Imatinib mesylate associated with delayed hematopoietic recovery after concomitant chemotherapy

Abstract

results indicate that the absolute degradation rate is approximately 50% per day (ie an increase of the Ct value with one cycle) in PB MNC.Although our data are based on a limited and heterogeneous set of samples, they clearly indicate that transcripts are rapidly degraded ex vivo and that the rate of degradation can differ between different types of transcripts, between PB and BM, and between patients. As such differential degradation will results in an over-or underestimation of MRD levels, samples should preferably be processed on the day of sampling; this processing should include at least the Ficoll density centrifugation-based separation of MNC and the cell lysis step of the RNA extraction. Even better, because changes in transcript levels can already occur within the initial 4 h, 5 samples should be collected in tubes with immediate stabilization of intracellular RNA, thereby preventing any degradation of control gene and/or fusion gene transcripts. Such reagents for stabilization of RNA have recently successfully been applied in a multi-center study (Mueller et al, Blood 2003; 102: 64a abstract We read with interest the paper by Ruchatz et al 1 on the effect of imatinib on hematopoietic recovery following idarubicin exposure in murine model. We describe an elderly patient with chronic myeloid leukemia (CML) and transformed large B-cell lymphoma treated with imatinib mesylate and combination chemotherapy.This is an 87-year-old male with a history of follicular lymphoma involving left cervical nodes in 1996, and he refused further therapy. He presented again in July 2000 with a markedly elevated WBC of 223 000/ml. A bone marrow examination confirmed the diagnosis of CML in chronic phase with cytogenetic study showing 45X,-Y,t(9; 22)(q34; q11) [25].

Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients

“…Despite the relatively high specificity of IM treatment towards the BCR-ABL fusion protein, off-target multikinase inhibitory effects occur and can interfere with normal hematopoiesis. 1, 2 For instance, non-specific inhibition of Flt3L has been associated with disruption of dendritic cell (DC) homeostasis and functions in both mice and humans. 3 In addition, studies have reported an interference of IM with T cell counts and activation.…”