Prediction of mobilisation failure in patients with non-Hodgkin's lymphoma

Abstract

Summary:Factors affecting progenitor cell mobilisation in patients with non-Hodgkin's lymphoma (NHL) are incompletely understood. We have analysed factors predicting mobilisation failure in 97 consecutive patients with NHL (59 males, 38 females; median age 49 years) who received mobilisation with intermediate- dose þ cells. In all, 18 patients (19%) failed to reach this threshold. In univariate analysis, premobilisation factors associated with mobilisation failure included BM involvement at the time of diagnosis (P ¼ 0.001) or prior to mobilisation (P ¼ 0.001) and low platelet count just prior to mobilisation (P ¼ 0.001). In multivariate analysis, only BM involvement at diagnosis (P ¼ 0.004) and platelet count just prior to mobilisation (P ¼ 0.01) were associated with mobilisation failure. A mathematical model based on these two factors and presented in the form of a receiver operating characteristics curve showed a sensitivity of 0.71 and a specificity of 0.77 in the prediction of mobilisation failure. Patients at a high risk of mobilisation failure may benefit from novel approaches.

Identification of prognostic factors for plerixafor‐based hematopoietic stem cell mobilization

“…Overall, the patients were characterized by features that are known to affect standard stem cell mobilization negatively, including advanced age, a diagnosis of NHL, previous radiotherapy, extensive treatment with chemotherapy, treatment with lenalidomide or purine analogues, previous autoSCT, or failure of at least one previous attempt at mobilization [7][8][9][10][11][12][13][14][15]. We observed that, despite these unfavorable characteristics, mobilization with plerixafor and G-CSF enabled the required number of stem cells to be collected in 67.5% of patients.…”

“…A number of factors are known to affect the outcome of stem cell mobilization negatively in the context of traditional mobilization regimens that are based on the administration of G-CSF with or without chemotherapy. These factors include advanced age, a diagnosis of non-Hodgkin's lymphoma (NHL), previous radiotherapy, extensive treatment with chemotherapy, treatment with lenalidomide or purine analogues, and the failure of at least one previous attempt at mobilization [7][8][9][10]. In this study, we decided to investigate whether the above-mentioned factors might allow the prediction of a suboptimal outcome for stem cell mobilization with plerixafor and G-CSF.…”

Plerixafor in patients with lymphoma and multiple myeloma: effectiveness in cases with very low circulating CD34+ cell levels and preemptive intervention vs remobilization

“…[7][8][9][10][11][12][13][14][15][16] However, the value of patient characteristics and prior treatment clinical factors to successfully score and accurately predict the risk of poor mobilization is controversial, and recent studies do suggest that they are inaccurate predictors and should not be used to identify candidates for optimized strategies to prevent mobilization failure. 17,18 At present, the measurement of preapheresis levels of CD34+ cells in PB 7,[19][20][21][22] is the most robust and recommended indicator to identify potential poor mobilizers and efficiently rescue them with novel mobilization strategies, including the use of plerixafor.…”

Plerixafor with and without chemotherapy in poor mobilizers: results from the German compassionate use program

“…Although poor mobilizers are difficult to identify in advance, the following risk factors for poor mobilization are accepted in general: age 460 years, progressive disease, severe BM involvement, previous chemo-and/or radiotherapy, type of chemotherapy, previously failed mobilization attempts, platelet counts o100 Â 10 9 /L before apheresis and the occurrence of neutropenic fever during mobilization. 3,[9][10][11][12][13] The bicyclam plerixafor (formerly known as AMD3100) was found to interrupt the interaction between the chemokine stroma-derived factor-1 alpha, which is constitutively expressed on BM stromal cells, 14,15 and its cognate receptor CXCR4 on CD34 þ HSC, 16 resulting in a rapid increase of PBSC. 12 Initially designed as a CXCR4 entry-inhibitor for the treatment of HIV-1 infections, 17 the transient leukocytosis monitored in healthy individuals, as well as in HIV positive patients, led to a change in its use.…”