Difference between Expression of Adhesion Molecules on CD34 ⁺ Cells from Bone Marrow and G‐CSF‐Stimulated Peripheral Blood

Abstract

c-kit, CD58, CD62L and CD49d were less expressed on CD34 + cells of PBSC than of BM, the difference being statistically significant for CD49d (p < 0.05). CD49e and CD37 were expressed more in PBSC than BM without being statistically significant. The mean fluorescence intensity for all adhesion molecules on CD34 + cells did not differ significantly between PBSC and BM. The significantly lower expression of CD49d on G-CSF-mobilized PBSCs might suggest that downregulation of this molecule may be involved in the process of peripheral stem cell mobilization.

Expression of Adhesion Molecules on CD34 + Cells in Peripheral Blood of Non‐Hodgkin's Lymphoma Patients Mobilized with Different Growth Factors

“…This decrease was observed in apheresis collections of all patients, regardless of the growth factor used for mobilization, and is consistent with results obtained by other groups [32][33][34][35][36][37][38]. The fact that "good mobilizers" and "poor mobilizers," as well as PBSCs from normal donors, had a similar pattern of coexpression of this molecule on CD34 + cells suggests a role for this molecule in the process of release of stem cells to the PB.…”

“…+ [24][25][26][27][28] and CD34 + cells coexpressing adhesion molecules such as CD62L (L-selectin) and CD49d (VLA-4) were the most studied [32][33][34][35][36][37][38]. Yet, the factors involved in the regulation of stem cell release from the BM to the circulation and the mechanism of homing are still poorly understood.…”

“…Other subsets of CD34 + cells express well-defined adhesion molecules such as Lselectin and very late-acting antigen (VLA)4 which are thought to play an important role in the release of CD34 + cells to the PB during mobilization and in homing to the BM in the process of engraftment. The extent of expression on CD34 + cells of adhesion molecules, such as VLA-4 (CD49d) and L-selectin (CD62L), has been shown to correlate with mobilization of PBSC [32][33][34][35][36][37] and in vivo treatment of mice with antibodies to VLA-4 [38] or VCAM-1 [39] + cells expressing Thy1, VLA-4, and L-selectin in all three arms of the study with a similar pattern of these CD34 + subsets observed in all patients, regardless of the mobilization regimen used.…”

Effect of thalidomide on stem cell collection and engraftment in patients with multiple myeloma

“…The authors speculated that an impaired ability to mobilize stem cells in the presence of thalidomide may be related to thalidomide's modulation of adhesion molecules in the bone marrow stroma. [24][25][26][27] Several factors have been identified as adversely affecting engraftment, including inadequate stem cell dose, previous exposure to an alkylating agent, increasing patient age, serum beta 2 -microglobulin, previous radiotherapy, and lack of growth factor use after infusion. [9][10][11][12][13][14][15][16]28 In our study, early platelet engraftment of 20 000/ml was affected by previous thalidomide use.…”

Thalidomide as salvage therapy for VAD-refractory multiple myeloma prior to autologous PBSCT

“…The process of stem cell mobilization involves modulation of adhesive interactions between bone marrow stroma and hematopoietic stem cells, Thal seems to modulate these adhesion molecules (integrins, selectins and immunoglobulinlike) with a reduction of circulating CD 34+ after mobilization. 3,4 Also, transplants should therefore not be attempted with minimally adequate numbers of stem cells reinfused since Thal could also hamper the adhesive process mediated by L-selectin. 5 Secondly, Thal given in combination with multiagent chemotherapy and dexamethasone is associated with a significantly increased risk of deep vein thrombosis(DVT) that has important clinical implications.…”