Clinical significance of LEA-1 expression in adult acute myeloid leukemia

Kawada, Hiroshi; Fukuda, Ryuki; Yoshida, Miyoko; Takei, Mieko; Kobayashi, N; Masumoto, Akira; Ogawa, Yoshiaki; Sasao, Tamotsu; Katayama, Nobuyuki; Watanabe, Shigeki; Umeda, Yoshikatsu; Yamauchi, Kunihiko; Yonekura, Shuji; Ichikawa, Yukinobu

doi:10.1016/0145-2126(95)00113-1

Cited by 11 publications

(10 citation statements)

References 25 publications

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“…Thus, the involvement of AML1 and CBF␤ in the CD11a gene transcription raises the possibility that CD11a/CD18 integrin expression might be altered in some of these lymphoproliferative disorders. In this regard, diminished or absent CD11a/CD18 expression has been noted in cases of B-lineage acute lymphoblastic leukemia (33), and the expression of CD11a/CD18 significantly correlates with splenomegaly, resistance to induction chemotherapies and short survival periods in AML patients (34). Therefore, it will be of interest to determine whether an association exists between AML1 or CBF␤ chromosomal translocations and the expression of the CD11a/CD18 integrin, a task we are currently undertaking.…”

Section: Discussionmentioning

confidence: 99%

Polyomavirus Enhancer-binding Protein 2/Core Binding Factor/Acute Myeloid Leukemia Factors Contribute to the Cell Type-specific Activity of the CD11a Integrin Gene Promoter

Puig‐Kröger¹,

López-Rodrı́guez²,

Relloso³

et al. 2000

Journal of Biological Chemistry

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The CD11a/CD18 leukocyte integrin (LFA-1; also known as ␣L/␤2) mediates leukocyte transendothelial migration during immune and inflammatory responses and participates in lymphoma metastasis. CD11a/CD18 leukocyte-restricted expression is controlled by the CD11a gene promoter, which confers tissue-specific expression to reporter genes in vitro and in vivo. DNase I protection analysis of the CD11a proximal gene promoter revealed DNA-protein interactions centered at position -110 (CD11a-110). Disruption of CD11a-110 reduced CD11a promoter activity in a cell type-specific manner, as it reduced its activity by 70% in Jurkat lymphoid cells, whereas the effect was considerably lower in K562 and HepG2 cells. Electrophoretic mobility shift assays showed evidence of cell type-specific differences in CD11a-110 binding and indicated its specific recognition by members of the polyomavirus enhancerbinding protein 2/core binding factor (CBF)/acute myeloid leukemia (AML) family of transcription factors. AML1B/CBF␤ transactivated the CD11a promoter, with AML1B/CBF␤-mediated transactivation being completely dependent on the integrity of the CD11a-110 element. Therefore, CBF/AML factors play a role in the cell type-restricted transcription of the CD11a integrin gene through recognition of CD11a-110. The involvement of CBF/AML factors in CD11a expression raises the possibility that CD11a/CD18 expression might be deregulated in acute myeloid and B-lineage acute lymphoblastic leukemias, thus contributing to their altered adhesion and metastatic potential.

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Section: Discussionmentioning

confidence: 99%

Polyomavirus Enhancer-binding Protein 2/Core Binding Factor/Acute Myeloid Leukemia Factors Contribute to the Cell Type-specific Activity of the CD11a Integrin Gene Promoter

Puig‐Kröger¹,

López-Rodrı́guez²,

Relloso³

et al. 2000

Journal of Biological Chemistry

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“…A long term administration of G-CSF together with anti-tumoral drugs including Ara-C has, therefore, been effectively used for the treatment of patients with AML [6,7,9]. On the other hand, both low concentrations of ACR and Ara-C show a time-dependent cytotoxicity to AML cells [10,11], and we also experienced a case of refractory AML who was successfully treated with continuous intravenous infusion of low-dose ACR and Ara-C [12]. These observa tions prompted us to treat the present case with a combi nation therapy of G-CSF and continuous intravenous in fusion of low-dose ACR and Ara-C.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Cell Surface Expression of T-Lymphoid Antigens and Adhesion Molecules on Acute Myeloid Leukaemia Cells after in vivo Administration of Granulocyte Colony-Stimulating Factor

Kawada

Ichikawa²,

Kobayashi³

et al. 1994

Acta Haematol

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We herein report a case of acute myeloid leukaemia (AML, FAB: MO) who showed upregulation of T-lymphoid antigens (CD2, CD7) and adhesion molecules (CD11a, CD11b, CD18) on leukaemic cells after in vivo administration of granulocyte colony-stimulating factor (G-CSF). To our knowledge, this is the first report which describes in vivo changes of cell surface antigen expression on AML cells after the administration of G-CSF.

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“…45,46 These differences in adhesion receptor expression may affect myeloblast trafficking and patient prognosis. 42,47 A study by the Eastern Cooperative Oncology Group suggested that CD11b ϩ AML may constitute a new leukemic syndrome with a poor response to chemotherapy and reduced survival. 45 However, the impact of adhesion receptor expression on clinical presentation and response to therapy was not examined for the patients studied in this report.…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell activation by myeloblasts: molecular mechanisms of leukostasis and leukemic cell dissemination

Stucki

Rivier

Gikic

et al. 2001

Blood

241

203

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Clinical significance of LEA-1 expression in adult acute myeloid leukemia

Cited by 11 publications

References 25 publications

Polyomavirus Enhancer-binding Protein 2/Core Binding Factor/Acute Myeloid Leukemia Factors Contribute to the Cell Type-specific Activity of the CD11a Integrin Gene Promoter

Polyomavirus Enhancer-binding Protein 2/Core Binding Factor/Acute Myeloid Leukemia Factors Contribute to the Cell Type-specific Activity of the CD11a Integrin Gene Promoter

Upregulation of Cell Surface Expression of T-Lymphoid Antigens and Adhesion Molecules on Acute Myeloid Leukaemia Cells after in vivo Administration of Granulocyte Colony-Stimulating Factor

Endothelial cell activation by myeloblasts: molecular mechanisms of leukostasis and leukemic cell dissemination

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