Etiology of acute myeloid leukemia following intensive therapy for AML – relapse, secondary disease or bad luck?

Abstract

Figure 1R-banded karyotype showing the paracentric inversion of chromosome 16 and double trisomies 9 and 22. diagnosis, as the bone marrow is not involved. 3,4 Our patient had a diagnosis of lymphoma before recognizing that it was a GS.Cytogenetic analysis of AML patients with chloroma have rarely been reported in the literature. However, it appears that patients with t(8;21)-associated AML type 2 are more prone than others to develop GS. Indeed, 4.5 to 38% of patients with t(8;21)(q22;q22) developed GS. 1,5 Several patients with AML type 4 in conjunction with GS and abnormalities of chromosome 16, mainly inv(16)(p13;q22) have also been reported. 3,[6][7][8] However, isolated granulocytic sarcoma of the small intestine preceding AML is rare; only two patients had a cytogenetic analysis using banding techniques. Le Beau et al 8 Etiology of acute myeloid leukemia following intensive therapy for AML -relapse, secondary disease or bad luck? Leukemia (2002) Our patient has several features in common with the latter case (inv(16) and double trisomies 9 and 22), but for the absence of eosinophilia and the type of AML which is definitely of the FAB type 2; however, the blasts composing the granulocytic sarcoma had some monocytic characteristics which were not found in the marrow at the diagnosis of the AML. Therefore, to the best of our knowledge, this is the first report of a case of GS preceding AML type 2 with inv(16). F Morel

A Case Report of the Second de Novo Acute Myeloid Leukemia (AML) Following Allogeneic Stem Cell Transplantation in a Patient with the First AML

“…This case is characterized by a longer latency period than in previous reports of secondary AML following hematologic and/or non hematologic malignancies [2,3] as well as rare cases of secondary AML following de novo AML [5,6], in the setting of an allograft. In our case, the new complex cytogenetic aberrations, as well as the allograft setting, suggested that the origin of the second AML might be biologically unrelated to the first.…”

“…Secondary AML is primarily associated with therapy-related myelodysplasia and/or therapy-related AML ( t -AML) as a late complication following cytotoxic therapy [1-3,5,6]. t -AML consists of 2 different syndromes: one with a long latency (5 to 7 years or more) observed following the administration of alkylating agents, which frequently show antecedent dysplastic changes and clonal abnormalities with loss of all or part of chromosome 5 or 7, or both.…”

“…However, in most cases, prior treatment was not for leukemia but for lymphoma and myeloma [2,3]. Indeed, although malignancies after HSCT has been well documented [4], secondary leukemia occurring after HSCT for AML is rare [5,6]. In addition, most reports of secondary AML follow autologous transplantation, and it is rare following allogeneic transplantation regardless of the primary disease [4], primarily because the anti-leukemic effects of the allogeneic graft reduce the risk of a secondary clone developing.…”

Secondary malignancies after hematopoietic stem cell transplantation

“…Secondary leukemia occurring after HSCT for AML is rare [41]. CHO et al reported a case of the second de novo acute myeloid leukemia following allogeneic HSCT for a first occurence of AML [42].…”