Clinical risk classification is inaccurate in predicting relapse in adult patients with acute lymphoblastic leukemia, sometimes resulting in patients receiving inappropriate chemotherapy or stem cell transplantation (SCT). We studied minimal residual disease (

This imatinib-based protocol improved long-term outcome of adult patients with Ph-positive ALL. With SCT, post-transplantation mortality and relapse remain the major hindrance to additional therapeutic improvement. Additional intensification of imatinib therapy should warrant a better molecular response and clinical outcome, both in patients selected for SCT and in those unable to undergo this procedure.

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We suggest that patients with late PTLDs and limited disease may benefit from local treatment. For patients who require chemotherapy, we suggest that it should be administered to minimize the risk of infection complications.

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Pulmonary distress symptoms and thrombotic complications are side‐effects of all‐trans‐retinoic acid (ATRA) therapy for remission induction in acute promyelocytic leukaemia (APL). The ATRA‐induced increase of leukaemic cell adhesive molecules may be responsible. To explore this we used a functional assay to study the effect of ATRA treatment on the adhesion of blast cells to cultured human endothelial cells (EC), endothelial cell matrix (ECM), and interleukin 1β‐activated EC (IL1 + EC). NB4 cells, a maturation‐inducible human promyelocytic leukaemia cell line, were treated with 1 μm ATRA or the vehicle (control), labelled with 51Cr and tested in the adhesion assay. ATRA increased NB4 adhesion to EC (P < 0.01), ECM (P < 0.001) and IL1 + EC (P = n.s.). An inhibition study with anti‐EC adhesion receptors MoAbs indicated that anti‐E‐selectin, anti‐VCAM‐1 and anti‐ICAM‐1 effectively inhibited cell adhesion to IL1 + EC (18 ± 7%, 45 ± 6.9% and 29 ± 6% inhibition, respectively) and to unstimulated EC. Preincubation of ATRA‐treated NB4 cells with MoAbs anti‐VLA4 and anti‐LFA1, the VCAM‐1 and ICAM‐1 counter‐receptors respectively, resulted in a significant inhibition of adhesion. Cytofluorimetric analysis of the NB4 cell membrane molecules confirmed the increase under ATRA of VLA4, LFA1, MAC1 and ICAM‐1. Therefore ATRA increases NB4 cell adhesion to the endothelium and the subendothelial matrix. These findings parallel the increment of NB4 surface adhesive molecules, among which VLA4 and LFA1 appear to play an important part. These mechanisms may contribute to the complications of ATRA therapy in APL.

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