Preferential cytogenetic response to continuous intravenous low-dose decitabine (DAC) administration in myelodysplastic syndrome with monosomy

human erythroblastic leukemia viral oncogene homolog 1 (ErbB1)/EGFR that is approved for the treatment of NSCLC6 and pancreatic cancer.7 Although erlotinib has not been studied in AML, gefitinib, another EGFR-TKI, can induce neutrophil differentiation in several EGFR AML cell lines.8,9 In this patient’s bone marrow biopsy, EGFR was expressed on stromal cells, including fibroblasts, but was undetectable on myeloblasts (Figure 1E). Erlotinib was well tolerated; complete remission was achieved within a month, and was durable for at least 6 months. In conclusion, this is the first report of a patient with AML who achieved complete remission following erlotinib. EGFR inhibitors may induce neutrophilic differentiation of AML blasts via effects on tyrosine kinases (or other targets) distinct from EGFR. Clinical trials of erlotinib in the treatment of AML are warranted.