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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Therapy-related acute myelomonocytic leukemia following successful treatment for acute promyelocytic leukemia.

We report a case of therapy-related acute myeloid leukemia (t-AML), M4 FAB subtype, with t(10;11)(p14;q21) chromosome abnormality developed in a patient treated for acute promyelocytic leukemia (APL) after 4 years of continuous complete remission (CCR). Two distinct forms of t-AML have been described: the classical type and the second type. Our case has many characteristics in common with the second type of t-AML such as: exposure to topoisomerase II active agents (idarubicin (IDA), mitoxantrone (MITOX), etoposide (VP16)), M4 FAB subtype, a latency period of 39 months and absence of a preleukemic phase. However, it differs in the chromosome 11 breakpoint (band q21 instead of q23) and absence of ALL-1 (Hrx, MLL, Htrx) gene involvement. This can represent the second observation of t-AML occurring after treatment for APL.[1]

References

  1. Therapy-related acute myelomonocytic leukemia following successful treatment for acute promyelocytic leukemia. Todisco, E., Testi, A.M., Avvisati, G., Moleti, M.L., Cedrone, M., Cimino, G., Mancini, F., Amadori, S., Mandelli, F. Leukemia (1995) [Pubmed]
 
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