Disease relevance of CD34

• MVD was evaluated by 2 observers after CD34 immunostaining and correlated with the following parameters: WHO classification, hormonal profile, tumor size, vascular endothelial growth factor expression, occurrence of metastasis, duration of survival [1].
• Differential long-term and multilineage engraftment potential from subfractions of human CD34+ cord blood cells transplanted into NOD/SCID mice [2].
• Increased erythropoietin-receptor expression on CD34-positive bone marrow cells from patients with chronic myeloid leukemia [3].
• In summary, the results show that the defects in the erythroid development in a subpopulation of patients with myelodysplasia is localized at an early stage of the erythroid differentiation and is associated with the persistent expression of the CD34 antigen and, in some cases, with the expression of Evi-1 [4].
• Differentiation of T-ALL cells was also evidenced through the downregulation of CD34 precursor cell antigen, the generation of CD4+ and CD8+ cells from CD4+ CD8+ precursors, and the acquisition of mature T-cell functions [5].

Psychiatry related information on CD34

• Utilization of FITC-QBEND10 instead of FICT-8G12 to estimate infrequent (usually less than or equal to 5%) CD34+ CHP for clinical decision-making in autologous transplantation of CHP exposes clinicians to the risk of either overestimating (false positive) or underestimating (false negative) these cells in peripheral blood [6].
• We studied the expression of a hemopoietic progenitor cell antigen, designated CD34, in brains from subjects with Alzheimer's disease (AD) and non-neurological controls [7].
• We have treated a series of 10 patients presenting with de novo (six) or relapsed (four) chronic lymphocytic leukaemia (CLL) with fludarabine as cytoreduction treatment and consolidation of the response with CD34 selected peripheral blood stem cell transplantation using cyclophosphamide and total body irradiation (TBI) as conditioning therapy [8].

High impact information on CD34

• Hematopoietic stem cells: are they CD34-positive or CD34-negative [9]?
• Although rhesus SP cells do not initially possess any hematopoietic colony-forming capability, they acquire the ability to form colonies after long-term culture on bone marrow stroma, coincident with their conversion to a CD34-positive phenotype [10].
• These studies suggest the existence of a hitherto unrecognized population of hematopoietic stem cells that lack the CD34 surface marker classically associated with primitive hematopoietic cells [10].
• Hematopoietic and vascular endothelial cells develop normally in the podocalyxin-deficient mice, possibly through functional compensation by other sialomucins (such as CD34) [11].
• Podocalyxin is a CD34-related sialomucin that is expressed at high levels by podocytes, and also by mesothelial cells, vascular endothelia, platelets, and hematopoietic stem cells [11].

Chemical compound and disease context of CD34

• All the eight leukemias that were either refractory to treatment or that relapsed afterwards were assigned to cluster B. In the latter cluster, CD34 upregulation and serine proteases downregulation is consistent with a maturation arrest and lack of granulocytic differentiation [12].
• We conclude that staining formalin-fixed, paraffin-embedded, high-grade lymphomas with anti-cyclin D-1 antibody is useful in confirming the diagnosis of MCL-BV, whereas positive reactions with CD99, CD34, and particularly TdT are more characteristic of LBL [13].
• Gastrointestinal stromal tumors (GISTs) coexpress CD34 and the Kit tyrosine-kinase receptor (CD117) [14].
• Similar results for VA and MVD were obtained with FvW and CD34 labeling.CONCLUSION(S): Leiomyomas have a smaller vascular area, a lower microvessel density, and a higher vascular luminal area than normal myometrium [15].
• METHODS: Endothelial cell and pericyte area were assessed by quantitative immunocytochemistry for CD34 and alpha-smooth muscle actin respectively, taking into consideration the dynamics of lutein cell hypertrophy and atrophy throughout the cycle and after HCG treatment [16].

Biological context of CD34

• The heparin binding PECAM-1 adhesion molecule is expressed by CD34+ hematopoietic precursor cells with early myeloid and B-lymphoid cell phenotypes [17].
• Induction of apoptosis by overnight incubation of CD34 cells in serum-deprived medium resulted in the upregulation of bcl-2 as a single population histogram [18].
• The reason for this may be the convergence of various unfavorable prognostic factors, such as (1) the high incidence of cytogenetic abnormalities; (2) the lack of differentiation features and the expression of immaturity markers such as CD34 and CD7; and (3) the frequent expression of P-170 [19].
• The other case differed by virtue of expression of CD34 and was also hyperdiploid with 55 chromosomes [20].
• We show here that SDF-1 may also be involved in hematopoiesis, promoting the proliferation of human CD34(+) cells purified from normal adult peripheral blood (PB) [21].

Anatomical context of CD34

• However, we demonstrate that SCID-repopulating cells present in the CD34(+) cell fraction of cord blood can be segregated into subpopulations with distinct repopulation characteristics [2].
• Progressive changes included: loss of CD34, acquisition of and graded increases in the level of cell surface CD19, and appearance of immature B cells expressing mu/kappa or mu/lambda cell surface Ig receptors [22].
• The cytoplasmic domain of stem cell antigen CD34 is essential for cytoadhesion signaling but not sufficient for proliferation signaling [23].
• Flow cytometric analysis of bone marrow cells based on the expression of CD34, Kit receptor, and G-CSFR demonstrated a reduced frequency of CD34(+)/Kit(+)/ G-CSFR(+) cells in patients with SCN [24].
• Expression of the CD34 gene in vascular endothelial cells [25].

Associations of CD34 with chemical compounds

• In addition, CD34, a glycoprotein found on immature cells of both myeloid and lymphoid lineages, was expressed on the blast cells of 48.2% of patients [26].
• Progenitor subpopulations were isolated from bone marrow of normal or 5-fluorouracil (5FU)-treated mice and separated by sorting based on the surface antigens Sca-1, c-kit, and CD34 [27].
• Analysis of transgenic human CD34-tTA mice by cross breeding with a strain carrying Cre recombinase under control of a tetracycline-responsive element demonstrated induction of Cre expression in mice in a pattern consistent with the expression of the human CD34 transgene [28].
• The further metabolism of arachidonic acid to eicosanoids by CD34(+) cells was not detected by either thin-layer chromatography, enzyme immunoassay, or differential spectroscopy [29].
• There are two consensus protein kinase C phosphorylation sites and one potential tyrosine kinase phosphorylation site in the cytoplasmic portion of CD34 [30].

Physical interactions of CD34

• Our investigations shed new light on signaling pathways of CD34 by demonstrating that CD34 couples to the hematopoietic adapter protein CrkL [31].
• Conversely, CD44 bound HA very weakly when exons V8-V10 were replaced with a CD34 mucin domain, which is heavily modified by O-linked glycans [32].
• It is expressed by the primitive CD34 positive haemopoietic stem cells and interacts with the Kit ligand for signal transduction [33].
• The pattern of CD31 immunolabelling was more complex and extensive than the vessel pattern shown by CD34 or factor VIII staining [34].
• Among the adhesion molecules, the integrins of the beta 1-subfamily are known to direct cell-cell and cell-matrix interactions and evidence has been provided that CD34-positive stem cells bind either to the bone marrow stroma or to the extracellular matrix proteins through the beta 1-integrins [35].

Regulatory relationships of CD34

• Chemokine SDF-1 enhances circulating CD34(+) cell proliferation in synergy with cytokines: possible role in progenitor survival [21].
• CD34 expression of this cell line and the ability of transforming growth factor-beta to inhibit the TNF-alpha induction of E-selectin was examined [36].
• The serum VEGF levels in hemodialysis patients were not different from those in control subjects and did not correlate with CD34+ MNC counts [37].
• CD38 co-expression analysis also showed that a small but distinct group of cells expressing low CD38 and no external CD34 antigen could be detected [38].
• CXCR-4 was expressed on PB CD34(+) cells [21].

Other interactions of CD34

• Supernatants of fresh leukemic cells from 24 AML patients contained significantly more VEGF than supernatants from bone marrow cells of 9 normal donors or of CD34-enriched cells from 3 normal volunteer donors as determined by an enzyme-linked immunosorbent assay [39].
• Neither CD34 nor CD33 antigens were identified on the cells [40].
• Hematopoietic precursors expressing strongly the CD34 antigen (CD34(s+)) and lacking CD38 or HLA-DR expression were analyzed by using three-color immunofluorescence staining [18].
• In synergy with cytokines, SDF-1 increased PB CD34(+) and CD34(high)CD38(low) cell expansion and colony formation [21].
• More than 75% of TdT+ cells in both the blood and marrow expressed the CD34, CD22, and HLA-DR antigens [41].

Analytical, diagnostic and therapeutic context of CD34

• In the current studies we demonstrate that human CD34(+)/CD38(-) cells can generate CD45(+)/CD34(-) progeny in a long-term xenograft model and that those CD45(+)/CD34(-) cells can regenerate CD34(+) progeny following secondary transplantation [42].
• An approximately 110 Kd protein can be identified by Western blot analysis with CD34 antibodies in detergent extracts of freshly isolated umbilical vessel endothelial cells, and CD34 mRNA is present in cultured umbilical vein cells as well as other tissues rich in vascular endothelium (breast, placenta) [25].
• Electron microscopy of umbilical artery, breast, and kidney capillary vessels reveals that in all three sites, CD34 molecules are concentrated on membrane processes, many of which interdigitate between adjacent endothelial cells [25].
• We show here that highly purified CD34++ Lineage marker-negative (CD34++Lin-) UCB cells generate T, natural killer (NK), and dendritic cells in a severe combined immunodeficient mouse fetal thymus organ culture (FTOC) [43].
• EPCs labeled with CD34, CD133, and vascular endothelial growth factor receptor-2 (VEGFR2) antibodies were counted by flow cytometry in the peripheral blood of 53 NSCLC patients [44].

References