance therapy versus three courses of standard-dose consolidation with maintenance therapy in adults with acute myeloid leukemia: the Japan Adult Leukemia Study Group AML97 study. Cancer. 2005;104:2726–2734.
Le Beau MM, Larson RA, Bitter MA, Vardiman JW, Golomb HM, Rowley JD. Association of an inversion of chromosome 16 with abnormal marrow eosinophils in acute myelomonocytic leukemia: a unique cytogenetic-clinicopathological association. N Engl J Med. 1983;309:630–636.
Johansson B, Mertens F, Mitelman F. Secondary chromosomal abnormalities in acute leukemias. Leukemia. 1994;8:953–962.
Castro PD, Liang LC, Nagarajan L. Deletion of chromosome 5q13.3 and 17p loci cooperate in myeloid neoplasms. Blood. 2000;95:2138–2143.
Babicka L, Ransdorfova S, Brezinova J, et al. Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH. Leuk Res. 2006. In press.
Liang H, Samanta S, Nagarajan L. SSBP2, a candidate tumor suppressor gene, induces growth arrest and differentiation of myeloid leukemia cells. Oncogene. 2005;24:2625–2634.
Longo L, Donti E, Mencarelli A, et al. Mapping of chromosome 17 breakpoints in acute myeloid leukemias. Oncogene. 1990;5:1557–1563.
Marcucci G, Mrozek K, Ruppert AS, et al. Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of patients with inv(16): a Cancer and Leukemia Group B study. J Clin Oncol. 2005;23:5705–5717.
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Sakai, R., Fujimaki, K., Yamazaki, E. et al. Acute Myelomonocytic Leukemia with Dysplastic Bone Marrow Eosinophils Showing t(5;17)(q13;q11) and a Secondary Chromosomal Aberration, inv(16)(p13q22). Int J Hematol 84, 417–420 (2006). https://doi.org/10.1532/IJH97.06054
- Acute myeloid leukemia
- Additional chromosomal abnormality