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Hematologic and cytogenetic response to lenalidomide monotherapy in acute myeloid leukemia arising from JAK2V617F positive, del(5)(q13q33) myelodysplastic syndrome

Leukemia volume 20, pages 2063–2064 (2006)Cite this article

After discussion of the therapeutic alternatives with the patient (including the likelihood of failure with induction chemotherapy with secondary AML (median survival 3–4 weeks3 with standard therapy in age >80 years), and the responses reported with lenalidomide for patients with interstitial chromosome 5q deletions and MDS,1 she elected to begin lenalidomide at a dose of 10 mg/day. She tolerated the agent well, without any adverse effects. After 3 months of treatment, she had normal peripheral blood counts, and no evidence of circulating blasts. A repeat marrow exam showed a slightly hypercellular marrow, with significant improvement in granulocytic maturation and with a significant decrease in the myeloblasts to 5% blasts (Figure 1b). Additionally, the karyotypic abnormalities had completely resolved to show a normal female karyotype. This would be considered a partial response by the International Working Group for Acute Myeloid Leukemia,4 nearly a complete response had the blast percentage been <5%. After 2 additional months of lenalidomide (still at 10 mg/day) the patient had evidence of disease progression, with recurrent leukopenia, thrombocytopenia and 10% blasts in the marrow. Additionally, repeat karyotypic analysis showed clonal progression, with 10/30 metaphases having the del(5)(q13q33), and 7 of them with multiple other structural abnormalities including loss of 17p. Alternative therapy was initiated.

To our knowledge, this is the first report of lenalidomide monotherapy resulting in achieveving a solid 5-month partial remission in an elderly patient with high-risk AML. The patient reported a high quality of life during this time, and was free of transfusions, hospitalization and infection. The coexistence of the JAK2V617F mutation, a finding more commonly associated with myeloproliferative disorders, is an additional intriguing aspect to this case. JAK2V167F has been described in 6.2% MDS patients with del(5)(q13q33),5 and the clinical significance is unknown. Few agents offer any legitimate therapeutic benefit to elderly patients with secondary AML. Lenalidomide may have activity as monotherapy against AML arising from del(5q)-associated chronic myeloid disorders. However, the apparent ability of the disorders to undergo clonal evolution suggests that combination or sequential therapy of lenalidomide with other novel or traditional agents should be explored.

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Authors and Affiliations

  1. Division of Hematology, Mayo Clinic, Rochester, MN, USA

    R A Mesa, A Tefferi & D P Steensma

  2. Division of Hematopathology, Mayo Clinic, Rochester, MN, USA

    C-Yang Li

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  1. R A Mesa
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  2. A Tefferi
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  4. D P Steensma
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Correspondence to R A Mesa.

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Mesa, R., Tefferi, A., Li, CY. et al. Hematologic and cytogenetic response to lenalidomide monotherapy in acute myeloid leukemia arising from JAK2V617F positive, del(5)(q13q33) myelodysplastic syndrome. Leukemia 20, 2063–2064 (2006). https://doi.org/10.1038/sj.leu.2404398

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