Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD54/Intercellular Adhesion Molecule-1 (ICAM-1) is a cell adhesion molecule largely distributed among normal and neoplastic tissues. Through the binding to its ligand(s) CD54 plays a key role in cell to cell interactions leading to the immune response. Recently, CD54 expression has been investigated on hematopoietic cells: the antigen is predominantly expressed in the early stages of normal hematopoiesis and during the activation of blood cells. As regards to hematological malignancies, CD54 is strongly expressed on neoplastic cells from "stem cell derived" neoplasms. In AML, CD54 expression is related with other differentiation-linked molecules such as CD34 and HLA-DR and is significantly correlated with FAB morphological classification. In lymphoproliferative disorders, a high CD54 expression is associated with germinal centre lymphomas. This review summarizes our current understanding of CD54 with emphasis on recent advances and reference to unresolved issues such as its prognostic role in the clinical outcome of oncohematological diseases.
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PMID:Expression and functional role of CD54/Intercellular Adhesion Molecule-1 (ICAM-1) on human blood cells. 136 19

Adhesion receptors from the very late activation (VLA) (beta 1) integrin subfamily play a role in the cooperation of hematopoietic progenitors with bone marrow stroma, and the disregulated expression of these molecules, as evaluated by immunophenotyping, has been implicated in the acquisition of the malignant phenotype by hematopoietic cells. In the present study, Northern hybridization was used to determine the pattern of expression of transcripts for VLA subunits in: (i) leukemic blasts obtained from the peripheral blood of ten patients with acute myelogenous leukemia (AML) of different FAB subclasses; (ii) the human leukemic cell lines KG-1, HL-60, K-562, HEL and U-937; and (iii) normal hematopoietic cells. Most of the AML blasts and the cultured leukemic cells expressed mRNAs for the beta 1 and alpha 5 subunits (the only exception among the cell lines was KG-1 cells) and these transcripts were also found in normal bone marrow progenitors, peripheral blood mononuclear cells (PBMNC), and peripheral blood monocytes. While the alpha 4 transcript was detected in all cultured cells but K-562, and in normal circulating monocytes, it occurred in blasts from only two AML patients and was weakly expressed in mature PBMNC. No specific pattern of expression of beta 1, alpha 5, and alpha 4 transcripts could be related to cell differentiation or maturation in the AML blasts and leukemic cell lines tested. None of the primary AML blasts or cultured cells showed mRNA messages for alpha 2, alpha 3 or alpha 6 chains of the beta 1 integrins. The results suggest that, in some cases of AML, the malignant phenotype of leukemic blasts may be associated with down-regulated transcription of the alpha 4 integrin subunit.
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PMID:Expression of beta 1 integrin mRNAs in human leukemic blasts. 752 92

Minimally differentiated acute myeloid leukemia (AML-M0) is a rare FAB subtype (2-3% of AMLs) of poor prognosis. The aim of our study was to characterize AML-M0 expression and regulation of adhesion/costimulatory molecule involved in immune recognition, to test blast in vitro immunogenicity, and to determine the percentage of leukemia progenitor cells. Here, we demonstrate that alloimmune recognition of AML-M0 in primary mixed lymphocyte reaction, as evaluated by IL-2 secretion of responding T cells, is reduced in comparison with more differentiated subtypes (128 +/- 95 pg/ml vs304 +/- 159 pg/ml, P < 0.05). These data are in line with low blast cell expression of major histocompatibility complex (MHC) class II DR molecules, and of the CD28 ligand B7-2, which plays an important role in AML immune recognition. Adhesion/costimulatory molecules were up-regulated by leukemic cell stimulation via CD40, and, although less efficiently, by gamma-IFN; both stimuli improved blast cell immunogenicity. We also demonstrate that AML-M0 have a very high percentage (40% +/- 30) of CD34+/CD38- leukemic clonogenic precursors in comparison with more differentiated AMLs (2.5% +/- 2) or non-leukemic CD34+hematopoietic precursors (1.8% +/- 0.8). Since the presence of a leukemic cell population at an early differentiation stage has been identified as a poor prognostic factor, we conclude that the high frequency of CD34+/CD38- blasts in AML-M0 may converge with already identified poor prognosis factors such as chemotherapy resistance and cytogenetic abnormalities. The clinical implications of AML-M0 impaired in vitroimmunogenicity and a high percentage of CD34+/CD38- blasts will require comparative analysis of additional patients. The increased immunogenicity of blast cells after CD40 triggering provide interesting clues for AML-M0 immunotherapy, that have to be confirmed with an in vivo leukemia model in mice.
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PMID:The immunophenotype of minimally differentiated acute myeloid leukemia (AML-M0): reduced immunogenicity and high frequency of CD34+/CD38- leukemic progenitors. 1051 51