Expression of intercellular adhesion molecule 1 (ICAM‐1) in childhood acute lymphoblastic leukaemia: correlation with clinical features and outcome

Abstract

Summary.To investigate whether expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in childhood acute lymphoblastic leukaemia (ALL) has an impact on the biological behaviour of the disease, we evaluated 751 children of the ALL-BFM 90 trial with B-cell precursor-(n = 677) or T-cell-ALL (n = 74) for CD54 expression within immunological subgroups, its correlation to certain clinical features, and therapy outcome.The highest percentage of patients expressing CD54 was found in common-and pre-B-ALL (76 . 1% and 61 . 4%, respectively). There was intermediate expression in pre-pre-B-ALL (47 . 8%), and the lowest expression was detected in T-ALL (12 . 2%).A significant positive correlation could be demonstrated between low CD54 expression (<20% stained blasts) and high peripheral leucocyte counts, central nervous system (CNS) involvement, and splenomegaly at the time of diagnosis (P < 0 . 01). In addition, CD54 expression was a favourable but not independent prognostic factor. Event-free survival estimate at 4 . 5 years was 86% for CD54 + patients (n = 463), compared with 78% for CD54¹ patients (n = 241) (P < 0 . 01). These findings demonstrate that CD54 expression has an impact on dissemination patterns and outcome of childhood ALL, and emphasizes the potential relevance of adhesion mechanisms in influencing clinical characteristics and prognosis of haematological malignancies.

The Burkitt-like lymphomas: a Southwest Oncology Group study delineating phenotypic, genotypic, and clinical features

“…The BLLs have a much higher incidence of CAM abnormalities than the DLBCLs, with frequent loss of LFA and ICAM antigens. These particular CAMs were previously found to have a high rate of loss of expression in BL [34][35][36][37][38][39][40] ; we here found CAM loss also to be a common feature of the BLLs. As previously observed, 41 a loss of CAMs results in abnormalities in T-and B-cell interactions and diminishes immune surveillance.…”

Detection of acute leukemia cells with mixed lineage leukemia (MLL) gene rearrangements by flow cytometry using monoclonal antibody 7.1

“…The significantly lower expression of the adhesion molecule CD54 (ICAM-1) in moab 7.1-positive pro-B-ALL with t(4;11) observed in our study compared to other pro-B-ALL cases might be of relevance for the higher incidence of hyperleukocytosis, organomegaly, and CNS involvement in this leukemia subtype, 5 as low CD54 expression correlates with these clinical parameters in childhood ALL. 31 Moreover, NG2 itself may contribute to extramedullary manifestations in acute leukemia. Increased NG2 expression was shown to enhance metastatic properties of melanoma cells, possibly by modulating binding events mediated through the adhesion molecules CD44 and ␣ 4 ␤ 1 integrin.…”

Thrombomodulin and von Willebrand Factor: Relation to Endothelial Dysfunction and Disease Outcome in Children with Acute Lymphoblastic Leukemia

“…Expression of β2-integrins is observed in most cases of ALL, as evidenced by CD18 (β2 subunit) and CD11a (LFA-1) expression. The ligand for LFA-1 is ICAM-1 (CD54), which is expressed on a wide variety of cells such as ECs, fibroblasts, and hemopoietic cells [14,15]. Human precursor B-ALL cells appear to bind to cellular and extracellular components of bone marrow stroma through a variety of mechanisms, including CD-44 attachment to hyaluronate and VLA integrin binding to fibronectin and VCAM.…”

“…Human precursor B-ALL cells appear to bind to cellular and extracellular components of bone marrow stroma through a variety of mechanisms, including CD-44 attachment to hyaluronate and VLA integrin binding to fibronectin and VCAM. The role of these molecules in the growth and dissemination of precursor B-ALL requires further investigation [13,14,15,16]. …”