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 to cells and matrices participates in the regulation of lymphocyte proliferation, maturation and tissue localization. Consequently, abnormal patterns of adhesion molecule expression may contribute to the pathophysiology of lymphoproliferative disorders. Integrins are major cell-surface adhesive proteins composed by alpha and beta subunits. In contrast to normal lymphocytes, Burkitt's lymphoma (BL) cells lack the beta2 integrin CD11a/CD18. To study the molecular mechanism underlying this deficiency, presence of the transcript for each subunit was analysed by Northern blotting in group I BL lines (BL biopsy-like) and, for comparison, Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs). While transcripts for both CD11a (alpha subunit) and CD18 (beta subunit) were readily detected in LCLs, BL lines contained the transcript for the alpha subunit only. Treatment of BL cells with phorbol ester for 72 h induced expression of the beta subunit mRNA and the CD11a and CD18 antigens on the cell surface. The results indicate that the CD11a/CD18 deficiency of BL is due to absence of the beta subunit transcript and that this defect is restored by stimulation of the cells.
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PMID:Adhesion molecule CD11a/CD18-deficient Burkitt's lymphoma cells lack the transcript for the beta, but not the alpha, integrin subunit. 902 Mar 71