Although rare, secondary clonal hematologic neoplasia may occur after successful therapy for acute promyelocytic leukemia (APL). These secondary clonal events may be considered therapy-related, but may also be due to an underlying background of clonal hematopoiesis from which both malignancies may develop. In this manuscript, we describe two patients with secondary clones after APL therapy characterized in one patient by deletion of chromosome 11q23 and, in the other, by monosomy of chromosome 7, and also provide a review of all secondary clonal disorders described after APL therapy. We suggest that since most reports identify karyotypic abnormalities not typically associated with chemotherapy, there may be another mechanism underlying secondary clonal development after complete response to initial APL therapy.
Keywords: 6-MP, 6-mercaptopurine; AML, acute myelocytic leukemia; APL, acute promyelocytic leukemia; ATG, antithymyocyte globulin; ATO, arsenic trioxide; ATRA, all-trans retinoic acid; Acute myelocytic leukemia (AML); CR, complete remission; FISH, fluorescence in situ hybridization; MDS, myelodysplastic syndrome; Myelodysplastic syndrome (MDS); PML-RARalpha, promyelocytic leukemia/Retinoic acid receptor alpha; Secondary clone; Therapy-related acute myelocytic leukemia (t-AML); Therapy-related myelodysplastic syndrome (t-MDS); t- MDS, therapy-related myelodysplastic syndrome; t-AML, therapy-related acute myelocytic leukemia.