Association of an inversion of chromosome 16 with abnormal marrow eosinophils in acute myelomonocytic leukemia. A unique cytogenetic-clinicopathological association
MM Le Beau, RA Larson, MA Bitter, JW Vardiman, HM Golomb, and JD Rowley
We identified 18 patients with an inversion of chromosome 16, inv(16)(p13q22), among 308 patients with newly diagnosed acute nonlymphocytic leukemia. Each of these 18 patients had acute myelomonocytic leukemia (M4 subtype) and eosinophils with distinctly abnormal morphology, cytochemical staining, and ultrastructure. These eosinophils constituted from 1 to 33 per cent of the nucleated marrow cells. In our series, every patient with acute myelomonocytic leukemia and abnormal eosinophils also had an abnormal chromosome 16. This subgroup of M4 patients had a good response to intensive therapy designed to induce remission; 13 of 17 treated patients entered a complete remission, and 10 remain in first remission. Thus, patients with an inversion of chromosome 16 appear to represent a unique cytogenetic-clinicopathological subtype of acute nonlymphocytic leukemia with a favorable prognosis.
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(2002). Real-time quantitation of minimal residual disease in inv(16)-positive acute myeloid leukemia may indicate risk for clinical relapse and may identify patients in a curable state. Blood
99: 443-449
[Abstract][Full Text]
McKenna, R. W.
(2000). Multifaceted Approach to the Diagnosis and Classification of Acute Leukemias. Clin. Chem.
46: 1252-1259
[Abstract][Full Text]
van der Kolk, D. M., Vellenga, E., van der Veen, A. Y., Noordhoek, L., Timmer-Bosscha, H., Ossenkoppele, G. J., Raymakers, R. A., Muller, M., van den Berg, E., de Vries, E. G. E.
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95: 3514-3519
[Abstract][Full Text]
Lowenberg, B., Downing, J. R., Burnett, A.
(1999). Acute Myeloid Leukemia. NEJM
341: 1051-1062
[Full Text]
Adya, N., Stacy, T., Speck, N. A., Liu, P. P.
(1998). The Leukemic Protein Core Binding Factor beta (CBFbeta )-Smooth-Muscle Myosin Heavy Chain Sequesters CBFalpha 2 into Cytoskeletal Filaments and Aggregates. Mol. Cell. Biol.
18: 7432-7443
[Abstract][Full Text]
Britos-Bray, M., Ramirez, M., Cao, W., Wang, X., Liu, P. P., Civin, C. I., Friedman, A. D.
(1998). CBFbeta -SMMHC, Expressed in M4eo Acute Myeloid Leukemia, Reduces p53 Induction and Slows Apoptosis in Hematopoietic Cells Exposed to DNA-Damaging Agents. Blood
92: 4344-4352
[Abstract][Full Text]
Kogan, S. C., Lagasse, E., Atwater, S., Bae, S.-c., Weissman, I., Ito, Y., Bishop, J. M.
(1998). The PEBP2beta MYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia. Proc. Natl. Acad. Sci. USA
95: 11863-11868
[Abstract][Full Text]
Viswanatha, D. S., Chen, I.-M., Liu, P. P., Slovak, M. L., Rankin, C., Head, D. R., Willman, C. L.
(1998). Characterization and Use of an Antibody Detecting the CBFbeta -SMMHC Fusion Protein in inv(16)/t(16;16)-Associated Acute Myeloid Leukemias. Blood
91: 1882-1890
[Abstract][Full Text]
Liu, P., Seidel, N., Bodine, D., Speck, N., Tarle, S., Collins, F.S.
(1994). Acute Myeloid Leukemia with Inv(16) Produces a Chimeric Transcription Factor with a Myosin Heavy Chain Tail. Cold Spring Harb Symp Quant Biol
59: 547-553
[Abstract]
Liu, P, Tarle, S., Hajra, A, Claxton, D., Marlton, P, Freedman, M, Siciliano, M., Collins, F.
(1993). Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia. Science
261: 1041-1044
[Abstract]
KOEFFLER, H. P.
(1987). Syndromes of Acute Nonlymphocytic Leukemia. ANN INTERN MED
107: 748-758
[Abstract]
Simmers, R., Sutherland, G., West, A, Richards, R.
(1987). Fragile sites at 16q22 are not at the breakpoint of the chromosomal rearrangement in AMMoL. Science
236: 92-94
[Abstract]